Journal articles on the topic 'Executor genes'
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1
Ji, Zhiyuan, Wei Guo, Xifeng Chen, Chunlian Wang, and Kaijun Zhao. "Plant Executor Genes." International Journal of Molecular Sciences 23, no. 3 (January 28, 2022): 1524. http://dx.doi.org/10.3390/ijms23031524.
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Executor (E) genes comprise a new type of plant resistance (R) genes, identified from host–Xanthomonas interactions. The Xanthomonas-secreted transcription activation-like effectors (TALEs) usually function as major virulence factors, which activate the expression of the so-called “susceptibility” (S) genes for disease development. This activation is achieved via the binding of the TALEs to the effector-binding element (EBE) in the S gene promoter. However, host plants have evolved EBEs in the promoters of some otherwise silent R genes, whose expression directly causes a host cell death that is characterized by a hypersensitive response (HR). Such R genes are called E genes because they trap the pathogen TALEs in order to activate expression, and the resulting HR prevents pathogen growth and disease development. Currently, deploying E gene resistance is becoming a major component in disease resistance breeding, especially for rice bacterial blight resistance. Currently, the biochemical mechanisms, or the working pathways of the E proteins, are still fuzzy. There is no significant nucleotide sequence homology among E genes, although E proteins share some structural motifs that are probably associated with the signal transduction in the effector-triggered immunity. Here, we summarize the current knowledge regarding TALE-type avirulence proteins, E gene activation, the E protein structural traits, and the classification of E genes, in order to sharpen our understanding of the plant E genes.
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Wang, Jun, Dongsheng Tian, Keyu Gu, Xiaobei Yang, Lanlan Wang, Xuan Zeng, and Zhongchao Yin. "Induction of Xa10-like Genes in Rice Cultivar Nipponbare Confers Disease Resistance to Rice Bacterial Blight." Molecular Plant-Microbe Interactions® 30, no. 6 (June 2017): 466–77. http://dx.doi.org/10.1094/mpmi-11-16-0229-r.
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Bacterial blight of rice, caused by Xanthomonas oryzae pv. oryzae, is one of the most destructive bacterial diseases throughout the major rice-growing regions in the world. The rice disease resistance (R) gene Xa10 confers race-specific disease resistance to X. oryzae pv. oryzae strains that deliver the corresponding transcription activator-like (TAL) effector AvrXa10. Upon bacterial infection, AvrXa10 binds specifically to the effector binding element in the promoter of the R gene and activates its expression. Xa10 encodes an executor R protein that triggers hypersensitive response and activates disease resistance. ‘Nipponbare’ rice carries two Xa10-like genes in its genome, of which one is the susceptible allele of the Xa23 gene, a Xa10-like TAL effector-dependent executor R gene isolated recently from ‘CBB23’ rice. However, the function of the two Xa10-like genes in disease resistance to X. oryzae pv. oryzae strains has not been investigated. Here, we designated the two Xa10-like genes as Xa10-Ni and Xa23-Ni and characterized their function for disease resistance to rice bacterial blight. Both Xa10-Ni and Xa23-Ni provided disease resistance to X. oryzae pv. oryzae strains that deliver the matching artificially designed TAL effectors (dTALE). Transgenic rice plants containing Xa10-Ni and Xa23-Ni under the Xa10 promoter provided specific disease resistance to X. oryzae pv. oryzae strains that deliver AvrXa10. Xa10-Ni and Xa23-Ni knock-out mutants abolished dTALE-dependent disease resistance to X. oryzae pv. oryzae. Heterologous expression of Xa10-Ni and Xa23-Ni in Nicotiana benthamiana triggered cell death. The 19-amino-acid residues at the N-terminal regions of XA10 or XA10-Ni are dispensable for their function in inducing cell death in N. benthamiana and the C-terminal regions of XA10, XA10-Ni, and XA23-Ni are interchangeable among each other without affecting their function. Like XA10, both XA10-Ni and XA23-Ni locate to the endoplasmic reticulum (ER) membrane, show self-interaction, and induce ER Ca2+ depletion in leaf cells of N. benthamiana. The results indicate that Xa10-Ni and Xa23-Ni in Nipponbare encode functional executor R proteins, which induce cell death in both monocotyledonous and dicotyledonous plants and have the potential of being engineered to provide broad-spectrum disease resistance to plant-pathogenic Xanthomonas spp.
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Liu, Zhiquan, Yujun Zhu, Huanbin Shi, Jiehua Qiu, Xinhua Ding, and Yanjun Kou. "Recent Progress in Rice Broad-Spectrum Disease Resistance." International Journal of Molecular Sciences 22, no. 21 (October 28, 2021): 11658. http://dx.doi.org/10.3390/ijms222111658.
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Rice is one of the most important food crops in the world. However, stable rice production is constrained by various diseases, in particular rice blast, sheath blight, bacterial blight, and virus diseases. Breeding and cultivation of resistant rice varieties is the most effective method to control the infection of pathogens. Exploitation and utilization of the genetic determinants of broad-spectrum resistance represent a desired way to improve the resistance of susceptible rice varieties. Recently, researchers have focused on the identification of rice broad-spectrum disease resistance genes, which include R genes, defense-regulator genes, and quantitative trait loci (QTL) against two or more pathogen species or many isolates of the same pathogen species. The cloning of broad-spectrum disease resistance genes and understanding their underlying mechanisms not only provide new genetic resources for breeding broad-spectrum rice varieties, but also promote the development of new disease resistance breeding strategies, such as editing susceptibility and executor R genes. In this review, the most recent advances in the identification of broad-spectrum disease resistance genes in rice and their application in crop improvement through biotechnology approaches during the past 10 years are summarized.
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Ji, Zhiyuan, Hongda Sun, Yena Wei, Man Li, Hongjie Wang, Jiangmin Xu, Cailin Lei, Chunlian Wang, and Kaijun Zhao. "Ectopic Expression of Executor Gene Xa23 Enhances Resistance to Both Bacterial and Fungal Diseases in Rice." International Journal of Molecular Sciences 23, no. 12 (June 11, 2022): 6545. http://dx.doi.org/10.3390/ijms23126545.
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Bacterial blight (BB) and bacterial leaf streak (BLS), caused by phytopathogenic bacteria Xanthomonas oryzae pv. oryzae (Xoo) and Xanthomonas oryzae pv. oryzicola (Xoc), respectively, are the most serious bacterial diseases of rice, while blast, caused by Magnaporthe oryzae (M. oryzae), is the most devastating fungal disease in rice. Generating broad-spectrum resistance to these diseases is one of the key approaches for the sustainable production of rice. Executor (E) genes are a unique type of plant resistance (R) genes, which can specifically trap transcription activator-like effectors (TALEs) of pathogens and trigger an intense defense reaction characterized by a hypersensitive response in the host. This strong resistance is a result of programed cell death induced by the E gene expression that is only activated upon the binding of a TALE to the effector-binding element (EBE) located in the E gene promoter during the pathogen infection. Our previous studies revealed that the E gene Xa23 has the broadest and highest resistance to BB. To investigate whether the Xa23-mediated resistance is efficient against Xanthomonas oryzae pv. oryzicola (Xoc), the causal agent of BLS, we generated a new version of Xa23, designated as Xa23p1.0, to specifically trap the conserved TALEs from multiple Xoc strains. The results showed that the Xa23p1.0 confers broad resistance against both BB and BLS in rice. Moreover, our further experiment on the Xa23p1.0 transgenic plants firstly demonstrated that the E-gene-mediated defensive reaction is also effective against M. oryzae, the causal agent of the most devastating fungal disease in rice. Our current work provides a new strategy to exploit the full potential of the E-gene-mediated disease resistance in rice.
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Yang, Xu, Kai Chen, Yaohui Wang, Dehong Yang, and Yongping Huang. "The Sex Determination Cascade in the Silkworm." Genes 12, no. 2 (February 23, 2021): 315. http://dx.doi.org/10.3390/genes12020315.
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In insects, sex determination pathways involve three levels of master regulators: primary signals, which determine the sex; executors, which control sex-specific differentiation of tissues and organs; and transducers, which link the primary signals to the executors. The primary signals differ widely among insect species. In Diptera alone, several unrelated primary sex determiners have been identified. However, the doublesex (dsx) gene is highly conserved as the executor component across multiple insect orders. The transducer level shows an intermediate level of conservation. In many, but not all examined insects, a key transducer role is performed by transformer (tra), which controls sex-specific splicing of dsx. In Lepidoptera, studies of sex determination have focused on the lepidopteran model species Bombyx mori (the silkworm). In B. mori, the primary signal of sex determination cascade starts from Fem, a female-specific PIWI-interacting RNA, and its targeting gene Masc, which is apparently specific to and conserved among Lepidoptera. Tra has not been found in Lepidoptera. Instead, the B. mori PSI protein binds directly to dsx pre-mRNA and regulates its alternative splicing to produce male- and female-specific transcripts. Despite this basic understanding of the molecular mechanisms underlying sex determination, the links among the primary signals, transducers and executors remain largely unknown in Lepidoptera. In this review, we focus on the latest findings regarding the functions and working mechanisms of genes involved in feminization and masculinization in Lepidoptera and discuss directions for future research of sex determination in the silkworm.
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Kibriya, Muhammad G., Maruf Raza, Mohammed Kamal, Zahidul Haq, Rupash Paul, Andrew Mareczko, Brandon L. Pierce, Habibul Ahsan, and Farzana Jasmine. "Relative Telomere Length Change in Colorectal Carcinoma and Its Association with Tumor Characteristics, Gene Expression and Microsatellite Instability." Cancers 14, no. 9 (April 30, 2022): 2250. http://dx.doi.org/10.3390/cancers14092250.
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We compared tumor and adjacent normal tissue samples from 165 colorectal carcinoma (CRC) patients to study change in relative telomere length (RTL) and its association with different histological and molecular features. To measure RTL, we used a Luminex-based assay. We observed shorter RTL in the CRC tissue compared to paired normal tissue (RTL 0.722 ± SD 0.277 vs. 0.809 ± SD 0.242, p = 0.00012). This magnitude of RTL shortening (by ~0.08) in tumor tissue is equivalent to RTL shortening seen in human leukocytes over 10 years of aging measured by the same assay. RTL was shorter in cancer tissue, irrespective of age group, gender, tumor pathology, location and microsatellite instability (MSI) status. RTL shortening was more prominent in low-grade CRC and in the presence of microsatellite instability (MSI). In a subset of patients, we also examined differential gene expression of (a) telomere-related genes, (b) genes in selected cancer-related pathways and (c) genes at the genome-wide level in CRC tissues to determine the association between gene expression and RTL changes. RTL shortening in CRC was associated with (a) upregulation of DNA replication genes, cyclin dependent-kinase genes (anti-tumor suppressor) and (b) downregulation of “caspase executor”, reducing apoptosis.
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Read, Andrew C., Mathilde Hutin, Matthew J. Moscou, Fabio C. Rinaldi, and Adam J. Bogdanove. "Cloning of the Rice Xo1 Resistance Gene and Interaction of the Xo1 Protein with the Defense-Suppressing Xanthomonas Effector Tal2h." Molecular Plant-Microbe Interactions® 33, no. 10 (October 2020): 1189–95. http://dx.doi.org/10.1094/mpmi-05-20-0131-sc.
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The Xo1 locus in the heirloom rice variety Carolina Gold Select confers resistance to bacterial leaf streak and bacterial blight, caused by Xanthomonas oryzae pv. oryzicola and X. oryzae pv. oryzae, respectively. Resistance is triggered by pathogen-delivered transcription activator-like effectors (TALEs) independent of their ability to activate transcription and is suppressed by truncated variants called truncTALEs, common among Asian strains. By transformation of the susceptible variety Nipponbare, we show that one of 14 nucleotide-binding, leucine-rich repeat (NLR) protein genes at the locus, with a zinc finger BED domain, is the Xo1 gene. Analyses of published transcriptomes revealed that the Xo1-mediated response is more similar to those mediated by two other NLR resistance genes than it is to the response associated with TALE-specific transcriptional activation of the executor resistance gene Xa23 and that a truncTALE dampens or abolishes activation of defense-associated genes by Xo1. In Nicotiana benthamiana leaves, fluorescently tagged Xo1 protein, like TALEs and truncTALEs, localized to the nucleus. And endogenous Xo1 specifically coimmunoprecipitated from rice leaves with a pathogen-delivered, epitope-tagged truncTALE. These observations suggest that suppression of Xo1-function by truncTALEs occurs through direct or indirect physical interaction. They further suggest that effector coimmunoprecipitation may be effective for identifying or characterizing other resistance genes.
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Xie, Zhen, Bingxiao Yan, Jianyao Shou, Jun Tang, Xin Wang, Keran Zhai, Jiyun Liu, et al. "A nucleotide-binding site-leucine-rich repeat receptor pair confers broad-spectrum disease resistance through physical association in rice." Philosophical Transactions of the Royal Society B: Biological Sciences 374, no. 1767 (January 14, 2019): 20180308. http://dx.doi.org/10.1098/rstb.2018.0308.
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Rice blast caused by Magnaporthe oryzae is the most destructive fungal disease in crops, greatly threatening rice production and food security worldwide. The identification and utilization of broad-spectrum resistance genes are considered to be the most economic and effective method to control the disease. In the past decade, many blast resistance ( R ) genes have been identified, which mainly encode nucleotide-binding leucine-rich repeat (NLR) receptor family and confer limited race-specific resistance to the fungal pathogen. Resistance genes conferring broad-spectrum blast resistance are still largely lacking. In this study, we carried out a map-based cloning of the new blast R locus Pizh in variety ZH11. A bacterial artificial chromosome (BAC) clone of 165 kb spanning the Pizh locus was sequenced and identified 9 NLR genes, among which only Pizh-1 and Pizh-2 were expressed. Genetic complementation experiments indicated that Pizh-1 but not Pizh-2 alone could confer blast resistance. Intriguingly, both mutations on Pizh-1 and Pizh-2 by CRISPR-Cas9 abolished the Pizh- mediated resistance. We also observed that Pizh-1 -mediated resistance was partially dependent on Pizh-2 . Pizh-1 and Pizh-2 form a complex of NLRs through direct interaction. This suggests that Pizh-1 may function as the executor NLR and Pizh-2 as a ‘helper’ NLR that shares functional redundancy with other NLRs. Our current study provides not only a good tool for rice disease resistance breeding but also deep insight into NLR association and function in plant immunity. This article is part of the theme issue ‘Biotic signalling sheds light on smart pest management’.
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Mihailovic, Smiljana, Vesna Coric, Tanja Radic, Ana Savic Radojevic, Marija Matic, Dejan Dragicevic, Milica Djokic, et al. "The Association of Polymorphisms in Nrf2 and Genes Involved in Redox Homeostasis in the Development and Progression of Clear Cell Renal Cell Carcinoma." Oxidative Medicine and Cellular Longevity 2021 (April 17, 2021): 1–15. http://dx.doi.org/10.1155/2021/6617969.
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Deleterious effects of SNPs found in genes encoding transcriptional factors, as well as antioxidant and detoxification enzymes, are disputable; however, their functional significance seems to modify the risk for clear cell renal cell carcinoma (ccRCC) development and progression. We investigated the effect of specific Nrf2, SOD2, GPX1 gene variants and GSTP1ABCD haplotype on ccRCC risk and prognosis and evaluated the association between GSTP1 and regulatory (JNK1/2) and executor (caspase-3) apoptotic molecule expression in ccRCC tissue samples and the presence of GSTP1 : JNK1/2 protein : protein interactions. Genotyping was performed in 223 ccRCC patients and 336 matched controls by PCR-CTTP and qPCR. Protein expression was analyzed using immunoblot, while the existence of GSTP1 : JNK1 protein : protein interactions was investigated by immunoprecipitation experiments. An increased risk of ccRCC development was found among carriers of variant genotypes of both SOD2 rs4880 and GSTP1 rs1695 polymorphisms. Nrf2 rs6721961 genetic polymorphism in combination with both rs4880 and rs1695 showed higher ccRCC risk as well. Haplotype analysis revealed significant risk of ccRCC development in carriers of the GSTP1C haplotype. Furthermore, GSTP1 variant forms seem to affect the overall survival in ccRCC patients, and the proposed molecular mechanism underlying the GSTP1 prognostic role might be the presence of GSTP1 : JNK1/2 protein : protein interactions.
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Madaro, Luca, Valeria Marrocco, Piera Fiore, Paola Aulino, Piera Smeriglio, Sergio Adamo, Mario Molinaro, and Marina Bouché. "PKCθ signaling is required for myoblast fusion by regulating the expression of caveolin-3 and β1D integrin upstream focal adhesion kinase." Molecular Biology of the Cell 22, no. 8 (April 15, 2011): 1409–19. http://dx.doi.org/10.1091/mbc.e10-10-0821.
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Fusion of mononucleated myoblasts to form multinucleated myofibers is an essential phase of skeletal myogenesis, which occurs during muscle development as well as during postnatal life for muscle growth, turnover, and regeneration. Many cell adhesion proteins, including integrins, have been shown to be important for myoblast fusion in vertebrates, and recently focal adhesion kinase (FAK), has been proposed as a key mediator of myoblast fusion. Here we focused on the possible role of PKCθ, the PKC isoform predominantly expressed in skeletal muscle, in myoblast fusion. We found that the expression of PKCθ is strongly up-regulated following freeze injury–induced muscle regeneration, as well as during in vitro differentiation of satellite cells (SCs; the muscle stem cells). Using both PKCθ knockout and muscle-specific PKCθ dominant-negative mutant mouse models, we observed delayed body and muscle fiber growth during the first weeks of postnatal life, when compared with wild-type (WT) mice. We also found that myofiber formation, during muscle regeneration after freeze injury, was markedly impaired in PKCθ mutant mice, as compared with WT. This phenotype was associated with reduced expression of the myogenic differentiation program executor, myogenin, but not with that of the SC marker Pax7. Indeed in vitro differentiation of primary muscle-derived SCs from PKCθ mutants resulted in the formation of thinner myotubes with reduced numbers of myonuclei and reduced fusion rate, when compared with WT cells. These effects were associated to reduced expression of the profusion genes caveolin-3 and β1D integrin and to reduced activation/phosphorylation of their up-stream regulator FAK. Indeed the exogenous expression of a constitutively active mutant form of PKCθ in muscle cells induced FAK phosphorylation. Moreover pharmacologically mediated full inhibition of FAK activity led to similar fusion defects in both WT and PKCθ-null myoblasts. We thus propose that PKCθ signaling regulates myoblast fusion by regulating, at least in part, FAK activity, essential for profusion gene expression.
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Xagorari, Angeliki, Sarantis Tsetsakos, Zoi Katana, Konstantinos Krikonis, Anastasia Kouvatsi, Katerina Chlichlia, Achilles Anagnostopoulos, and Damianos Sotiropoulos. "CD34+ Derived Microparticles Regulate Apoptosis in Normal and Acute Myeloid Leukemia Cells." Blood 132, Supplement 1 (November 29, 2018): 5090. http://dx.doi.org/10.1182/blood-2018-99-114425.
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Abstract Introduction Microparticles (MPs) are small vesicles 100nm-1μm derived from the apoptotic or stimulated cells. The mechanism of their production is distinctive from exosomes or apoptotic bodies. MPs have been detected in the blood in many pathological conditions associated mainly with endothelial injury, thrombosis and inflammation. Our previous study showed that MPs originated also from CD34+ cells of umbilical cord blood, which is an alternative source for hemopoeitic stem cell transplantation. MPs considered as markers of cell activation, as well as apoptosis. Apoptosis is a complex interaction network regulated either through death receptor like FAS or through the internal pathway of Bcl2, Bax. The two pathways activate the executor of cell death program, caspases. The aim of this study is to elucidate the role of MPs in apoptosis of hemopoietic cells. Methods Umbilical cord blood units (UCB) were collected after informed consent. The units that were used in this study, were rejected as not appropriate for transplantation due to low volume. The HL60 promyelocytic leukemia cell line was cultured in RPMI (Life Technologies) supplemented with 10% fetal calf serum (FCS) and 1% penicillin-strepromycin. CD34+ MPs were isolated from the plasma of UCBs after centrifugation and magnetic bead MACS purification (Miltenyi Biotec). The number of CD34+ MPs was estimated by flow cytometry using CD34-PE and Annexin V-FITC Abs. Mononuclear cells (MNC) were collected after density gradient centrifugation on lymphoprep (Fresenius) and were cultured for 3 and 6 days in the presence of CD34+ MPs. Viability assays were performed using 7-AAD in flow cytometry. In another set of experiments different numbers of CD34+ MPs were used in MNC cultures. RNA was extracted from MNC using Qiagen RNA extraction kit and reverse transcribed into cDNA using Superscript II reverse transcriptase (Invitrogen) with random primers (Promega). RT-PCR was performed using Platinum Pfx polymerase (Invitrogen). The primers for FAS, BCL2, BAX, caspase 3, survivin and GAPDH genes were used. The PCR products were analysed in an agarose gel electrophoresis. Results Cell viability increased in UCB derived MNC (UCB-MNC) incubated with CD34+ MPs (800 /ml) after 3 day vs. 6 days of culture. The UCB-MNC viability was higher using 800/ml CD34+ MPs vs. 400/ml. In contrast, CD34+ MPs (800 /ml vs. 400/ml) did not affect the viability in one day MNC culture. Purified CD34+ MPs were applied to UCB-MNC cultures and by RT-PCR was shown increased expression of BCL2 gene as well as FAS and caspase-3 genes. The promyelocytc cell line HL60 has been used in order to analyze the effect of CD34+ MPs in leukemic cells. The expression of Bcl2 was decreased in HL60 cells co-incubated with CD34+ MPs. This result shows an opposite effect of CD34+ MPs in the apoptotic gene Bcl2 for the HL60 cells indicating that there are different mechanisms of MP function in various cell types. Conclusions In this study we have identified and monitored the time- and dose-dependent effect of CD34-derived microparticles in the viability of UCB mononuclear cells. Additionally, CD34+ MPs function is accosiated with the high expression of the pro- and anti-apoptotic Bcl2 and apoptotic FAS. In contrast CD34+ MPs decreases the expression of Bcl2 in the promyelocytic leukemia cell line HL60. Therefore the stem cell derived microparticles might serve as a potential regulator of apoptosis in normal and malignant hematopoietic cells. Disclosures No relevant conflicts of interest to declare.
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Frey, Patrick, Antoine Devisme, Monika Schrempp, Geoffroy Andrieux, Melanie Boerries, and Andreas Hecht. "Canonical BMP Signaling Executes Epithelial-Mesenchymal Transition Downstream of SNAIL1." Cancers 12, no. 4 (April 21, 2020): 1019. http://dx.doi.org/10.3390/cancers12041019.
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Epithelial-mesenchymal transition (EMT) is a pivotal process in development and disease. In carcinogenesis, various signaling pathways are known to trigger EMT by inducing the expression of EMT transcription factors (EMT-TFs) like SNAIL1, ultimately promoting invasion, metastasis and chemoresistance. However, how EMT is executed downstream of EMT-TFs is incompletely understood. Here, using human colorectal cancer (CRC) and mammary cell line models of EMT, we demonstrate that SNAIL1 critically relies on bone morphogenetic protein (BMP) signaling for EMT execution. This activity requires the transcription factor SMAD4 common to BMP/TGFβ pathways, but is TGFβ signaling-independent. Further, we define a signature of BMP-dependent genes in the EMT-transcriptome, which orchestrate EMT-induced invasiveness, and are found to be regulated in human CRC transcriptomes and in developmental EMT processes. Collectively, our findings substantially augment the knowledge of mechanistic routes whereby EMT can be effectuated, which is relevant for the conceptual understanding and therapeutic targeting of EMT processes.
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Ramasubramanian, Abilasha. "FASTK family of genes linked to cancer." Bioinformation 18, no. 3 (March 31, 2022): 206–13. http://dx.doi.org/10.6026/97320630018206.
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Fas Activated Serine/Threonine Kinase (FASTK) family is a protein family encoded in the nuclear genome that spans the mitochondria and executes numerous functions, and consists of FASTK, the founding member along with 5 homologous proteins FASTKD1-5. Up regulation of FASTK family members have not only been implicated in tumour progression and invasion but also in increased resistance to chemotherapy proven by their knockdown leading to increased sensitivity to drugs. Thus, this review reports the implication of FASTK proteins in cancer and hence provides a scope to emphasise the role of these proteins in Oral Cancer.
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Agafonov, Aleksandr, Kimmo Mattila, Cuong Duong Tuan, Lars Tiede, Inge Alexander Raknes, and Lars Ailo Bongo. "META-pipe cloud setup and execution." F1000Research 6 (November 29, 2017): 2060. http://dx.doi.org/10.12688/f1000research.13204.1.
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META-pipe is a complete service for the analysis of marine metagenomic data. It provides assembly of high-throughput sequence data, functional annotation of predicted genes, and taxonomic profiling. The functional annotation is computationally demanding and is therefore currently run on a high-performance computing cluster in Norway. However, additional compute resources are necessary to open the service to all ELIXIR users. We describe our approach for setting up and executing the functional analysis of META-pipe on additional academic and commercial clouds. Our goal is to provide a powerful analysis service that is easy to use and to maintain. Our design therefore uses a distributed architecture where we combine central servers with multiple distributed backends that execute the computationally intensive jobs. We believe our experiences developing and operating META-pipe provides a useful model for others that plan to provide a portal based data analysis service in ELIXIR and other organizations with geographically distributed compute and storage resources.
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Agafonov, Aleksandr, Kimmo Mattila, Cuong Duong Tuan, Lars Tiede, Inge Alexander Raknes, and Lars Ailo Bongo. "META-pipe cloud setup and execution." F1000Research 6 (January 18, 2018): 2060. http://dx.doi.org/10.12688/f1000research.13204.2.
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META-pipe is a complete service for the analysis of marine metagenomic data. It provides assembly of high-throughput sequence data, functional annotation of predicted genes, and taxonomic profiling. The functional annotation is computationally demanding and is therefore currently run on a high-performance computing cluster in Norway. However, additional compute resources are necessary to open the service to all ELIXIR users. We describe our approach for setting up and executing the functional analysis of META-pipe on additional academic and commercial clouds. Our goal is to provide a powerful analysis service that is easy to use and to maintain. Our design therefore uses a distributed architecture where we combine central servers with multiple distributed backends that execute the computationally intensive jobs. We believe our experiences developing and operating META-pipe provides a useful model for others that plan to provide a portal based data analysis service in ELIXIR and other organizations with geographically distributed compute and storage resources.
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Agafonov, Aleksandr, Kimmo Mattila, Cuong Duong Tuan, Lars Tiede, Inge Alexander Raknes, and Lars Ailo Bongo. "META-pipe cloud setup and execution." F1000Research 6 (May 2, 2019): 2060. http://dx.doi.org/10.12688/f1000research.13204.3.
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META-pipe is a complete service for the analysis of marine metagenomic data. It provides assembly of high-throughput sequence data, functional annotation of predicted genes, and taxonomic profiling. The functional annotation is computationally demanding and is therefore currently run on a high-performance computing cluster in Norway. However, additional compute resources are necessary to open the service to all ELIXIR users. We describe our approach for setting up and executing the functional analysis of META-pipe on additional academic and commercial clouds. Our goal is to provide a powerful analysis service that is easy to use and to maintain. Our design therefore uses a distributed architecture where we combine central servers with multiple distributed backends that execute the computationally intensive jobs. We believe our experiences developing and operating META-pipe provides a useful model for others that plan to provide a portal based data analysis service in ELIXIR and other organizations with geographically distributed compute and storage resources.
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Rantong, Gaolathe, and Arunika H. L. A. N. Gunawardena. "Programmed cell death: genes involved in signaling, regulation, and execution in plants and animals." Botany 93, no. 4 (April 2015): 193–210. http://dx.doi.org/10.1139/cjb-2014-0152.
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Programmed cell death (PCD) is a suicide mechanism adopted by multicellular organisms that is essential for development and resistance to different forms of stress. In plants, PCD is involved from embryogenesis to death of the whole plant. PCD is genetically regulated and the molecular pathways involved in different forms of this process in animals are relatively more understood than in plants. At the morphological level, apoptosis, one of the forms of PCD in animals, and plant PCD have some similarities such as cell shrinkage, shrinkage of the nucleus, and DNA fragmentation. Because morphological characteristics are a product of the genetically encoded PCD mechanism, it is of interest to figure out how much of the apoptotic pathway is shared with plant PCD in terms of the genes involved. Evidence of some level of similarities has been gathered in the last decade, supporting conservation during signaling, regulation, and execution of apoptosis and plant PCD. A continued search into the genomes of plants has provided insights about homologues of apoptosis genes present in plants, and functional analysis provides evidence about which genes are carrying out similar roles during apoptosis and plant PCD. This review is aimed at updating on the progress of plant PCD mechanism research and highlighting some of the similarities and differences between plant and mammalian PCD mechanisms, with special focus on the commonalities.
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Nakata, Yuichiro, Norimasa Yamasaki, Takeshi Ueda, Kenichiro Ikeda, Akiko Nagamachi, Toshiya Inaba, and Hiroaki Honda. "JMJD3 Plays Essential Roles in the Maintenance of Hematopoietic Stem Cells and Leukemic Stem Cells through the Regulation of p16INK4a." Blood 128, no. 22 (December 2, 2016): 2653. http://dx.doi.org/10.1182/blood.v128.22.2653.2653.
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Abstract Hematopoiesis is a complex process that involves the interplay between lineage-specific transcription and epigenetic regulation, including histone modifications. Tri-methylation of histone H3 at Lys27 (H3K27me3) is an epigenetic mark for transcriptional repression. Jumonji domain-containing 3 (JMJD3) acts as a histone demethylase for H3K27 and contributes to various cellular processes including senescence and differentiation through transcriptional regulation. In the hematopoietic system, JMJD3 has been reported to be required for M2 macrophage development and terminal thymocyte differentiation. However, the roles of JMJD3 in normal hematopoiesis and leukemogenesis are still largely elusive. To address this issue, we generated pIpC-inducible Jmjd3 conditional KO (cKO) mice. Jmjd3-deficient (Jmjd3Δ/Δ) mice grew healthy and did not show obvious hematopoietic abnormalities, except a slight decrease of myeloid cells. To investigate the role of JMJD3in hematopoietic stem cell (HSC) function, a competitive repopulation assay was performed using control and Jmjd3Δ/Δ HSCs. The results showed that the chimerism of Jmjd3Δ/Δ cells was significantly decreased compared with that of control cells in all the hematopoietic lineages, indicating that JMJD3 is essential for long-term repopulating ability of HSCs. To further investigate the effect of Jmjd3 deletion in leukemogenesis, c-kit+ bone marrow (BM) cells from control and Jmjd3 cKO mice were transduced with MLL-AF9 fusion protein that rapidly induces acute leukemia. L-GMPs (the fraction containing leukemic stem cells (LSCs)) were sorted from MLL-AF9-transduced BM cells and subjected to colony replating and bone marrow transplantation (BMT) assays. In contrast control L-GMPs that continued to form colonies after multiple rounds of replating, Jmjd3Δ/Δ L-GMPs ceased to proliferate after third rounds of replating. In addition, recipients transplanted with Jmjd3Δ/Δ L-GMPs exhibited a significant delay in the onset of leukemia compared with those transplanted with controlL-GMPs. These results indicate that JMJD3 plays essential roles in maintaining stem cell properties not only in normal HSCs but also in LSCs. We next investigated underlying molecular mechanisms. Previous studies demonstrated the INK4a/ARF locus, a key executor of cellular senescence, is regulated by JMJD3. Thus, we examined whether JMJD3 regulates INK4a/ARF locus in hematopoietic cells under proliferative and oncogenic stresses. We found that enforced expression of Jmjd3 in in vitro-cultured and cytokine-stimulated hematopoietic stem-progenitor cells (HSPCs) significantly upregulated the expression of p16INK4a compared with control cells. In addition, transformation of HSPCs by MLL-AF9 induced expression of Jmjd3, but not other H3K27me3-related genes, such as Utx and EZH2, which was accompanied by the upregulation of p16INK4a. In contrast, no obvious expressional change was observed in p19ARF in both cases. In Jmjd3Δ/Δ HSPCs, no upregulation of p16INK4a was detected in HSPCs by cytokine-induced proliferation or MLL-AF9-induced transformation, where H3K27me3 was tightly associated with promoter region of p16INK4a locus. These results strongly suggest that proliferative and oncogenic stresses induces the expression of Jmjd3 in HSPCs, which subsequently upregulates p16INK4a through demethylating H3K27me3 on the p16INK4a promoter and consequently maintains stem cell potential by inhibiting excessive entry into cell cycle. Deficiency of Jmjd3 fails upregulation of p16INK4a, which induces continuous and excessive cell proliferation and finally causes exhaustion of stem cell pool. In conclusion, we propose the idea that JMJD3-p16INK4a axis plays essential roles in maintaining HSC and LSC pool size under proliferative and oncogenic stresses. Disclosures No relevant conflicts of interest to declare.
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ROGOV, SERGEY I., KUVAT T. MOMYNALIEV, and VADIM M. GOVORUN. "COEXPRESSIONFINDER: A NEW ALGORITHM FOR FINDING GROUPS OF COEXPRESSED GENES." Journal of Bioinformatics and Computational Biology 04, no. 04 (August 2006): 853–64. http://dx.doi.org/10.1142/s0219720006002193.
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Results: A new algorithm is developed which is intended to find groups of genes whose expression values change in a concordant manner in a series of experiments with DNA arrays. This algorithm is named as CoexpressionFinder. It can find more complete and internally coordinated groups of gene expression vectors than hierarchical clustering. Also, it finds more genes having coordinated expression. The algorithm's design allows parallel execution. Availability: The algorithm is implemented as a Java application which is freely available at: and .
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Deng, Siqi, Shijie Shen, Saeed El-Ashram, Huan Lu, Dan Luo, Guomin Ye, Zhen feng, et al. "Selecting Hub Genes and Predicting Target Genes of microRNAs in Tuberculosis via the Bioinformatics Analysis." Genetics Research 2021 (October 31, 2021): 1–11. http://dx.doi.org/10.1155/2021/6226291.
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Tuberculosis (TB) is the world's most prevalently infectious disease. Molecular mechanisms behind tuberculosis remain unknown. microRNA (miRNA) is involved in a wide variety of diseases. To validate the significant genes and miRNAs in the current sample, two messenger RNA (mRNA) expression profile datasets and three miRNA expression profile datasets were downloaded from the Gene Expression Omnibus (GEO) database. The differentially expressed (DE) genes (DEGs) and miRNAs (DE miRNAs) between healthy and TB patients were filtered out. Enrichment analysis was executed, and a protein-protein interaction (PPI) network was developed to understand the enrich pathways and hub genes of TB. Additionally, the target genes of miRNA were predicted and overlapping target genes were identified. We studied a total of 181 DEGs (135 downregulated and 46 upregulated genes) and two DE miRNAs (2 downregulated miRNAs) from two gene profile datasets and three miRNA profile datasets, respectively. 10 hub genes were defined based on high degree of connectivity. A PPI network's top module was constructed. The 23 DEGs identified have a significant relationship with miRNAs. 25 critically significant Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were discovered. The detailed study revealed that, in tuberculosis, the DE miRNA and DEGs form an interaction network. The identification of novel target genes and main pathways would aid with our understanding of miRNA's function in tuberculosis progression.
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Ishii, Hideshi, Andrea Vecchione, Yusuke Furukawa, Carlo M. Croce, Kay Huebner, and Louise YY Fong. "Differentially expressed genes execute zinc-induced apoptosis in precancerous esophageal epithelium of zinc-deficient rats." Oncogene 23, no. 49 (September 13, 2004): 8040–48. http://dx.doi.org/10.1038/sj.onc.1207974.
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Seo, Jong Bae, Hyang Mi Moon, Woo Sik Kim, Yun Sok Lee, Hyun Woo Jeong, Eung Jae Yoo, Jungyeob Ham, et al. "Activated Liver X Receptors Stimulate Adipocyte Differentiation through Induction of Peroxisome Proliferator-Activated Receptor γ Expression." Molecular and Cellular Biology 24, no. 8 (April 15, 2004): 3430–44. http://dx.doi.org/10.1128/mcb.24.8.3430-3444.2004.
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ABSTRACT Liver X receptors (LXRs) are nuclear hormone receptors that regulate cholesterol and fatty acid metabolism in liver tissue and in macrophages. Although LXR activation enhances lipogenesis, it is not well understood whether LXRs are involved in adipocyte differentiation. Here, we show that LXR activation stimulated the execution of adipogenesis, as determined by lipid droplet accumulation and adipocyte-specific gene expression in vivo and in vitro. In adipocytes, LXR activation with T0901317 primarily enhanced the expression of lipogenic genes such as the ADD1/SREBP1c and FAS genes and substantially increased the expression of the adipocyte-specific genes encoding PPARγ (peroxisome proliferator-activated receptor γ) and aP2. Administration of the LXR agonist T0901317 to lean mice promoted the expression of most lipogenic and adipogenic genes in fat and liver tissues. It is of interest that the PPARγ gene is a novel target gene of LXR, since the PPARγ promoter contains the conserved binding site of LXR and was transactivated by the expression of LXRα. Moreover, activated LXRα exhibited an increase of DNA binding to its target gene promoters, such as ADD1/SREBP1c and PPARγ, which appeared to be closely associated with hyperacetylation of histone H3 in the promoter regions of those genes. Furthermore, the suppression of LXRα by small interfering RNA attenuated adipocyte differentiation. Taken together, these results suggest that LXR plays a role in the execution of adipocyte differentiation by regulation of lipogenesis and adipocyte-specific gene expression.
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Sheng, Minjie, Haiying Cai, Ming Cheng, Jing Li, Jian Zhang, and Lihua Liu. "Identification of Novel Choroidal Neovascularization-Related Genes Using Laplacian Heat Diffusion Algorithm." BioMed Research International 2021 (September 6, 2021): 1–10. http://dx.doi.org/10.1155/2021/2295412.
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Choroidal neovascularization (CNV) is a type of eye disease that can cause vision loss. In recent years, many studies have attempted to investigate the major pathological processes and molecular pathogenic mechanisms of CNV. Because many diseases are related to genes, the genes associated with CNV need to be identified. In this study, we proposed a network-based approach for identifying novel CNV-associated genes. To execute such method, we first employed a protein-protein interaction network reported in STRING. Then, we applied a network diffusion algorithm, Laplacian heat diffusion, on this network by selecting validated CNV-related genes as the seed nodes. As a result, some novel genes that had unknown but strong relationships with validated genes were identified. Furthermore, we used a screening procedure to extract the most essential genes. Eleven latent CNV-related genes were finally obtained. Extensive analyses were performed to confirm that these genes are novel CNV-related genes.
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Ma, Liang-Xiao, Ya-Jun Wang, Jing-Fang Wang, Xuan Li, and Pei Hao. "Expression Sensitivity Analysis of Human Disease Related Genes." BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/637424.
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Background. Genome-wide association studies (GWAS) have shown its revolutionary power in seeking the influenced loci on complex diseases genetically. Thousands of replicated loci for common traits are helpful in diseases risk assessment. However it is still difficult to elucidate the variations in these loci that directly cause susceptibility to diseases by disrupting the expression or function of a protein currently.Results. We evaluate the expression features of disease related genes and find that different diseases related genes show different expression perturbation sensitivities in various conditions. It is worth noting that the expression of some robust disease-genes doesn’t show significant change in their corresponding diseases, these genes might be easily ignored in the expression profile analysis.Conclusion. Gene ontology enrichment analysis indicates that robust disease-genes execute essential function in comparison with sensitive disease-genes. The diseases associated with robust genes seem to be relatively lethal like cancer and aging. On the other hand, the diseases associated with sensitive genes are apparently nonlethal like psych and chemical dependency diseases.
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Reilly, Molly B., Tessa Tekieli, Cyril Cros, G. Robert Aguilar, James Lao, Itai Antoine Toker, Berta Vidal, et al. "Widespread employment of conserved C. elegans homeobox genes in neuronal identity specification." PLOS Genetics 18, no. 9 (September 30, 2022): e1010372. http://dx.doi.org/10.1371/journal.pgen.1010372.
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Homeobox genes are prominent regulators of neuronal identity, but the extent to which their function has been probed in animal nervous systems remains limited. In the nematode Caenorhabditis elegans, each individual neuron class is defined by the expression of unique combinations of homeobox genes, prompting the question of whether each neuron class indeed requires a homeobox gene for its proper identity specification. We present here progress in addressing this question by extending previous mutant analysis of homeobox gene family members and describing multiple examples of homeobox gene function in different parts of the C. elegans nervous system. To probe homeobox function, we make use of a number of reporter gene tools, including a novel multicolor reporter transgene, NeuroPAL, which permits simultaneous monitoring of the execution of multiple differentiation programs throughout the entire nervous system. Using these tools, we add to the previous characterization of homeobox gene function by identifying neuronal differentiation defects for 14 homeobox genes in 24 distinct neuron classes that are mostly unrelated by location, function and lineage history. 12 of these 24 neuron classes had no homeobox gene function ascribed to them before, while in the other 12 neuron classes, we extend the combinatorial code of transcription factors required for specifying terminal differentiation programs. Furthermore, we demonstrate that in a particular lineage, homeotic identity transformations occur upon loss of a homeobox gene and we show that these transformations are the result of changes in homeobox codes. Combining the present with past analyses, 113 of the 118 neuron classes of C. elegans are now known to require a homeobox gene for proper execution of terminal differentiation programs. Such broad deployment indicates that homeobox function in neuronal identity specification may be an ancestral feature of animal nervous systems.
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Gloeckner, G., and C. F. Beck. "Genes involved in light control of sexual differentiation in Chlamydomonas reinhardtii." Genetics 141, no. 3 (November 1, 1995): 937–43. http://dx.doi.org/10.1093/genetics/141.3.937.
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Abstract Gamete formation requires the sequential action of two extrinsic cues, nitrogen deprivation and blue light. The mutants described here are specifically altered in the light-dependent step. Mutations lrg1, lrg3, and lrg4 overcome this light dependence while mutation lrg2 results in a delayed execution of the light-mediated step. The four mutations are linked. The recessive nature of the lrg1, lrg3, and lrg4 mutations implies that they encode elements of negative control in this light response pathway. Analyses of diploids suggest an interaction between the gene products of the mutated loci with a central role for lrg4. The lrg4 mutation is unique also because it overcomes the light dependence of Chlamydomonas zygote germination when present in homozygous form. These data indicate that there are common components in the signal chains that control gametogenesis and zygote germination.
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Jensen, Travis L., Michael Frasketi, Kevin Conway, Leigh Villarroel, Heather Hill, Konstantinos Krampis, and Johannes B. Goll. "RSEQREP: RNA-Seq Reports, an open-source cloud-enabled framework for reproducible RNA-Seq data processing, analysis, and result reporting." F1000Research 6 (December 21, 2017): 2162. http://dx.doi.org/10.12688/f1000research.13049.1.
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RNA-Seq is increasingly being used to measure human RNA expression on a genome-wide scale. Expression profiles can be interrogated to identify and functionally characterize treatment-responsive genes. Ultimately, such controlled studies promise to reveal insights into molecular mechanisms of treatment effects, identify biomarkers, and realize personalized medicine. RNA-Seq Reports (RSEQREP) is a new open-source cloud-enabled framework that allows users to execute start-to-end gene-level RNA-Seq analysis on a preconfigured RSEQREP Amazon Virtual Machine Image (AMI) hosted by AWS or on their own Ubuntu Linux machine. The framework works with unstranded, stranded, and paired-end sequence FASTQ files stored locally, on Amazon Simple Storage Service (S3), or at the Sequence Read Archive (SRA). RSEQREP automatically executes a series of customizable steps including reference alignment, CRAM compression, reference alignment QC, data normalization, multivariate data visualization, identification of differentially expressed genes, heatmaps, co-expressed gene clusters, enriched pathways, and a series of custom visualizations. The framework outputs a file collection that includes a dynamically generated PDF report using R, knitr, and LaTeX, as well as publication-ready table and figure files. A user-friendly configuration file handles sample metadata entry, processing, analysis, and reporting options. The configuration supports time series RNA-Seq experimental designs with at least one pre- and one post-treatment sample for each subject, as well as multiple treatment groups and specimen types. All RSEQREP analyses components are built using open-source R code and R/Bioconductor packages allowing for further customization. As a use case, we provide RSEQREP results for a trivalent influenza vaccine (TIV) RNA-Seq study that collected 1 pre-TIV and 10 post-TIV vaccination samples (days 1-10) for 5 subjects and two specimen types (peripheral blood mononuclear cells and B-cells).
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Jensen, Travis L., Michael Frasketi, Kevin Conway, Leigh Villarroel, Heather Hill, Konstantinos Krampis, and Johannes B. Goll. "RSEQREP: RNA-Seq Reports, an open-source cloud-enabled framework for reproducible RNA-Seq data processing, analysis, and result reporting." F1000Research 6 (April 13, 2018): 2162. http://dx.doi.org/10.12688/f1000research.13049.2.
Full textAbstract:
RNA-Seq is increasingly being used to measure human RNA expression on a genome-wide scale. Expression profiles can be interrogated to identify and functionally characterize treatment-responsive genes. Ultimately, such controlled studies promise to reveal insights into molecular mechanisms of treatment effects, identify biomarkers, and realize personalized medicine. RNA-Seq Reports (RSEQREP) is a new open-source cloud-enabled framework that allows users to execute start-to-end gene-level RNA-Seq analysis on a preconfigured RSEQREP Amazon Virtual Machine Image (AMI) hosted by AWS or on their own Ubuntu Linux machine via a Docker container or installation script. The framework works with unstranded, stranded, and paired-end sequence FASTQ files stored locally, on Amazon Simple Storage Service (S3), or at the Sequence Read Archive (SRA). RSEQREP automatically executes a series of customizable steps including reference alignment, CRAM compression, reference alignment QC, data normalization, multivariate data visualization, identification of differentially expressed genes, heatmaps, co-expressed gene clusters, enriched pathways, and a series of custom visualizations. The framework outputs a file collection that includes a dynamically generated PDF report using R, knitr, and LaTeX, as well as publication-ready table and figure files. A user-friendly configuration file handles sample metadata entry, processing, analysis, and reporting options. The configuration supports time series RNA-Seq experimental designs with at least one pre- and one post-treatment sample for each subject, as well as multiple treatment groups and specimen types. All RSEQREP analyses components are built using open-source R code and R/Bioconductor packages allowing for further customization. As a use case, we provide RSEQREP results for a trivalent influenza vaccine (TIV) RNA-Seq study that collected 1 pre-TIV and 10 post-TIV vaccination samples (days 1-10) for 5 subjects and two specimen types (peripheral blood mononuclear cells and B-cells).
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Czyz, Malgorzata, Malgorzata Sztiller-Sikorska, Anna Gajos-Michniewicz, Marta Osrodek, and Mariusz L. Hartman. "Plasticity of Drug-Naïve and Vemurafenib- or Trametinib-Resistant Melanoma Cells in Execution of Differentiation/Pigmentation Program." Journal of Oncology 2019 (July 3, 2019): 1–15. http://dx.doi.org/10.1155/2019/1697913.
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Melanoma plasticity creates a plethora of opportunities for cancer cells to escape treatment. Thus, therapies must target all cancer cell subpopulations bearing the potential to contribute to disease. The role of the differentiation/pigmentation program in intrinsic and acquired drug resistance is largely uncharacterized. MITF level and expression of MITF-dependent pigmentation-related genes, MLANA, PMEL, TYR, and DCT, in drug-naïve and vemurafenib- or trametinib-treated patient-derived melanoma cell lines and their drug-resistant counterparts were analysed and referred to genomic alterations. Variability in execution of pigmentation/differentiation program was detected in patient-derived melanoma cell lines. Acute treatment with vemurafenib or trametinib enhanced expression of pigmentation-related genes in MITF-Mhigh melanoma cells, partially as the consequence of transcriptional reprograming. During development of resistance, changes in pigmentation program were not unidirectional, but also not universal as expression of different pigmentation-related genes was diversely affected. In selected resistant cell lines, differentiation/pigmentation was promoted and might be considered as one of drug-tolerant phenotypes. In other resistant lines, dedifferentiation was induced. Upon drug withdrawal (“drug holiday”), the dedifferentiation process in resistant cells either was enhanced but reversed by drug reexposure suggesting involvement of epigenetic mechanisms or was irreversible. The irreversible dedifferentiation might be connected with homozygous loss-of-function mutation in MC1R, as MC1RR151C +/+ variant was found exclusively in drug-naïve MITF-Mlow dedifferentiated cells and drug-resistant cells derived from MITFhigh/MC1RWT cells undergoing irreversible dedifferentiation. MC1RR151C +/+ variant might be further investigated as a parameter potentially impacting melanoma patient stratification and aiding in treatment decision.
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Coutant, Anthony, Katherine Roper, Daniel Trejo-Banos, Dominique Bouthinon, Martin Carpenter, Jacek Grzebyta, Guillaume Santini, et al. "Closed-loop cycles of experiment design, execution, and learning accelerate systems biology model development in yeast." Proceedings of the National Academy of Sciences 116, no. 36 (August 16, 2019): 18142–47. http://dx.doi.org/10.1073/pnas.1900548116.
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One of the most challenging tasks in modern science is the development of systems biology models: Existing models are often very complex but generally have low predictive performance. The construction of high-fidelity models will require hundreds/thousands of cycles of model improvement, yet few current systems biology research studies complete even a single cycle. We combined multiple software tools with integrated laboratory robotics to execute three cycles of model improvement of the prototypical eukaryotic cellular transformation, the yeast (Saccharomyces cerevisiae) diauxic shift. In the first cycle, a model outperforming the best previous diauxic shift model was developed using bioinformatic and systems biology tools. In the second cycle, the model was further improved using automatically planned experiments. In the third cycle, hypothesis-led experiments improved the model to a greater extent than achieved using high-throughput experiments. All of the experiments were formalized and communicated to a cloud laboratory automation system (Eve) for automatic execution, and the results stored on the semantic web for reuse. The final model adds a substantial amount of knowledge about the yeast diauxic shift: 92 genes (+45%), and 1,048 interactions (+147%). This knowledge is also relevant to understanding cancer, the immune system, and aging. We conclude that systems biology software tools can be combined and integrated with laboratory robots in closed-loop cycles.
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Mikkilineni, Rao. "Information Processing, Information Networking, Cognitive Apparatuses and Sentient Software Systems." Proceedings 47, no. 1 (May 13, 2020): 27. http://dx.doi.org/10.3390/proceedings2020047027.
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In the physical world, computing processes, message communication networks and cognitive apparatuses are the building blocks of sentient beings. Genes and neural networks provide complementary information processing models that enable execution of mechanisms dealing with “life” using physical, chemical and biological processes. A cognizing agent architecture (mind) provides the orchestration of body and the brain to manage the “life” processes to deal with fluctuations and maintain survival and sustenance. We present a new information processing architecture that enables “digital genes” and “digital neurons” with cognizing agent architecture to design and implement sentient, resilient and intelligent systems in the digital world.
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Mikkilineni, Rao. "Information Processing, Information Networking, Cognitive Apparatuses and Sentient Software Systems." Proceedings 47, no. 1 (May 13, 2020): 27. http://dx.doi.org/10.3390/proceedings47010027.
Full textAbstract:
In the physical world, computing processes, message communication networks and cognitive apparatuses are the building blocks of sentient beings. Genes and neural networks provide complementary information processing models that enable execution of mechanisms dealing with “life” using physical, chemical and biological processes. A cognizing agent architecture (mind) provides the orchestration of body and the brain to manage the “life” processes to deal with fluctuations and maintain survival and sustenance. We present a new information processing architecture that enables “digital genes” and “digital neurons” with cognizing agent architecture to design and implement sentient, resilient and intelligent systems in the digital world.
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Findley, Seth D., Melanie R. Mormile, Andrea Sommer-Hurley, Xue-Cheng Zhang, Peter Tipton, Krista Arnett, James H. Porter, Monty Kerley, and Gary Stacey. "Activity-Based Metagenomic Screening and Biochemical Characterization of Bovine Ruminal Protozoan Glycoside Hydrolases." Applied and Environmental Microbiology 77, no. 22 (September 23, 2011): 8106–13. http://dx.doi.org/10.1128/aem.05925-11.
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ABSTRACTThe rumen, the foregut of herbivorous ruminant animals such as cattle, functions as a bioreactor to process complex plant material. Among the numerous and diverse microbes involved in ruminal digestion are the ruminal protozoans, which are single-celled, ciliated eukaryotic organisms. An activity-based screen was executed to identify genes encoding fibrolytic enzymes present in the metatranscriptome of a bovine ruminal protozoan-enriched cDNA expression library. Of the four novel genes identified, two were characterized in biochemical assays. Our results provide evidence for the effective use of functional metagenomics to retrieve novel enzymes from microbial populations that cannot be maintained in axenic cultures.
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van Kessel, Julia C., Steven T. Rutherford, Jian-Ping Cong, Sofia Quinodoz, James Healy, and Bonnie L. Bassler. "Quorum Sensing Regulates the Osmotic Stress Response in Vibrio harveyi." Journal of Bacteriology 197, no. 1 (October 13, 2014): 73–80. http://dx.doi.org/10.1128/jb.02246-14.
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Bacteria use a chemical communication process called quorum sensing to monitor cell density and to alter behavior in response to fluctuations in population numbers. Previous studies withVibrio harveyihave shown that LuxR, the master quorum-sensing regulator, activates and represses >600 genes. These include six genes that encode homologs of theEscherichia coliBet and ProU systems for synthesis and transport, respectively, of glycine betaine, an osmoprotectant used during osmotic stress. Here we show that LuxR activates expression of the glycine betaine operonbetIBA-proXWV, which enhances growth recovery under osmotic stress conditions. BetI, an autorepressor of theV. harveyibetIBA-proXWVoperon, activates the expression of genes encoding regulatory small RNAs that control quorum-sensing transitions. Connecting quorum-sensing and glycine betaine pathways presumably enablesV. harveyito tune its execution of collective behaviors to its tolerance to stress.
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Scaloppi, Maurice Fabian, Samir Moura Kadri, Daniel Diego Mendes, Paulo Eduardo Martins Ribolla, and Ricardo de Oliveira Orsi. "Colony Transport Affects the Expression of Some Genes Related to the Apis mellifera L. Immune System." Sociobiology 69, no. 4 (December 28, 2022): e7522. http://dx.doi.org/10.13102/sociobiology.v69i4.7522.
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Migratory beekeeping can harm the bee colonies if not executed properly. Here, colonies of Apis mellifera were transported (for one or two hours) or not, following proper technical standards. To analyze gene expression (defensin-1, abaecin, and HSP70), forager bees were collected immediately, 24, and 72 hours after transportation. Bee mortality and population growth were measured before and after transportation. This study concludes that transporting honey bee colonies for 2 hours promotes immune system gene expression, although there are no significant changes in bee mortality and population growth of the colonies.
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Kim, Jung-Hwan, Dong-Min Kang, Young-Jin Cho, Jin-Won Hyun, and Mi-Jeong Ahn. "Medicarpin Increases Antioxidant Genes by Inducing NRF2 Transcriptional Level in HeLa Cells." Antioxidants 11, no. 2 (February 18, 2022): 421. http://dx.doi.org/10.3390/antiox11020421.
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The nuclear factor erythroid-derived 2-related factor 2 (NRF2) plays a pivotal role in the regulation of genes involved in oxidative stress and drug detoxification. Therefore, it is important to find NRF2 inducers to protect cells from excessive oxidative damage. Here, we investigated the effect of medicarpin isolated from the root of Robinia pseudoacacia L. on the activity of NRF2 in HeLa cells. Medicarpin significantly induced the antioxidant response elements (ARE)-luciferase activity in a concentration-dependent manner. Furthermore, medicarpin not only induced HO-1, GCLC, and NQO1 mRNA by translocating NRF2 to the nucleus but also induced the mRNA level of NRF2. To verify the NRF2 induction mechanism by medicarpin, ~2 kb of NRF2 promoter-luciferase assay was executed. As a result, medicarpin significantly induced NRF2-luciferase activity. Moreover, medicarpin strongly inhibited the ubiquitin-dependent proteasomal degradation of NRF2. Thus, medicarpin might protect cells by promoting the NRF2 transcriptional activity.
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Bowerman, Bruce. "The near demise and subsequent revival of classical genetics for investigating Caenorhabditis elegans embryogenesis: RNAi meets next-generation DNA sequencing." Molecular Biology of the Cell 22, no. 19 (October 2011): 3556–58. http://dx.doi.org/10.1091/mbc.e11-03-0185.
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Molecular genetic investigation of the early Caenorhabditis elegans embryo has contributed substantially to the discovery and general understanding of the genes, pathways, and mechanisms that regulate and execute developmental and cell biological processes. Initially, worm geneticists relied exclusively on a classical genetics approach, isolating mutants with interesting phenotypes after mutagenesis and then determining the identity of the affected genes. Subsequently, the discovery of RNA interference (RNAi) led to a much greater reliance on a reverse genetics approach: reducing the function of known genes with RNAi and then observing the phenotypic consequences. Now the advent of next-generation DNA sequencing technologies and the ensuing ease and affordability of whole-genome sequencing are reviving the use of classical genetics to investigate early C. elegans embryogenesis.
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Krwawicz, Joanna, Katarzyna D. Arczewska, Elzbieta Speina, Agnieszka Maciejewska, and Elzbieta Grzesiuk. "Bacterial DNA repair genes and their eukaryotic homologues: 1. Mutations in genes involved in base excision repair (BER) and DNA-end processors and their implication in mutagenesis and human disease." Acta Biochimica Polonica 54, no. 3 (September 24, 2007): 413–34. http://dx.doi.org/10.18388/abp.2007_3219.
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Base excision repair (BER) pathway executed by a complex network of proteins is the major system responsible for the removal of damaged DNA bases and repair of DNA single strand breaks (SSBs) generated by environmental agents, such as certain cancer therapies, or arising spontaneously during cellular metabolism. Both modified DNA bases and SSBs with ends other than 3'-OH and 5'-P are repaired either by replacement of a single or of more nucleotides in the processes called short-patch BER (SP-BER) or long-patch BER (LP-BER), respectively. In contrast to Escherichia coli cells, in human ones, the two BER sub-pathways are operated by different sets of proteins. In this review the selection between SP- and LP-BER and mutations in BER and end-processors genes and their contribution to bacterial mutagenesis and human diseases are considered.
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De Kesel, Jonas, Ramsés Gómez-Rodríguez, Eli Bonneure, Sven Mangelinckx, and Tina Kyndt. "The Use of PTI-Marker Genes to Identify Novel Compounds that Establish Induced Resistance in Rice." International Journal of Molecular Sciences 21, no. 1 (January 2, 2020): 317. http://dx.doi.org/10.3390/ijms21010317.
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Compounds that establish induced resistance (IR) in plants are promising alternatives for the pesticides that are progressively being banned worldwide. Screening platforms to identify IR-establishing compounds have been developed, but none were specifically designed for monocot plants. Here, we propose the use of an RT-qPCR screening platform, based on conserved immunity marker genes of rice as proxy for IR induction. Central regulators of biotic stress responses of rice were identified with a weighted gene co-expression network analysis (WGCNA), using more than 350 microarray datasets of rice under various sorts of biotic stress. Candidate genes were narrowed down to six immunity marker genes, based on consistent association with pattern-triggered immunity (PTI), both in rice plants as in rice cell suspension cultures (RCSCs). By monitoring the expression of these genes in RCSCs upon treatment with candidate IR-inducing compounds, we showed that our marker genes can predict IR induction in rice. Diproline, a novel IR-establishing compound for monocots that was detected with these marker genes, was shown to induce rice resistance against root-knot nematodes, without fitness costs. Gene expression profiling of the here-described PTI-marker genes can be executed on fully-grown plants or in RCSCs, providing a novel and versatile tool to predict IR induction.
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Neela, Praveen Kumar, Anjana Atteeri, Pavan Kumar Mamillapalli, Vasu Murthy Sesham, Sreekanth Keesara, Jaya Chandra, Udayini Monica, and Vasavi Mohan. "Genetics of Dentofacial and Orthodontic Abnormalities." Global Medical Genetics 07, no. 04 (December 2020): 095–100. http://dx.doi.org/10.1055/s-0040-1722303.
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AbstractThe development of craniofacial complex and dental structures is a complex and delicate process guided by specific genetic mechanisms. Genetic and environmental factors can influence the execution of these mechanisms and result in abnormalities. An insight into the mechanisms and genes involved in the development of orofacial and dental structures has gradually gained by pedigree analysis of families and twin studies as well as experimental studies on vertebrate models. The development of novel treatment techniques depends on in-depth knowledge of the various molecular or cellular processes and genes involved in the development of the orofacial complex. This review article focuses on the role of genes in the development of nonsyndromic orofacial, dentofacial variations, malocclusions, excluding cleft lip palate, and the advancements in the field of molecular genetics and its application to obtain better treatment outcomes.
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Price, Donald, Simon Rabinovitch, Patrick H. O'Farrell, and Shelagh D. Campbell. "Drosophila wee1 Has an Essential Role in the Nuclear Divisions of Early Embryogenesis." Genetics 155, no. 1 (May 1, 2000): 159–66. http://dx.doi.org/10.1093/genetics/155.1.159.
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Abstract In Drosophila, the maternally expressed mei-41 and grp genes are required for successful execution of the nuclear division cycles of early embryogenesis. In fission yeast, genes encoding similar kinases (rad3 and chk1, respectively) are components of a cell cycle checkpoint that delays mitosis by inhibitory phosphorylation of Cdk1. We have identified mutations in a gene encoding a Cdk1 inhibitory kinase, Drosophila wee1 (Dwee1). Like mei-41 and grp, Dwee1 is zygotically dispensable but is required maternally for completing the embryonic nuclear cycles. The arrest phenotype of Dwee1 mutants, as well as genetic interactions between Dwee1, grp, and mei-41 mutations, suggest that Dwee1 is functioning in the same regulatory pathway as these genes. These findings imply that inhibitory phosphorylation of Cdk1 by Dwee1 is required for proper regulation of the early syncytial cycles of embryogenesis.
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Tavtigian, S. V., S. D. Zabludoff, and B. J. Wold. "Cloning of mid-G1 serum response genes and identification of a subset regulated by conditional myc expression." Molecular Biology of the Cell 5, no. 3 (March 1994): 375–88. http://dx.doi.org/10.1091/mbc.5.3.375.
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The emergence of cells from a quiescent G0 arrested state into the cell cycle is a multistep process that begins with the immediate early response to mitogens and extends into a specialized G1 phase. Many immediate early serum response genes including c-fos, c-myc, and c-jun are transcriptional regulators. To understand their roles in regulating cell cycle entry and progression, the identities of their regulatory targets must be determined. In this work we have cloned cDNA copies of messenger RNAs that are either up- or down-regulated at a mid-G1 point in the serum response (midserum-response [mid-SR]). The mid-SR panel is expected to include both direct and indirect targets of immediate early regulators. This expectation was confirmed by the identification of several transcriptional targets of conditional c-myc activity. In terms of cellular function, the mid-SR class is also expected to include execution genes needed for progression through G1 and into S-phase. DNA sequence data showed that the mid-SR panel included several genes already known to be involved in cell cycle progression or growth transformation, suggesting that previously unknown cDNAs in the same group are good candidates for other G1 execution functions. In functional assays of G0-->S-phase progression, c-myc expression can bypass the requirement for serum mitogens and drive a large fraction of G0 arrested cells through G1 into S-phase. However, beyond this general similarity, little is known about the relation of a serum-driven progression to a myc-driven progression. Using the mid-SR collection as molecular reporters, we found that the myc driven G1 differs qualitatively from the serum driven case. Instead of simply activating a subset of serum response genes, as might be expected, myc regulated some genes inversely relative to serum stimulation. This suggests that a myc driven progression from G0 may have novel properties with implications for its action in oncogenesis.
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Lloyd Evans, Dyfed, and Shailesh Vinay Joshi. "Herbicide targets and detoxification proteins in sugarcane: from gene assembly to structure modelling." Genome 60, no. 7 (July 2017): 601–17. http://dx.doi.org/10.1139/gen-2016-0152.
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In a genome context, sugarcane is a classic orphan crop, in that no genome and only very few genes have been assembled. We have devised a novel exome assembly methodology that has allowed us to assemble and characterize 49 genes that serve as herbicide targets, safener interacting proteins, and members of herbicide detoxification pathways within the sugarcane genome. We have structurally modelled the products of each of these genes, as well as determining allelic, genomic, and RNA-Seq based polymorphisms for each gene. This study provides the largest collection of sugarcane structures modelled to date. We demonstrate that sugarcane genes are highly polymorphic, revealing that each genotype is evolving both uniquely and independently. In addition, we present an exome assembly system for orphan crops that can be executed on commodity infrastructure, making exome assembly practical for any group. In terms of knowledge about herbicide modes of action and detoxification, we have advanced sugarcane from a crop where no information about any herbicide-associated gene was available to the situation where sugarcane is now a species with the single largest collection of known and annotated herbicide-associated genes.
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Mazzarella, Luca, Helle F. Jørgensen, Jorge Soza-Ried, Anna V. Terry, Stella Pearson, Georges Lacaud, Valerie Kouskoff, Matthias Merkenschlager, and Amanda G. Fisher. "Embryonic stem cell–derived hemangioblasts remain epigenetically plastic and require PRC1 to prevent neural gene expression." Blood 117, no. 1 (January 6, 2011): 83–87. http://dx.doi.org/10.1182/blood-2010-03-273128.
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Abstract Many lineage-specific developmental regulator genes are transcriptionally primed in embryonic stem (ES) cells; RNA PolII is bound at their promoters but is prevented from productive elongation by the activity of polycomb repressive complexes (PRC) 1 and 2. This epigenetically poised state is thought to enable ES cells to rapidly execute multiple differentiation programs and is recognized by a simultaneous enrichment for trimethylation of lysine 4 and trimethylation of lysine 27 of histone H3 (bivalent chromatin) across promoter regions. Here we show that the chromatin profile of this important cohort of genes is progressively modified as ES cells differentiate toward blood-forming precursors. Surprisingly however, neural specifying genes, such as Nkx2-2, Nkx2-9, and Sox1, remain bivalent and primed even in committed hemangioblasts, as conditional deletion of PRC1 results in overt and inappropriate expression of neural genes in hemangioblasts. These data reinforce the importance of PRC1 for normal hematopoietic differentiation and reveal an unexpected epigenetic plasticity of mesoderm-committed hemangioblasts.
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Jensen, Travis L., William F. Hooper, Sami R. Cherikh, and Johannes B. Goll. "RP-REP Ribosomal Profiling Reports: an open-source cloud-enabled framework for reproducible ribosomal profiling data processing, analysis, and result reporting." F1000Research 10 (February 24, 2021): 143. http://dx.doi.org/10.12688/f1000research.40668.1.
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Ribosomal profiling is an emerging experimental technology to measure protein synthesis by sequencing short mRNA fragments undergoing translation in ribosomes. Applied on the genome wide scale, this is a powerful tool to profile global protein synthesis within cell populations of interest. Such information can be utilized for biomarker discovery and detection of treatment-responsive genes. However, analysis of ribosomal profiling data requires careful preprocessing to reduce the impact of artifacts and dedicated statistical methods for visualizing and modeling the high-dimensional discrete read count data. Here we present Ribosomal Profiling Reports (RP-REP), a new open-source cloud-enabled software that allows users to execute start-to-end gene-level ribosomal profiling and RNA-Seq analysis on a pre-configured Amazon Virtual Machine Image (AMI) hosted on AWS or on the user’s own Ubuntu Linux server. The software works with FASTQ files stored locally, on AWS S3, or at the Sequence Read Archive (SRA). RP-REP automatically executes a series of customizable steps including filtering of contaminant RNA, enrichment of true ribosomal footprints, reference alignment and gene translation quantification, gene body coverage, CRAM compression, reference alignment QC, data normalization, multivariate data visualization, identification of differentially translated genes, and generation of heatmaps, co-translated gene clusters, enriched pathways, and other custom visualizations. RP-REP provides functionality to contrast RNA-SEQ and ribosomal profiling results, and calculates translational efficiency per gene. The software outputs a PDF report and publication-ready table and figure files. As a use case, we provide RP-REP results for a dengue virus study that tested cytosol and endoplasmic reticulum cellular fractions of human Huh7 cells pre-infection and at 6 h, 12 h, 24 h, and 40 h post-infection. Case study results, Ubuntu installation scripts, and the most recent RP-REP source code are accessible at GitHub. The cloud-ready AMI is available at AWS (AMI ID: RPREP RSEQREP (Ribosome Profiling and RNA-Seq Reports) v2.1 (ami-00b92f52d763145d3)).
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Li, Mengping, Keun Pyo Lee, Tong Liu, Vivek Dogra, Jianli Duan, Mengshuang Li, Weiman Xing, and Chanhong Kim. "Antagonistic modules regulate photosynthesis-associated nuclear genes via GOLDEN2-LIKE transcription factors." Plant Physiology 188, no. 4 (December 24, 2021): 2308–24. http://dx.doi.org/10.1093/plphys/kiab600.
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Abstract GOLDEN2-LIKE (GLK) transcription factors drive the expression of photosynthesis-associated nuclear genes (PhANGs) indispensable for chloroplast biogenesis. Salicylic acid (SA)-induced SIGMA FACTOR-BINDING PROTEIN 1 (SIB1), a transcription coregulator and positive regulator of cell death, interacts with GLK1 and GLK2 to reinforce the expression of PhANGs, leading to photoinhibition of photosystem II and singlet oxygen (1O2) burst in chloroplasts. 1O2 then contributes to SA-induced cell death via EXECUTER 1 (EX1; 1O2 sensor protein)-mediated retrograde signaling upon reaching a critical level. This earlier finding has initiated research on the potential role of GLK1/2 and EX1 in SA signaling. Consistent with this view, we reveal that LESION-SIMULATING DISEASE 1 (LSD1), a transcription coregulator and negative regulator of SA-primed cell death, interacts with GLK1/2 to repress their activities in Arabidopsis (Arabidopsis thaliana). Overexpression of LSD1 repressed GLK target genes, including PhANGs, whereas loss of LSD1 enhanced their expression. Remarkably, LSD1 overexpression inhibited chloroplast biogenesis, resembling the characteristic glk1glk2 double mutant phenotype. Subsequent chromatin immunoprecipitation coupled with expression analyses further revealed that LSD1 inhibits the DNA-binding activity of GLK1 toward its target promoters. SA-induced nuclear-targeted SIB1 proteins appeared to interrupt the LSD1–GLK interaction, and the subsequent SIB1–GLK interaction activated EX1-mediated 1O2 signaling, elucidating antagonistic modules SIB1 and LSD1 in the regulation of GLK activity. Taken together, we provide a working model that SIB1 and LSD1, mutually exclusive SA-signaling components, antagonistically regulate GLK1/2 to fine-tune the expression of PhANGs, thereby modulating 1O2 homeostasis and related stress responses.
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Villalobos-Cid, Manuel, Francisco Salinas, Eduardo I. Kessi-Pérez, Matteo De Chiara, Gianni Liti, Mario Inostroza-Ponta, and Claudio Martínez. "Comparison of Phylogenetic Tree Topologies for Nitrogen Associated Genes Partially Reconstruct the Evolutionary History of Saccharomyces cerevisiae." Microorganisms 8, no. 1 (December 23, 2019): 32. http://dx.doi.org/10.3390/microorganisms8010032.
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Massive sequencing projects executed in Saccharomyces cerevisiae have revealed in detail its population structure. The recent “1002 yeast genomes project” has become the most complete catalogue of yeast genetic diversity and a powerful resource to analyse the evolutionary history of genes affecting specific phenotypes. In this work, we selected 22 nitrogen associated genes and analysed the sequence information from the 1011 strains of the “1002 yeast genomes project”. We constructed a total evidence (TE) phylogenetic tree using concatenated information, which showed a 27% topology similarity with the reference (REF) tree of the “1002 yeast genomes project”. We also generated individual phylogenetic trees for each gene and compared their topologies, identifying genes with similar topologies (suggesting a shared evolutionary history). Furthermore, we pruned the constructed phylogenetic trees to compare the REF tree topology versus the TE tree and the individual genes trees, considering each phylogenetic cluster/subcluster within the population, observing genes with cluster/subcluster topologies of high similarity to the REF tree. Finally, we used the pruned versions of the phylogenetic trees to compare four strains considered as representatives of S. cerevisiae clean lineages, observing for 15 genes that its cluster topologies match 100% the REF tree, supporting that these strains represent main lineages of yeast population. Altogether, our results showed the potential of tree topologies comparison for exploring the evolutionary history of a specific group of genes.
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Ambrozkiewicz, Mateusz C., Katherine J. Cuthill, Dermot Harnett, Hiroshi Kawabe, and Victor Tarabykin. "Molecular Evolution, Neurodevelopmental Roles and Clinical Significance of HECT-Type UBE3 E3 Ubiquitin Ligases." Cells 9, no. 11 (November 10, 2020): 2455. http://dx.doi.org/10.3390/cells9112455.
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Protein ubiquitination belongs to the best characterized pathways of protein degradation in the cell; however, our current knowledge on its physiological consequences is just the tip of an iceberg. The divergence of enzymatic executors of ubiquitination led to some 600–700 E3 ubiquitin ligases embedded in the human genome. Notably, mutations in around 13% of these genes are causative of severe neurological diseases. Despite this, molecular and cellular context of ubiquitination remains poorly characterized, especially in the developing brain. In this review article, we summarize recent findings on brain-expressed HECT-type E3 UBE3 ligases and their murine orthologues, comprising Angelman syndrome UBE3A, Kaufman oculocerebrofacial syndrome UBE3B and autism spectrum disorder-associated UBE3C. We summarize evolutionary emergence of three UBE3 genes, the biochemistry of UBE3 enzymes, their biology and clinical relevance in brain disorders. Particularly, we highlight that uninterrupted action of UBE3 ligases is a sine qua non for cortical circuit assembly and higher cognitive functions of the neocortex.
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Wani, Nisar, and Khalid Raza. "MKL-GRNI: A parallel multiple kernel learning approach for supervised inference of large-scale gene regulatory networks." PeerJ Computer Science 7 (January 28, 2021): e363. http://dx.doi.org/10.7717/peerj-cs.363.
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High throughput multi-omics data generation coupled with heterogeneous genomic data fusion are defining new ways to build computational inference models. These models are scalable and can support very large genome sizes with the added advantage of exploiting additional biological knowledge from the integration framework. However, the limitation with such an arrangement is the huge computational cost involved when learning from very large datasets in a sequential execution environment. To overcome this issue, we present a multiple kernel learning (MKL) based gene regulatory network (GRN) inference approach wherein multiple heterogeneous datasets are fused using MKL paradigm. We formulate the GRN learning problem as a supervised classification problem, whereby genes regulated by a specific transcription factor are separated from other non-regulated genes. A parallel execution architecture is devised to learn a large scale GRN by decomposing the initial classification problem into a number of subproblems that run as multiple processes on a multi-processor machine. We evaluate the approach in terms of increased speedup and inference potential using genomic data from Escherichia coli, Saccharomyces cerevisiae and Homo sapiens. The results thus obtained demonstrate that the proposed method exhibits better classification accuracy and enhanced speedup compared to other state-of-the-art methods while learning large scale GRNs from multiple and heterogeneous datasets.
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Köhler, Tim, Stefanie Wesche, Naimeh Taheri, Gerhard H. Braus, and Hans-Ulrich Mösch. "Dual Role of the Saccharomyces cerevisiae TEA/ATTS Family Transcription Factor Tec1p in Regulation of Gene Expression and Cellular Development." Eukaryotic Cell 1, no. 5 (October 2002): 673–86. http://dx.doi.org/10.1128/ec.1.5.673-686.2002.
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ABSTRACT In Saccharomyces cerevisiae, the transcription factors Tec1p and Ste12p are required for haploid invasive and diploid pseudohyphal growth. Tec1p and Ste12p have been postulated to regulate these developmental processes primarily by cooperative binding to filamentous and invasion-responsive elements (FREs), which are combined enhancer elements that consist of a Tec1p-binding site (TCS) and an Ste12p-binding site (PRE). They are present in the promoter regions of target genes, e.g., FLO11. Here, we show that Tec1p efficiently activates target gene expression and cellular development in the absence of Ste12p. We further demonstrate that TCS elements alone are sufficient to mediate Tec1p-driven gene expression by a mechanism termed TCS control that is operative even when Ste12p is absent. Mutational analysis of TEC1 revealed that TCS control, FLO11 expression, and haploid invasive growth require the C terminus of Tec1p. In contrast, the Ste12p-dependent FRE control mechanism is sufficiently executed by the N-terminal portion of Tec1p, which contains the TEA/ATTS DNA-binding domain. Our study suggests that regulation of haploid invasive and diploid pseudohyphal growth by Ste12p and Tec1p is not only executed by combinatorial control but involves additional control mechanisms in which Ste12p activates TEC1 expression via clustered PREs and where Tec1p regulates expression of target genes, e.g., FLO11, by TCS control.