Journal articles on the topic 'Restoration genomics'
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van Oppen, Madeleine J. H., and Melinda A. Coleman. "Advancing the protection of marine life through genomics." PLOS Biology 20, no. 10 (October 17, 2022): e3001801. http://dx.doi.org/10.1371/journal.pbio.3001801.
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The rapid growth in genomic techniques provides the potential to transform how we protect, manage, and conserve marine life. Further, solutions to boost the resilience of marine species to climate change and other disturbances that characterize the Anthropocene require transformative approaches, made more effective if guided by genomic data. Although genetic techniques have been employed in marine conservation for decades and the availability of genomic data is rapidly expanding, widespread application still lags behind other data types. This Essay reviews how genetics and genomics have been utilized in management initiatives for ocean conservation and restoration, highlights success stories, and presents a pathway forward to enhance the uptake of genomic data for protecting our oceans.
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Hodgins, Kathryn A., and Joslin L. Moore. "Adapting to a warming world: Ecological restoration, climate change, and genomics." American Journal of Botany 103, no. 4 (March 28, 2016): 590–92. http://dx.doi.org/10.3732/ajb.1600049.
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SHINZATO, Chuya. "New Approaches for Coral Reef Conservation and Restoration Using Genomics Techniques." TRENDS IN THE SCIENCES 22, no. 3 (2017): 3_92–3_95. http://dx.doi.org/10.5363/tits.22.3_92.
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Wheeler, Nicholas, and Ronald Sederoff. "Role of genomics in the potential restoration of the American chestnut." Tree Genetics & Genomes 5, no. 1 (October 29, 2008): 181–87. http://dx.doi.org/10.1007/s11295-008-0180-y.
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Byrne, Margaret. "A molecular journey in conservation genetics." Pacific Conservation Biology 24, no. 3 (2018): 235. http://dx.doi.org/10.1071/pc18025.
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Genetics, and more recently genomics, has become an integral part of conservation science. From the early days of DNA fingerprinting through development of hybridisation based and polymerase chain reaction based markers, to applications of genomics, genetics has provided many insights to improve management of plants, animals and their ecosystems. I share my journey of discovery in genetics and genomics, and their application in conservation of plants through understanding evolutionary history, population genetics of rare and threatened species, molecular taxonomy, fragmentation and the role of pollen dispersal, restoration in a risk management context, and adaptation to climate change.
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Wood, Georgina, Ezequiel M. Marzinelli, Adriana Vergés, Alexandra H. Campbell, Peter D. Steinberg, and Melinda A. Coleman. "Using genomics to design and evaluate the performance of underwater forest restoration." Journal of Applied Ecology 57, no. 10 (July 23, 2020): 1988–98. http://dx.doi.org/10.1111/1365-2664.13707.
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Lin, Jiunn-Chang, Tsang-Pai Liu, and Pei-Ming Yang. "CDKN2A-Inactivated Pancreatic Ductal Adenocarcinoma Exhibits Therapeutic Sensitivity to Paclitaxel: A Bioinformatics Study." Journal of Clinical Medicine 9, no. 12 (December 12, 2020): 4019. http://dx.doi.org/10.3390/jcm9124019.
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The mutation of cyclin dependent kinase inhibitor 2A (CDKN2A) is frequently found in pancreatic ductal adenocarcinoma (PDAC). However, its prognostic and therapeutic roles in PDAC have not been extensively investigated yet. In this study, we mined and integrated the cancer genomics and chemogenomics data to investigate the roles of CDKN2A genetic alterations in PDAC patients’ prognosis and treatment. We found that functional CDKN2A inactivation caused by mutations and deep deletions predicted poor prognosis in PDAC patients. CDKN2A inactivation was associated with the upregulation of genes related to estrogen response, which can be overcome by CDKN2A restoration. Chemosensitivity profiling of PDAC cell lines and patient-derived organoids found that CDKN2A inactivation was associated with the increased sensitivity to paclitaxel and SN-38 (the active metabolite of irinotecan). However, only paclitaxel can mimic the effect of CDKN2A restoration, and its drug sensitivity was correlated with genes related to estrogen response. Therefore, our study suggested that CDKN2A-inactivated PDAC patients could benefit from the precision treatment with paclitaxel, whose albumin-stabilized nanoparticle formulation (nab-paclitaxel) has been approved for treating PDAC.
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Meyer, Mary Hockenberry, Stan Hokanson, Susan Galatowitsch, and James Luby. "Public Gardens: Fulfilling the University's Research Mission." HortTechnology 20, no. 3 (June 2010): 522–27. http://dx.doi.org/10.21273/horttech.20.3.522.
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Research at botanic gardens, from medieval times to the present day, has evolved to encompass a wide range of topics. The Minnesota Landscape Arboretum, part of the University of Minnesota, is an example of a diverse, successful research program within a public university garden setting. Collaboration, mission, organization, and publications are keys to a successful research program. Future research for public gardens, including putting collections to work for conservation, understanding global change, ecological genomics, restoration ecology, seed banking, and citizen science are collaborative ideas for all botanic gardens to consider. Research can strengthen the botanic garden's role by providing public value while improving ties to the university.
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Shryock, Daniel F., Caroline A. Havrilla, Lesley A. DeFalco, Todd C. Esque, Nathan A. Custer, and Troy E. Wood. "Landscape genomics of Sphaeralcea ambigua in the Mojave Desert: a multivariate, spatially-explicit approach to guide ecological restoration." Conservation Genetics 16, no. 6 (June 18, 2015): 1303–17. http://dx.doi.org/10.1007/s10592-015-0741-1.
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Weiman, Shannon, Samantha Joye, Joel Kostka, Kenneth Halanych, and Rita Colwell. "GoMRI Insights into Microbial Genomics and Hydrocarbon Bioremediation Response in Marine Ecosystems." Oceanography 34, no. 1 (March 1, 2021): 124–35. http://dx.doi.org/10.5670/oceanog.2021.121.
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The Deepwater Horizon oil spill represents one of the most damaging environmental catastrophes of our generation. It contaminated vast areas of the open ocean, the deep sea, and the shoreline of the Gulf region and disrupted its ecosystems, with both residual and long-term impacts. At the core of all of these ecosystems are microbial communities that perform essential biogeochemical processes and ecosystem services such as carbon and nutrient cycling. Despite their importance, relatively little was known about marine microbes that degrade hydrocarbons in the Gulf of Mexico prior to the Deepwater Horizon spill, nor the effect of hydrocarbons on the microbiology of the Gulf region. Research carried out through the Gulf of Mexico Research Initiative (GoMRI) revealed cooperative microbial communities operating at the heart of bioremediation services with highly adaptive and complex dynamics. In addition, these efforts established new methods for assessing and monitoring ecosystem health, whereby microbial population genetics can serve as indicators of biogeochemical disruptions and/or restoration status in marine and coastal environments. Although much research is still needed to fully understand and engage microbially mediated bioremediation services, GoMRI constructed a strong foundation of methods, discoveries, and overarching principles to build upon. These insights and tools will help scientists better prepare for, and respond to, future environmental catastrophes, from oil tanker spills to long-term disruptions of climate change.
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Dreijerink, Koen M. A., H. T. Marc Timmers, and Myles Brown. "Twenty years of menin: emerging opportunities for restoration of transcriptional regulation in MEN1." Endocrine-Related Cancer 24, no. 10 (October 2017): T135—T145. http://dx.doi.org/10.1530/erc-17-0281.
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Since the discovery of the multiple endocrine neoplasia type 1 (MEN1) gene in 1997, elucidation of the molecular function of its protein product, menin, has been a challenge. Biochemical, proteomics, genetics and genomics approaches have identified various potential roles, which converge on gene expression regulation. The most consistent findings show that menin connects transcription factors and chromatin-modifying enzymes, in particular, the histone H3K4 methyltransferase complexes MLL1 and MLL2. Chromatin immunoprecipitation combined with next-generation sequencing has enabled studying genome-wide dynamics of chromatin binding by menin. We propose that menin regulates cell type-specific transcriptional programs by linking chromatin regulatory complexes to specific transcription factors. In this fashion, the MEN1 gene is a tumor suppressor gene in the endocrine tissues that are affected in MEN1. Recent studies have hinted at possibilities to pharmacologically restore the epigenetic changes caused by loss of menin function as therapeutic strategies for MEN1, for example, by inhibition of histone demethylases. The current lack of appropriate cellular model systems for MEN1-associated tumors is a limitation for compound testing, which needs to be addressed in the near future. In this review, we look back at the past twenty years of research on menin and the mechanism of disease of MEN1. In addition, we discuss how the current understanding of the molecular function of menin offers future directions to develop novel treatments for MEN1-associated endocrine tumors.
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Dmitrenko, Olga, Andrey Chaplin, Anna Balbutskaya, Tamara Pkhakadze, and Sergey Alkhovsky. "In Silico Genome-Scale Analysis of Molecular Mechanisms Contributing to the Development of a Persistent Infection with Methicillin-Resistant Staphylococcus aureus (MRSA) ST239." International Journal of Molecular Sciences 23, no. 24 (December 16, 2022): 16086. http://dx.doi.org/10.3390/ijms232416086.
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The increasing frequency of isolation of methicillin-resistant Staphylococcus aureus (MRSA) limits the chances for the effective antibacterial therapy of staphylococcal diseases and results in the development of persistent infection such as bacteremia and osteomyelitis. The aim of this study was to identify features of the MRSAST239 0943-1505-2016 (SA943) genome that contribute to the formation of both acute and chronic musculoskeletal infections. The analysis was performed using comparative genomics data of the dominant epidemic S. aureus lineages, namely ST1, ST8, ST30, ST36, and ST239. The SA943 genome encodes proteins that provide resistance to the host’s immune system, suppress immunological memory, and form biofilms. The molecular mechanisms of adaptation responsible for the development of persistent infection were as follows: amino acid substitution in PBP2 and PBP2a, providing resistance to ceftaroline; loss of a large part of prophage DNA and restoration of the nucleotide sequence of beta-hemolysin, that greatly facilitates the escape of phagocytosed bacteria from the phagosome and formation of biofilms; dysfunction of the AgrA system due to the presence of psm-mec and several amino acid substitutions in the AgrC; partial deletion of the nucleotide sequence in genomic island vSAβ resulting in the loss of two proteases of Spl—operon; and deletion of SD repeats in the SdrE amino acid sequence.
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Lettoof, Damian C., Vicki A. Thomson, Jari Cornelis, Philip W. Bateman, Fabien Aubret, Marthe M. Gagnon, and Brenton von Takach. "Bioindicator snake shows genomic signatures of natural and anthropogenic barriers to gene flow." PLOS ONE 16, no. 10 (October 29, 2021): e0259124. http://dx.doi.org/10.1371/journal.pone.0259124.
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Urbanisation alters landscapes, introduces wildlife to novel stressors, and fragments habitats into remnant ‘islands’. Within these islands, isolated wildlife populations can experience genetic drift and subsequently suffer from inbreeding depression and reduced adaptive potential. The Western tiger snake (Notechis scutatus occidentalis) is a predator of wetlands in the Swan Coastal Plain, a unique bioregion that has suffered substantial degradation through the development of the city of Perth, Western Australia. Within the urban matrix, tiger snakes now only persist in a handful of wetlands where they are known to bioaccumulate a suite of contaminants, and have recently been suggested as a relevant bioindicator of ecosystem health. Here, we used genome-wide single nucleotide polymorphism (SNP) data to explore the contemporary population genomics of seven tiger snake populations across the urban matrix. Specifically, we used population genomic structure and diversity, effective population sizes (Ne), and heterozygosity-fitness correlations to assess fitness of each population with respect to urbanisation. We found that population genomic structure was strongest across the northern and southern sides of a major river system, with the northern cluster of populations exhibiting lower heterozygosities than the southern cluster, likely due to a lack of historical gene flow. We also observed an increasing signal of inbreeding and genetic drift with increasing geographic isolation due to urbanisation. Effective population sizes (Ne) at most sites were small (< 100), with Ne appearing to reflect the area of available habitat rather than the degree of adjacent urbanisation. This suggests that ecosystem management and restoration may be the best method to buffer the further loss of genetic diversity in urban wetlands. If tiger snake populations continue to decline in urban areas, our results provide a baseline measure of genomic diversity, as well as highlighting which ‘islands’ of habitat are most in need of management and protection.
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Zhang, Ling, Xia Niu, Yanghui Bi, Heyang Cui, Hongyi Li, and Xiaolong Cheng. "Potential Role of Targeting KDR and Proteasome Inhibitors in the Therapy of Esophageal Squamous Cell Carcinoma." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382094806. http://dx.doi.org/10.1177/1533033820948060.
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Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive cancer types in China. In recent years, progress has been made in various types of cancer genomics including ESCC. However, the clinical significance of genomic variation of ESCC remains poorly defined. In the present study, genomic sequencing data from 469 ESCC cases were analyzed and potential therapeutic targets in the Druggable Genome Interaction Database (DGIdb) were screened. A series of potential therapeutic target genes and pathways were identified, of which treatment of ESCC with bortezomib (a specific inhibitor targeting proteasome) potently inhibited the proliferation of 5 ESCC cell lines and administration of bortezomib led to significant tumor xenograft regression in SCID mice. It was also identified that kinase insert domain receptor (KDR), which had drug recommendations from all 6 sources integrated by the DGldb and harbored significant amplification in ESCC, might be a downstream target of zinc finger protein 750 (ZNF750). ZNF750 acts as a transcription factor and has been demonstrated to harbor frequently inactivating mutations in ESCC by previous independent studies. In the present study, KDR was upregulated upon ZNF750 knockdown and the rescue of ZNF750 also led to marked restoration of KDR. KDR knockdown in stable ZNF750-knockdown KYSE150 and KYSE140 ESCC cells significantly attenuated the promotion of cell growth, colony formation, invasion and migration induced by ZNF750 knockdown. Further experiments found that apatinib treatment, a potent inhibitor of KDR, resulted in profound inhibition of cell proliferation and invasion. Collectively, the present study provided insight for genomic alterations as potential therapeutic targets in ESCC and supported the possibility of a therapeutic strategy targeting the proteasome in ESCC. The present results also suggested that targeting KDR may be an effective way to treat ESCC, not only in KDR variant cases, but also in individuals with ZNF750 mutations and deletions.
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Bacali, Cecilia, Romana Vulturar, Smaranda Buduru, Angela Cozma, Adriana Fodor, Adina Chiș, Ondine Lucaciu, Laura Damian, and Mirela Liliana Moldovan. "Oral Microbiome: Getting to Know and Befriend Neighbors, a Biological Approach." Biomedicines 10, no. 3 (March 14, 2022): 671. http://dx.doi.org/10.3390/biomedicines10030671.
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The oral microbiome, forming a biofilm that covers the oral structures, contains a high number of microorganisms. Biofilm formation starts from the salivary pellicle that allows bacterial adhesion–colonization–proliferation, co-aggregation and biofilm maturation in a complex microbial community. There is a constant bidirectional crosstalk between human host and its oral microbiome. The paper presents the fundamentals regarding the oral microbiome and its relationship to modulator factors, oral and systemic health. The modern studies of oral microorganisms and relationships with the host benefits are based on genomics, transcriptomics, proteomics and metabolomics. Pharmaceuticals such as antimicrobials, prebiotics, probiotics, surface active or abrasive agents and plant-derived ingredients may influence the oral microbiome. Many studies found associations between oral dysbiosis and systemic disorders, including autoimmune diseases, cardiovascular, diabetes, cancers and neurodegenerative disorders. We outline the general and individual factors influencing the host–microbial balance and the possibility to use the analysis of the oral microbiome in prevention, diagnosis and treatment in personalized medicine. Future therapies should take in account the restoration of the normal symbiotic relation with the oral microbiome.
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Gambari, Roberto. "The Role of OMICS Research in Understanding Phenotype Variation in Thalassaemia: The THALAMOSS Project." Thalassemia Reports 4, no. 3 (December 4, 2014): 4877. http://dx.doi.org/10.4081/thal.2014.4877.
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The β-thalassaemias are a group of severe and rare anaemias with monogenic inheritance, a complex systemic phenotype and several treatment-related complications, caused by more than 300 mutations of the β-globin gene. Novel therapeutic protocols, most of which are based on still experimental treatments, show great promise but significant variability of success between patients. These strategies include chemical/molecular induction of the endogenous β-like γ-globin gene or the restoration of clinically relevant β-globin levels by gene therapy. A small number of modifiers with significant impact on disease penetrance, severity and efficacy of treatments are known, but most remain elusive. Improvements of existing treatment regimens and optimization and application of novel treatments will critically depend on the characterization of additional disease modifiers and the stratification of patients for customized treatment regimens. This requires extensive analyses based on “OMICS”, an English-language neologism which refer to different but connected fields in molecular biology and biochemistry, such as genomics, transcriptomics, exomics, proteomics, metabolomics. The major objective of OMICS is a collective characterization of pools of biological molecules (gene sequences, transcripts, proteins and protein domains) controlling biological structures, functions and dynamics, including several involved in pathological conditions. One of the most interesting observations of genomics in β-thalassaemias is the association between genomic sequences and high fetal haemoglobin (HbF) levels, in consideration of the fact that high HbF levels are usually associated with milder forms of β-thalassaemia. Related to this issue, is the possibility to predict response to different therapeutic protocols on the basis of genomic analyses. For instance, three major loci (Xmn1-HBG2 single nucleotide polymorphism, HBS1L-MYB intergenic region on chromosome 6q, and BCL11A) contribute to high HbF production. Pharmacogenomic analysis of the effects of hydroxyurea (HU) on HbF production in a collection of β-thalassemia and sickle cell disease (SCD) patients allowed the identification of genomic signatures associated with high HbF. Therefore, it can hypothesized that genomic studies might predict the response of patients to treatments based on hydroxyurea, which is at present the most used HbF inducer in pharmacological therapy of β-thalassaemia. Transcriptomic/proteomic studies allowed to identify the zinc finger transcription factor B-cell lymphoma/leukemia 11A (BCL11A) as the major repressor of HbF expression. The field of research on g-globin gene repressors (including BCL11A) is of top interest, since several approaches can lead to pharmacologically-mediated inhibition of the expression of g-globin gene repressors, leading to gglobin gene activation. Among these strategies, we underline direct targeting of the transcription factors by aptamers or decoy molecules, as well as inhibition of the mRNA coding g-globin gene repressors with shRNAs, antisense molecules, peptide nucleic acids (PNAs) and microRNAs. In this respect, the THALAMOSS FP7 Project (THALAssaemia MOdular Stratification System for personalized therapy of β-thalassemia, www.thalamoss.eu) aims develop a universal sets of markers and techniques for stratification of β-thalassaemia patients into treatment subgroups for (a) onset and frequency of blood transfusions, (b) choice of iron chelation, (c) induction of fetal hemoglobin, (d) prospective efficacy of gene-therapy. The impact of THALAMOSS is the provision of novel biomarkers for distinct treatment subgroups in β-thalassaemia (500–1000 samples from participating medical centres), identified by combined genomics, proteomics, transcriptomics and tissue culture assays, the development of new or improved products for the cell isolation, characterization and treatment of β-thalassaemia patients and the establishment of routine techniques for detection of these markers and stratification of patients into treatment groups. Translation of these activities into the product portfolio and R&D methodology of participating SMEs will be a major boost for them as well as for the field. THALAMOSS tools and technologies will (a) facilitate identification of novel diagnostic tests, drugs and treatments specific to patient subgroups and (b) guide conventional and novel therapeutic approaches for β-thalassaemia, including personalized medical treatments.
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Westergaard, Kristine Bakke, Magni Olsen Kyrkjeeide, and Marie Kristine Brandrud. "Using genomics to guide seed‐sourcing at the right taxonomical level for ecological restoration projects: The complex case of Carex bigelowii s.lat. in Norway." Ecology and Evolution 11, no. 23 (November 17, 2021): 17117–31. http://dx.doi.org/10.1002/ece3.8350.
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Wang, Richard R. C., Xingfeng Li, Matthew D. Robbins, Steve R. Larson, Shaun B. Bushman, Thomas A. Jones, and Aaron Thomas. "DNA sequence-based mapping and comparative genomics of the St genome of Pseudoroegneria spicata (Pursh) Á. Löve versus wheat (Triticum aestivum L.) and barley (Hordeum vulgare L.)." Genome 63, no. 9 (September 2020): 445–57. http://dx.doi.org/10.1139/gen-2019-0152.
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Bluebunch wheatgrass (referred to as BBWG) [Pseudoroegneria spicata (Pursh) Á. Löve] is an important rangeland Triticeae grass used for forage, conservation, and restoration. This diploid has the basic St genome that occurs also in many polyploid Triticeae species, which serve as a gene reservoir for wheat improvement. Until now, the St genome in diploid species of Pseudoroegneria has not been mapped. Using a double-cross mapping populations, we mapped 230 expressed sequence tag derived simple sequence repeat (EST-SSR) and 3468 genotyping-by-sequencing (GBS) markers to 14 linkage groups (LGs), two each for the seven homologous groups of the St genome. The 227 GBS markers of BBWG that matched those in a previous study helped identify the unclassified seven LGs of the St sub-genome among 21 LGs of Thinopyrum intermedium (Host) Barkworth & D.R. Dewey. Comparisons of GBS sequences in BBWG to whole-genome sequences in bread wheat (Triticum aestivum L.) and barley (Hordeum vulgare L.) revealed that the St genome shared a homology of 35% and 24%, a synteny of 86% and 84%, and a collinearity of 0.85 and 0.86, with ABD and H, respectively. This first-draft molecular map of the St genome will be useful in breeding cereal and forage crops.
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Chatterjee Bhowmick, Diti, Miwon Ahn, Eunjin Oh, Rajakrishnan Veluthakal, and Debbie C. Thurmond. "Conventional and Unconventional Mechanisms by which Exocytosis Proteins Oversee β-cell Function and Protection." International Journal of Molecular Sciences 22, no. 4 (February 12, 2021): 1833. http://dx.doi.org/10.3390/ijms22041833.
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Type 2 diabetes (T2D) is one of the prominent causes of morbidity and mortality in the United States and beyond, reaching global pandemic proportions. One hallmark of T2D is dysfunctional glucose-stimulated insulin secretion from the pancreatic β-cell. Insulin is secreted via the recruitment of insulin secretory granules to the plasma membrane, where the soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) and SNARE regulators work together to dock the secretory granules and release insulin into the circulation. SNARE proteins and their regulators include the Syntaxins, SNAPs, Sec1/Munc18, VAMPs, and double C2-domain proteins. Recent studies using genomics, proteomics, and biochemical approaches have linked deficiencies of exocytosis proteins with the onset and progression of T2D. Promising results are also emerging wherein restoration or enhancement of certain exocytosis proteins to β-cells improves whole-body glucose homeostasis, enhances β-cell function, and surprisingly, protection of β-cell mass. Intriguingly, overexpression and knockout studies have revealed novel functions of certain exocytosis proteins, like Syntaxin 4, suggesting that exocytosis proteins can impact a variety of pathways, including inflammatory signaling and aging. In this review, we present the conventional and unconventional functions of β-cell exocytosis proteins in normal physiology and T2D and describe how these insights might improve clinical care for T2D.
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Vyas, Usha, and Natarajan Ranganathan. "Probiotics, Prebiotics, and Synbiotics: Gut and Beyond." Gastroenterology Research and Practice 2012 (2012): 1–16. http://dx.doi.org/10.1155/2012/872716.
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The human intestinal tract has been colonized by thousands of species of bacteria during the coevolution of man and microbes. Gut-borne microbes outnumber the total number of body tissue cells by a factor of ten. Recent metagenomic analysis of the human gut microbiota has revealed the presence of some 3.3 million genes, as compared to the mere 23 thousand genes present in the cells of the tissues in the entire human body. Evidence for various beneficial roles of the intestinal microbiota in human health and disease is expanding rapidly. Perturbation of the intestinal microbiota may lead to chronic diseases such as autoimmune diseases, colon cancers, gastric ulcers, cardiovascular disease, functional bowel diseases, and obesity. Restoration of the gut microbiota may be difficult to accomplish, but the use of probiotics has led to promising results in a large number of well-designed (clinical) studies. Microbiomics has spurred a dramatic increase in scientific, industrial, and public interest in probiotics and prebiotics as possible agents for gut microbiota management and control. Genomics and bioinformatics tools may allow us to establish mechanistic relationships among gut microbiota, health status, and the effects of drugs in the individual. This will hopefully provide perspectives for personalized gut microbiota management.
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Tomiya, Susumu, and Julie A. Meachen. "Postcranial diversity and recent ecomorphic impoverishment of North American gray wolves." Biology Letters 14, no. 1 (January 2018): 20170613. http://dx.doi.org/10.1098/rsbl.2017.0613.
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Recent advances in genomics and palaeontology have begun to unravel the complex evolutionary history of the gray wolf, Canis lupus . Still, much of their phenotypic variation across time and space remains to be documented. We examined the limb morphology of the fossil and modern North American gray wolves from the late Quaternary (< ca 70 ka) to better understand their postcranial diversity through time. We found that the late-Pleistocene gray wolves were characterized by short-leggedness on both sides of the Cordilleran–Laurentide ice sheets, and that this trait survived well into the Holocene despite the collapse of Pleistocene megafauna and disappearance of the ‘Beringian wolf' from Alaska. By contrast, extant populations in the Midwestern USA and northwestern North America are distinguished by their elongate limbs with long distal segments, which appear to have evolved during the Holocene possibly in response to a new level or type of prey depletion. One of the consequences of recent extirpation of the Plains ( Canis lupus nubilus ) and Mexican wolves ( C. l. baileyi ) from much of the USA is an unprecedented loss of postcranial diversity through removal of short-legged forms. Conservation of these wolves is thus critical to restoration of the ecophenotypic diversity and evolutionary potential of gray wolves in North America.
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Yap, Charles, Abulhassan Ali, Amogh Prabhakar, Akul Prabhakar, Aman Pal, Ying Yi Lim, and Pramath Kakodkar. "Comprehensive literature review on COVID-19 vaccines and role of SARS-CoV-2 variants in the pandemic." Therapeutic Advances in Vaccines and Immunotherapy 9 (January 2021): 251513552110597. http://dx.doi.org/10.1177/25151355211059791.
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Since the outbreak of the COVID-19 pandemic, there has been a rapid expansion in vaccine research focusing on exploiting the novel discoveries on the pathophysiology, genomics, and molecular biology of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Although the current preventive measures are primarily socially distancing by maintaining a 1 m distance, it is supplemented using facial masks and other personal hygiene measures. However, the induction of vaccines as primary prevention is crucial to eradicating the disease to attempt restoration to normalcy. This literature review aims to describe the physiology of the vaccines and how the spike protein is used as a target to elicit an antibody-dependent immune response in humans. Furthermore, the overview, dosing strategies, efficacy, and side effects will be discussed for the notable vaccines: BioNTech/Pfizer, Moderna, AstraZeneca, Janssen, Gamaleya, and SinoVac. In addition, the development of other prominent COVID-19 vaccines will be highlighted alongside the sustainability of the vaccine-mediated immune response and current contraindications. As the research is rapidly expanding, we have looked at the association between pregnancy and COVID-19 vaccinations, in addition to the current reviews on the mixing of vaccines. Finally, the prominent emerging variants of concern are described, and the efficacy of the notable vaccines toward these variants has been summarized.
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Siqueira, Marcos Vinicius Bohrer Monteiro, Patricia Sanae Sujii, Miklos Bajay, Carolina Grando, Kaiser Schwarcz, Camila Macrini, and Maria Imaculada Zucchi. "How can molecular ecology contribute to forest restoration?" Journal of Biotechnology and Biodiversity 4, no. 4 (November 1, 2013): 316–21. http://dx.doi.org/10.20873/jbb.uft.cemaf.v4n4.siqueira.
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The advance of scientific knowledge in various areas of molecular ecology has allowed the adoption of new strategies, particularly in forest restoration. The fusion of multidisciplinary areas and the implementation of management methodologies in order to get better results in forest restoration are current realities. In order to review the main ideas about the role of molecular techniques in the service of ecology restoration, this paper outlines how forest recovery can benefit from genetic and genomic plant population studies. The next challenges in conservation genetics can be brought by the quest for more efficient forest restorations from the point of view of biodiversity as well as the ecological ynamics as a whole. It is believed that in the coming years we will observe integrated strategies in molecular ecology with specific methodologies for restoration in tropical forests.
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Yang, Pei-Ming, Li-Shan Lin, and Tsang-Pai Liu. "Sorafenib Inhibits Ribonucleotide Reductase Regulatory Subunit M2 (RRM2) in Hepatocellular Carcinoma Cells." Biomolecules 10, no. 1 (January 9, 2020): 117. http://dx.doi.org/10.3390/biom10010117.
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The main curative treatments for hepatocellular carcinoma (HCC) are surgical resection and liver transplantation, which only benefits 15% to 25% of patients. In addition, HCC is highly refractory and resistant to cytotoxic chemotherapy. Although several multi-kinase inhibitors, such as sorafenib, regorafenib, and lenvatinib, have been approved for treating advanced HCC, only a short increase of median overall survival in HCC patients was achieved. Therefore, there is an urgent need to design more effective strategies for advanced HCC patients. Human ribonucleotide reductase is responsible for the conversion of ribonucleoside diphosphate to 2′-deoxyribonucleoside diphosphate to maintain the homeostasis of nucleotide pools. In this study, mining the cancer genomics and proteomics data revealed that ribonucleotide reductase regulatory subunit M2 (RRM2) serves as a prognosis biomarker and a therapeutic target for HCC. The RNA sequencing (RNA-Seq) analysis and public microarray data mining found that RRM2 was a novel molecular target of sorafenib in HCC cells. In vitro experiments validated that sorafenib inhibits RRM2 expression in HCC cells, which is positively associated with the anticancer activity of sorafenib. Although both RRM2 knockdown and sorafenib induced autophagy in HCC cells, restoration of RRM2 expression did not rescue HCC cells from sorafenib-induced autophagy and growth inhibition. However, long-term colony formation assay indicated that RRM2 overexpression partially rescues HCC cells from the cytotoxicity of sorafenib. Therefore, this study identifies that RRM2 is a novel target of sorafenib, partially contributing to its anticancer activity in HCC cells.
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LeBlanc, Jason J., Ross J. Davidson, and Paul S. Hoffman. "Compensatory Functions of Two Alkyl Hydroperoxide Reductases in the Oxidative Defense System of Legionella pneumophila." Journal of Bacteriology 188, no. 17 (September 1, 2006): 6235–44. http://dx.doi.org/10.1128/jb.00635-06.
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ABSTRACT Legionella pneumophila expresses two catalase-peroxidase enzymes that exhibit strong peroxidatic but weak catalatic activities, suggesting that other enzymes participate in decomposition of hydrogen peroxide (H2O2). Comparative genomics revealed that L. pneumophila and its close relative Coxiella burnetii each contain two peroxide-scavenging alkyl hydroperoxide reductase (AhpC) systems: AhpC1, which is similar to the Helicobacter pylori AhpC system, and AhpC2 AhpD (AhpC2D), which is similar to the AhpC AhpD system of Mycobacterium tuberculosis. To establish a catalatic function for these two systems, we expressed L. pneumophila ahpC1 or ahpC2 in a catalase/peroxidase mutant of Escherichia coli and demonstrated restoration of H2O2 resistance by a disk diffusion assay. ahpC1::Km and ahpC2D::Km chromosomal deletion mutants were two- to eightfold more sensitive to H2O2, tert-butyl hydroperoxide, cumene hydroperoxide, and paraquat than the wild-type L. pneumophila, a phenotype that could be restored by trans-complementation. Reciprocal strategies to construct double mutants were unsuccessful. Mutant strains were not enfeebled for growth in vitro or in a U937 cell infection model. Green fluorescence protein reporter assays revealed expression to be dependent on the stage of growth, with ahpC1 appearing after the exponential phase and ahpC2 appearing during early exponential phase. Quantitative real-time PCR showed that ahpC1 mRNA levels were ∼7- to 10-fold higher than ahpC2D mRNA levels. However, expression of ahpC2D was significantly increased in the ahpC1 mutant, whereas ahpC1 expression was unchanged in the ahpC2D mutant. These results indicate that AhpC1 or AhpC2D (or both) provide an essential hydrogen peroxide-scavenging function to L. pneumophila and that the compensatory activity of the ahpC2D system is most likely induced in response to oxidative stress.
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Jones, Thomas A., Thomas A. Monaco, Steven R. Larson, Erik P. Hamerlynck, and Jared L. Crain. "Using Genomic Selection to Develop Performance-Based Restoration Plant Materials." International Journal of Molecular Sciences 23, no. 15 (July 27, 2022): 8275. http://dx.doi.org/10.3390/ijms23158275.
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Effective native plant materials are critical to restoring the structure and function of extensively modified ecosystems, such as the sagebrush steppe of North America’s Intermountain West. The reestablishment of native bunchgrasses, e.g., bluebunch wheatgrass (Pseudoroegneria spicata [Pursh] À. Löve), is the first step for recovery from invasive species and frequent wildfire and towards greater ecosystem resiliency. Effective native plant material exhibits functional traits that confer ecological fitness, phenotypic plasticity that enables adaptation to the local environment, and genetic variation that facilitates rapid evolution to local conditions, i.e., local adaptation. Here we illustrate a multi-disciplinary approach based on genomic selection to develop plant materials that address environmental issues that constrain local populations in altered ecosystems. Based on DNA sequence, genomic selection allows rapid screening of large numbers of seedlings, even for traits expressed only in more mature plants. Plants are genotyped and phenotyped in a training population to develop a genome model for the desired phenotype. Populations with modified phenotypes can be used to identify plant syndromes and test basic hypotheses regarding relationships of traits to adaptation and to one another. The effectiveness of genomic selection in crop and livestock breeding suggests this approach has tremendous potential for improving restoration outcomes for species such as bluebunch wheatgrass.
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Kaufman, Jacob. "Interferon gamma resistance in setting of LKB1 loss: Phenotypic characterization and investigation of mechanism." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e21015-e21015. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e21015.
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e21015 Background: NSCLC Patients with LKB1 loss respond poorly to immune checkpoint inhibitors (ICI). Determining mechanisms of the underlying immune resistance and strategies to overcome it are urgent and unmet clinical needs. Methods: We re-expressed WT LKB1 into LKB1 mutant NSCLC cell lines and measured effects on immune associated phenotypes in vitro. Specifically, we evaluated response to exogenous interferon gamma (IFNG), as well T-cell mediated cytotoxicity using a T-cell co-culture assay. To identify IFNG signaling changes influenced by LKB1, we evaluated the differential effects of LKB1 on IFNG induced gene expression using RNAseq. Finally, we performed a whole genome loss of function screen using CRISPR-Cas9 library (TKOv3) to identify genes and pathways that modify susceptibility to IFNG in the LKB1 mutant and LKB1 WT state in the A549 cell line. Results: Across multiple LKB1 mutant cell lines, restoration of WT LKB1 enhanced anti-proliferative effects of IFNG in vitro. Furthermore, WT LKB1 enhanced T-cell mediated cytotoxicity in T-cell co-culture assays using anti-NY-ESO TCR and expression of NY-ESO antigen into an HLA matched NSCLC cell line, H2023 (17% vs 40% cell death; P < 0.01). IFNG treatment induced expression of a core set of interferon-driven genes in both the mutant and LKB1 WT state. However, differentially expressed gene classes included downregulation of proliferation-associated genes in the LKB1 WT state, as well as upregulation of ferroptosis genes, and enhanced IFNG-driven expression of immune evasion genes including PDL1, PDL2, TRAF1, and IDO1 in the LKB1 WT state. PDL1 expression was assessed by flow cytometry and found to be upregulated upon expression of LKB1. Our functional genomics screen identified genes whose inhibition enhanced IFNG susceptibility in the A549 mutant state, and genes whose inhibition restored IFNG resistance in the A549 LKB1 WT state. Preliminary analysis identifies candidate signaling and metabolic pathways that appear to confer IFNG sensitivity in the mutant state without significant effect on IFNG sensitivity after LKB1 add-back. These include modifiers of the Hippo/YAP pathway as well as modifiers of ferroptosis, which will form the basis for further mechanistic experiments. Conclusions: ICI resistance caused by LKB1 loss is associated with insensitivity to IFNG, and can be modified in vitro by re-expression of WT LKB1. An integrated approach to evaluate modifiers of IFNG effects identifies resistance mechanisms that may be potential therapeutic targets.
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Opalko, A. I., and O. P. Serzhuk. "Lysenkoizm phenomenon in the genomic era." Visnik ukrains'kogo tovaristva genetikiv i selekcioneriv 15, no. 1 (October 1, 2017): 69–77. http://dx.doi.org/10.7124/visnyk.utgis.15.1.715.
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During the round table meetings «Retrospective analysis of the learning efficiency in a genetics (Current Issues and Trends)», devoted to the 80-th anniversary of Yurii Mykolaiovych Mishkurov, a knowledge specialist of didactic problems of genetics at high school, the actual questions about a new round of perigenetics mythicize which are observed in Genomic era were discussed in the form of open discussion. An attempt to reveal the phenomenon of popularity of pseudogenetic and other pseudoscientific theories, which are spread by current television was done, the role of a teacher in forming a scientific picture of the world and in particular manifestation of heredity and variability was appreciated. It is proposed to file a petition for the correction of the curriculum and returning the subject «Applied Genetics and the basics of cytology» to the list of compulsory disciplines of Master’s degree in specialities: 201 — «Agronomy», 202 — «Plants Protection and Quarantine», 203 — «Horticulture and Viticulture», 205 — «Forestry», 206 — «Landscape Gardening» and for restoration in full volume of contact hours (lectures, laboratory and practical classes), term paper, training practice and planning of hours to control self-learning of students. The content of a Bachelor’s degree program on «Genetics» regarding the restoration of training practice and controlling of selflearning of students must be updated.Keywords: Bologna process, teaching of genetics, pseudoscience, heredity and variability, public consciousness.
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Cross, Hugh, Ed Biffin, Kor-jent van Dijk, Andrew Lowe, and Michelle Waycott. "Effective application of next-generation sequencing (NGS) approaches in systematics and population genetics: case studies in Eucalyptus and Acacia." Australian Systematic Botany 29, no. 3 (2016): 235. http://dx.doi.org/10.1071/sb16019.
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Next-generation sequencing (NGS) provides numerous tools for population and systematic studies. These tools are a boon to researchers working with non-model and poorly characterised organisms where little or no genomic resources exist. Several techniques have been developed to subsample the genomes of multiple individuals from related populations and species, so as to discover variable regions. We describe here the use of a modified AFLPseq method that provides a rapid and cost-effective approach to screening variable gene regions (SNPs) for multiple samples. Our method provides an adaptable toolkit for multiple downstream applications, which can be scaled up or down depending on the needs of the research question and budget. Using minor modifications to the protocol, we successfully recovered variable and useful markers that were applied to three case studies examining different scales of biological organisation, namely, from within populations to phylogenetic questions at the genus level and above. The case studies on Acacia and Eucalyptus generated genomic data across multiple taxonomic hierarchies, including demonstrating the detection of Acacia pinguifolia J.M.Black individuals used in restoration and their population origins, regional phylogeography of Acacia pycnantha Benth., and SNP-marker conservatism across some 70million years of divergence among the Myrtaceae.
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Jordan, Rebecca, Suzanne M. Prober, Ary A. Hoffmann, and Shannon K. Dillon. "Combined Analyses of Phenotype, Genotype and Climate Implicate Local Adaptation as a Driver of Diversity in Eucalyptus microcarpa (Grey Box)." Forests 11, no. 5 (April 28, 2020): 495. http://dx.doi.org/10.3390/f11050495.
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Trees are a keystone species in many ecosystems and a critical component of ecological restoration. Understanding their capacity to respond to climate change is essential for conserving biodiversity and determining appropriate restoration seed sources. Patterns of local adaptation to climate between populations within a species can inform such conservation decisions and are often investigated from either a quantitative trait or molecular genetic basis. Here, we present findings from a combined analysis of phenotype (quantitative genetic analysis), genotype (single nucleotide polymorphism (SNP) trait associations), and climate associations. We draw on the strength of this combined approach to investigate pre-existing climate adaptation and its genetic basis in Eucalyptus microcarpa (Grey box), an important tree for ecological restoration in south-eastern Australia. Phenotypic data from a 26-year-old provenance trial demonstrated significant genetic variation in growth and leaf traits at both the family and provenance levels. Growth traits were only associated with temperature, whilst leaf traits were associated with temperature, precipitation and aridity. Genotyping of 40 putatively adaptive SNPs from previous genome-wide analyses identified 9 SNPs associated with these traits. Drawing on previous SNP–climate association results, several associations were identified between all three comparisons of phenotype, genotype and climate. By combining phenotypic with genomic analyses, these results corroborate genomic findings and enhance understanding of climate adaptation in E. microcarpa. We discuss the implication of these results for conservation management and restoration under climate change.
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Gudima, S. O. "Restoration in vivo of defective hepatitis delta virus RNA genomes." RNA 12, no. 6 (April 17, 2006): 1061–73. http://dx.doi.org/10.1261/rna.2328806.
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Pavlova, K. S. "Skin care as a way to recover microbiome in patients with atopic dermatitis." Russian Journal of Allergy 11, no. 1 (December 15, 2014): 17–22. http://dx.doi.org/10.36691/rja526.
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Recently microbiome of the skin was characterized using genomic technologies in norm and in pathology. Microbiome of the affected skin in atopic dermatitis is characterized by a lack of the variety of bacteria, decrease of the Actinomycetes and Proteobacteries species and increase of Staphylococci colonization (Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus haemolyticus and others). Restoration of the skin barrier function is the most important goal in the overall concept of the atopic dermatitis treatment. Recent studies demonstrated the possibility of reductionof inflammation, xerosis, itching and restoration of skin microbiome of the affected areas by emollients use (Lipikar Baume AP, La Roche Posay), as a result of the skin barrier function improvement.
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Prober, Suzanne M., Brad M. Potts, Tanya Bailey, Margaret Byrne, Shannon Dillon, Peter A. Harrison, Ary A. Hoffmann, et al. "Climate adaptation and ecological restoration in eucalypts." Proceedings of the Royal Society of Victoria 128, no. 1 (2016): 40. http://dx.doi.org/10.1071/rs16004.
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Eucalypts are the cornerstone of ecological restoration efforts across the highly modified agricultural landscapes of southern Australia. ‘Local provenancing’ is the established strategy for sourcing germplasm for ecological restoration plantings, yet this approach gives little consideration to the persistence of these plantings under future climates. This paper provides a synopsis of recent and ongoing research that the authors are undertaking on climate adaptation in eucalypts, combining new genomic approaches with ecophysiological evidence from provenance trials. These studies explore how adaptive diversity is distributed within and among populations, whether populations are buffered against change through capacity for phenotypic plasticity, and how this informs provenancing strategies. Results to date suggest that eucalypts have some capacity to respond to future environmental instability through adaptive phenotypic plasticity or selection of putatively adaptive alleles. Despite this, growing evidence suggests that eucalypts will still be vulnerable to change. Provenancing strategies that exploit adaptations found in non-local provenances could thus confer greater climate-resilience in ecological restoration plantings, although they will also need to account for potential interactions between climate adaptations and other factors (e.g. cryptic evolutionary variation, non-climate-related adaptations, herbivory and elevated CO2).
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Duan, Yuange, Wanzhi Cai, and Hu Li. "Chloroplast C-to-U RNA editing in vascular plants is adaptive due to its restorative effect: testing the restorative hypothesis." RNA 29, no. 2 (January 17, 2023): 141–52. http://dx.doi.org/10.1261/rna.079450.122.
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The adaptiveness of nonsynonymous RNA editing (recoding) could be conferred by the flexibility of the temporal-spatially controllable proteomic diversity, or by its restorative effect which fixes unfavorable genomic mutations at the RNA level. These two complementary hypotheses, namely, the diversifying hypothesis and the restorative hypothesis, have distinct predictions on the landscape of RNA editing sites. We collected the chloroplast C-to-U RNA editomes of 21 vascular plants (11 angiosperms, four gymnosperms, and six ferns) from a previous study, aiming to testify whether the plant editomes typically conform to the restorative hypothesis. All predictions made by the restorative hypothesis are verified: (i) nonsynonymous editing sites are more frequent and have higher editing levels than synonymous sites; (ii) nonsynonymous editing levels are extremely high and show weak tissue-specificity in plants; (iii) on the inferred genomic sites with recent T-to-C mutations, nonsynonymous sites but not synonymous sites are compensated by C-to-U RNA editing. In conclusion, nonsynonymous C-to-U RNA editing in plants is adaptive due to its restorative effects. The recoding levels are high and are constantly required across the whole plant so that the recoding events could perfectly mimic DNA mutations. The evolutionary significance of plant RNA editing is systematically demonstrated at the genome-wide level.
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Li, Jie, Yujiao Sun, Xiaoyue Zhang, Chengzhong Pan, Shurong Zhang, and Binghui Zheng. "Water Quality and Microbial Community in the Context of Ecological Restoration: A Case Study of the Yongding River, Beijing, China." International Journal of Environmental Research and Public Health 19, no. 20 (October 11, 2022): 13056. http://dx.doi.org/10.3390/ijerph192013056.
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Ecological water replenishment via interbasin water diversion projects provides opportunities for ecological river restoration. Untangling water quality changes, microbiota dynamics, and community functions is necessary for sustainable ecological management. Using the Yongding River as a case study, we monitored the water quality and applied genomic sequencing to investigate microbial communities of the river in different stages after ecological water replenishment. Our results showed that river water quality represented by chemical oxygen demand (COD), total nitrogen (TN), and chlorophyll-a (Chl-a) did not change significantly during months after water replenishment. The bacterial community composition varied in different months and river subsections. The Cyanobium_PCC-6307, CL500-29 marine group, and Pseudomonas were dominant in the later stages after water replenishment. Water temperature, pH, and nutrient levels significantly affected the microbial community composition, and ecological restoration may have the potential to influence nitrogen cycling in the river. Our results can provide ecological insights into sustainable water quality maintenance and river management following ecological restoration enabled by ecological water replenishment.
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Frazier, Courtney L., Joseph San Filippo, Alan M. Lambowitz, and David A. Mills. "Genetic Manipulation of Lactococcus lactis by Using Targeted Group II Introns: Generation of Stable Insertions without Selection." Applied and Environmental Microbiology 69, no. 2 (February 2003): 1121–28. http://dx.doi.org/10.1128/aem.69.2.1121-1128.2003.
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ABSTRACT Despite their commercial importance, there are relatively few facile methods for genomic manipulation of the lactic acid bacteria. Here, the lactococcal group II intron, Ll.ltrB, was targeted to insert efficiently into genes encoding malate decarboxylase (mleS) and tetracycline resistance (tetM) within the Lactococcus lactis genome. Integrants were readily identified and maintained in the absence of a selectable marker. Since splicing of the Ll.ltrB intron depends on the intron-encoded protein, targeted invasion with an intron lacking the intron open reading frame disrupted TetM and MleS function, and MleS activity could be partially restored by expressing the intron-encoded protein in trans. Restoration of splicing from intron variants lacking the intron-encoded protein illustrates how targeted group II introns could be used for conditional expression of any gene. Furthermore, the modified Ll.ltrB intron was used to separately deliver a phage resistance gene (abiD) and a tetracycline resistance marker (tetM) into mleS, without the need for selection to drive the integration or to maintain the integrant. Our findings demonstrate the utility of targeted group II introns as a potential food-grade mechanism for delivery of industrially important traits into the genomes of lactococci.
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Spencer, David, David Russler-Germain, Nichole M. Helton, Tamara L. Lamprecht, Marwan Shinawi, Peter Westervelt, Jacqueline E. Payton, et al. "DNMT3A-Dependent DNA Methylation May Act As a Tumor Suppressor-Not a Tumor Promoter-during AML Progression." Blood 128, no. 22 (December 2, 2016): 1050. http://dx.doi.org/10.1182/blood.v128.22.1050.1050.
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Abstract Altered DNA methylation is a well-known feature of acute myeloid leukemia (AML) genomes, but the mechanisms underlying these changes and their relevance for AML pathogenesis are unclear. We previously showed that DNMT3A is the predominant de novo methyltransferase expressed in AML cells, and that the DNMT3AR882H mutation in AML creates a dominant negative protein that reduces in vitro DNA methylation activity by ~80%. Since DNMT3A provides themajority of the methylation activity in AML cells, we hypothesized that AML samples with and without DNMT3AR882H could reveal novel insights about the role of this enzyme in AML initiation and progression. We performed whole-genome bisulfite sequencing (WGBS) of 38 primary human AML samples and 17 normal human hematopoietic cell samples, as well as a remission sample from a patient with a persistent DNMT3AR882H mutation, and blood samples from a non-leukemic patient with a constitutional DNMT3AR882H mutation. We first identified 3,848 differentially methylated regions ('DMRs') between DNMT3AR882H and DNMT3AWT AMLs, virtually all of which were hypomethylated in the DNMT3AR882H AMLs. Further, 28% (1,087/3,848) of these DMRs were also hypomethylated when compared to CD34 cells, implying that these regions are truly hypomethylated in the AML cells with the R882H mutation. In contrast, 72% (2,759/3,848) of the DMRs were unmethylated in bothDNMT3AR882H AMLs and CD34 cells, but were hypermethylated in the DNMT3AWT AML samples. These loci were associated with CpG dense regions, suggesting that they represent abnormal CpG island hypermethylation that occurs only in AML samples with wild-type DNMT3A. Analysis of 21 additional primary AML samples with wild-type DNMT3A identified 4,912 hypermethylated regions compared to CD34 cells, of which 4,544 (92%) were significantly less methylated in DNMT3AR882H AMLs, implying that functional DNMT3A mediates abnormal CpG island hypermethylation in AML. WGBS analysis of two non-leukemic hematopoietic samples with DNMT3AR882H mutations was also performed to understand the direct effects of DNMT3AR882H in non-transformed myeloid cells. These samples included peripheral blood (PB) neutrophils and monocytes from a newly identified 9-year old patient with an overgrowth syndrome and developmental delay (Tatton-Brown et. al., Nature Genetics 2014), who was found to have a heterozygous DNMT3AR882H mutation in all skin and peripheral blood cells. His CBC was normal, and he had no evidence of clonal hematopoiesis by exome sequencing. We identified 2,051 DMRs in his PB myeloid cells, all of which were hypomethylated compared to control PB myeloid cells from his healthy 13-year old brother (and also normal CD34 cells), demonstrating that DNMT3AR882H directly causes focal methylation loss. We also performed WGBS on cells expanded from single stem/progenitor cells from an AML patient with a persistent DNMT3AR882H mutation during remission. Expanded cells with DNMT3AR882H were hypomethylated relative to wild-type DNMT3A cells expanded from the same sample. The majority of the hypomethylated regions were also present in the patient's AML cells, implying that DNMT3AR882H-associated hypomethylation in pre-leukemic cells is maintained during AML progression. These findings demonstrate that DNMT3AR882H-associated hypomethylation precedes leukemia development, and may therefore represent an important initiating phenotype for AML. Our data also suggest that the abnormal hypermethylation of CpG islands in AML cells is DNMT3A-dependent, and must occur during disease progression. This hypermethylation is absent in AMLs with DNMT3AR882H, revealing that it is not required for leukemia progression. We therefore propose a model where DNMT3A-dependent DNA methylation in AML cells acts as a 'brake' that prevents abnormal self-renewal; the abnormal CpG island hypermethylation in DNMT3AWT AMLs may be an adaptive response that is ultimately overcome during leukemia progression. The absence of this 'braking' activity in AMLs with DNMT3AR882H may contribute directly to leukemia initiation. The restoration of DNMT3A activity in AML cells with the DNMT3AR882H mutation is therefore a therapeutic goal. Disclosures Spencer: Cofactor Genomics: Consultancy.
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Humphrey, Christine E., Nicole Burnett, Shivangi Dubey, and John A. Kyndt. "Genomic and Phylogenetic Characterization of Rhodopseudomonas infernalis sp. nov., Isolated from the Hell Creek Watershed (Nebraska)." Microorganisms 10, no. 10 (October 13, 2022): 2024. http://dx.doi.org/10.3390/microorganisms10102024.
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The genus Rhodopseudomonas is known for its versatile metabolic capabilities and has been proposed to be used in a wide variety of innovative applications, ranging from biohydrogen and electricity production, bioremediation and as biostimulant in agriculture. Here, we report the isolation, characterization and genome sequence analysis of a novel Rhodopseudomonas species, strain HC1, isolated from the Hell Creek urban native restoration area. Whole genome-based analysis, average nucleotide identity (ANI) comparison, and growth characteristics identified this isolate as a new species of the Rhodopseudomonas genus, for which we propose the name Rhodopseudomonas infernalis sp. nov. Besides containing several nitrogenases for nitrogen fixation and hydrogen production, the HC1 genome encodes a unique gene cluster, not found in any other Rhodopseudomonas species, which encodes genes for the degradation of yet-unidentified aromatic PCB-type chemicals with potentially interesting biotechnological applications. The genomic features of Rps. infernalis HC1 indicate that it plays a positive role in the degradation of anthropogenic substances and aids the restoration of the Hell Creek watershed by contributing to N2 and carbon fixation and plant growth; however, the genome also contains several antibiotic resistance genes, indicating a broad range of antibiotic resistance in this environmental isolate.
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Vendelbo, Nikolaj Meisner, Khalid Mahmood, Pernille Sarup, Peter Skov Kristensen, Jihad Orabi, and Ahmed Jahoor. "Genomic Scan of Male Fertility Restoration Genes in a ‘Gülzow’ Type Hybrid Breeding System of Rye (Secale cereale L.)." International Journal of Molecular Sciences 22, no. 17 (August 27, 2021): 9277. http://dx.doi.org/10.3390/ijms22179277.
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Efficient and stable restoration of male fertility (Rf) is a prerequisite for large-scale hybrid seed production but remains an inherent issue in the predominant fertility control system of rye (Secale cereale L.). The ‘Gülzow’ (G)-type cytoplasmic male sterility (CMS) system in hybrid rye breeding exhibits a superior Rf. While having received little scientific attention, one major G-type Rf gene has been identified on 4RL (Rfg1) and two minor genes on 3R (Rfg2) and 6R (Rfg3) chromosomes. Here, we report a comprehensive investigation of the genetics underlying restoration of male fertility in a large G-type CMS breeding system using recent advents in rye genomic resources. This includes: (I) genome-wide association studies (GWAS) on G-type germplasm; (II) GWAS on a biparental mapping population; and (III) an RNA sequence study to investigate the expression of genes residing in Rf-associated regions in G-type rye hybrids. Our findings provide compelling evidence of a novel major G-type non-PPR Rf gene on the 3RL chromosome belonging to the mitochondrial transcription termination factor gene family. We provisionally denote the identified novel Rf gene on 3RL RfNOS1. The discovery made in this study is distinct from known P- and C-type systems in rye as well as recognized CMS systems in barley (Hordeum vulgare L.) and wheat (Triticum aestivum L.). We believe this study constitutes a stepping stone towards understanding the restoration of male fertility in the G-type CMS system and potential resources for addressing the inherent issues of the P-type system.
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Gökçe, Ali Fuat, John McCallum, Yutaka Sato, and Michael J. Havey. "Molecular Tagging of the Ms Locus in Onion." Journal of the American Society for Horticultural Science 127, no. 4 (July 2002): 576–82. http://dx.doi.org/10.21273/jashs.127.4.576.
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Cytoplasmic-genic male sterility (CMS) is used to produce hybrid onion (Allium cepa L.) seed. For the most widely used source of onion CMS, male sterility is conditioned by the interaction of the male-sterile (S) cytoplasm and the homozygous recessive genotype at a nuclear male-fertility restoration locus (Ms). Maintainer lines are used to seed propagate male-sterile lines, possess normal (N) male-fertile cytoplasm, and are homozyous recessive at the Ms locus. Due to the biennial nature of onion, it takes 4 to 8 years of crossing and scoring of progeny phenotypes to establish if maintainer lines can be extracted from an uncharacterized population or family. Identification of nuclear markers tightly linked to the Ms locus would allow for molecular-facilitated selection of maintainer lines. We evaluated testcross progenies from a segregating family for nuclear restoration of male fertility over at least three environments. Although segregations in the F2 family fit the expected 1:2:1 ratio (P = 0.973), the proportion of male-sterile testcross progenies showed significant (P < 0.01) year effects and it is therefore imperative to score male-fertility restoration over environments. Too many male-sterile testcross progenies were often observed, indicating that the dominant allele conditioning male-fertility restoration for S cytoplasm may not show complete penetrance. Segregations of amplified fragment length polymorphisms and restriction fragment length polymorphisms (RFLPs) revealed RFLPs flanking the Ms locus at 0.9 and 8.6 cM. An onion cDNA showing highly significant homology to the aldehyde dehydrogenase conditioned by the rf2 locus of maize was identified and mapped to linkage group I, independent of the Ms locus. A sample of commercial onion germplasm was evaluated for putative allelic diversity at the RFLP loci linked to Ms. The genomic region corresponding to the cDNA (AOB272) revealing the closest RFLP to Ms was sequenced to reveal numerous single nucleotide polymorphisms. Single-stranded conformational polymorphisms and single nucleotide extensions were developed that revealed genomic variation at AOB272-EcoRI. The use of these molecular markers to select maintainer lines in onion is discussed.
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Zheng, Mingmin, Tian Yang, Xiaowei Liu, Guihua Lü, Peng Zhang, Bin Jiang, Shufeng Zhou, et al. "qRf8-1, a Novel QTL for the Fertility Restoration of Maize CMS-C Identified by QTL-seq." G3: Genes|Genomes|Genetics 10, no. 7 (May 29, 2020): 2457–64. http://dx.doi.org/10.1534/g3.120.401192.
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C-type cytoplasmic male sterility (CMS-C), one of the three major CMS types in maize, has a promising application prospect in hybrid seed production. However, the complex genetic mechanism underlying the fertility restoration of CMS-C remains poorly understood. The maize inbred line A619 is one of the rare strong restorer lines carrying the restorer gene Rf4, but different fertility segregation ratios are found in several F2 populations derived from crosses between isocytoplasmic allonucleus CMS-C lines and A619. In the present study, the segregation ratios of fertile to sterile plants in the (CHuangzaosi × A619) F2 and BC1F1 populations (36.77:1 and 2.36:1, respectively) did not follow a typical monogenic model of inheritance, which suggested that some F2 and BC1F1 plants displayed restored fertility even without Rf4. To determine the hidden locus affecting fertility restoration, next-generation sequencing-based QTL-seq was performed with two specific extreme bulks consisting of 30 fertile and 30 sterile rf4rf4 individuals from the F2 population. A major QTL related to fertility restoration, designated qRf8-1, was detected on the long arm of chromosome 8 in A619. Subsequently, qRf8-1 was further validated and narrowed down to a 17.93-Mb genomic interval by insertion and deletion (InDel) and simple sequence repeat (SSR) marker-based traditional QTL mapping, explaining 12.59% (LOD = 25.06) of the phenotypic variation. Thus, using genetic analyses and molecular markers, we revealed another fertility restoration system acting in parallel with Rf4 in A619 that could rescue the male sterility of CHuangzaosi. This study not only expands the original fertility restoration system but also provides valuable insights into the complex genetic mechanisms underlying the fertility restoration of CMS-C.
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Gruenthal, K. M., D. A. Witting, T. Ford, M. J. Neuman, J. P. Williams, D. J. Pondella, A. Bird, et al. "Development and application of genomic tools to the restoration of green abalone in southern California." Conservation Genetics 15, no. 1 (August 21, 2013): 109–21. http://dx.doi.org/10.1007/s10592-013-0524-5.
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Wenzel, Tim, Thomas Büch, Nicole Urban, Ulrike Weirauch, Katrin Schierle, Achim Aigner, Michael Schaefer, and Hermann Kalwa. "Restoration of MARCK enhances chemosensitivity in cancer." Journal of Cancer Research and Clinical Oncology 146, no. 4 (February 13, 2020): 843–58. http://dx.doi.org/10.1007/s00432-020-03149-2.
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Abstract Purpose Increased ATP-binding-cassette (ABC) transporter activity is a major cause of chemotherapy resistance in cancer. The ABC transporter family member ABCB1 is often overexpressed in colorectal cancer (CRC). Phosphatidylinositol-4,5-bisphosphat (PI(4,5)P2)-dependent pathways are involved in the regulation of ABCB1 function. The protein Myristoylated Alanine-Rich C-Kinase Substrate (MARCKS) is a pivotal regulator of PI(4,5)P2 and inactivated in many CRC cancers via genetic deletion or hyperphosphorylation. Therefore, MARCKS may critically impact ABCB1. Methods CRC samples as well as CRC cell lines were tested for a connection between MARCKS and ABCB1 via immunofluorescence and Western-blot analysis. ABCB1 function was studied via calcein influx assay under treatment with known ABCB1 inhibitors (verapamil, tariquidar) as well as the kinase inhibitor bosutinib. ABCB1 internalization and MARCKS translocation was analyzed via confocal microscopy exploiting the endocytosis inhibitors chlorpromazine and dynasore. Abundance of PI(4,5)P2 was monitored by intramolecular fluorescence resonance energy transfer (FRET). Reproductive cell survival was studied via colorimetric WST-1 and clonogenic assays in combination with exposure to the chemotherapeutics doxorubicin and 5-fuorouracil (5-FU). Results We found increased ABCB1 expression in MARCKS negative CRC patient tumor samples and established CRC cell lines. Mechanistically, the reconstitution of MARCKS function via recombinant expression or the pharmacological inhibition of MARCKS phosphorylation led to a substantial decrease in ABCB1 activity. In CRC cells, bosutinib treatment resulted in a MARCKS translocation from the cytosol to the plasma membrane, while simultaneously, ABCB1 was relocated to intracellular compartments. Inhibition of MARCKS phosphorylation via bosutinib rendered cells more sensitive to the chemotherapeutics doxorubicin and 5-FU. Conclusions Cells devoid of MARCKS function showed incomplete ABCB1 internalization, leading to higher ABCB1 activity enhancing chemoresistance. Vice versa our data suggest the prevention of MARCKS inhibition by reversing hyperphosphorylation or genomic restoration after deletion as two promising approaches to overcome tumor cell resistance towards chemotherapeutic ABCB1 substrates.
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Steininger, Anne, Markus Möbs, Reinhard Ullmann, Karl Köchert, Stephan Kreher, Björn Lamprecht, Ioannis Anagnostopoulos, et al. "Genomic loss of the putative tumor suppressor gene E2A in human lymphoma." Journal of Experimental Medicine 208, no. 8 (July 25, 2011): 1585–93. http://dx.doi.org/10.1084/jem.20101785.
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The transcription factor E2A is essential for lymphocyte development. In this study, we describe a recurrent E2A gene deletion in at least 70% of patients with Sézary syndrome (SS), a subtype of T cell lymphoma. Loss of E2A results in enhanced proliferation and cell cycle progression via derepression of the protooncogene MYC and the cell cycle regulator CDK6. Furthermore, by examining the gene expression profile of SS cells after restoration of E2A expression, we identify several E2A-regulated genes that interfere with oncogenic signaling pathways, including the Ras pathway. Several of these genes are down-regulated or lost in primary SS tumor cells. These data demonstrate a tumor suppressor function of E2A in human lymphoid cells and could help to develop new treatment strategies for human lymphomas with altered E2A activity.
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Zhu, Qianzheng, Gulzar Wani, Hany H. Arab, Mohamed A. El-Mahdy, Alo Ray, and Altaf A. Wani. "Chromatin restoration following nucleotide excision repair involves the incorporation of ubiquitinated H2A at damaged genomic sites." DNA Repair 8, no. 2 (February 2009): 262–73. http://dx.doi.org/10.1016/j.dnarep.2008.11.007.
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Yu, Sung-Lim, Mi-Sun Kang, Ho-Yeol Kim, Sung Haeng Lee, and Sung-Keun Lee. "Restoration of proliferation ability with increased genomic instability from Rad2p-induced mitotic catastrophe in Saccharomyces cerevisiae." Molecular & Cellular Toxicology 7, no. 3 (September 2011): 195–206. http://dx.doi.org/10.1007/s13273-011-0026-9.
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Widyastuti, Yuni, Muhamad Yunus, Bambang Sapta Purwoko, and Satoto Satoto. "DIVERSITY AND CAPABILITY ANALYSES OF FERTILITY RESTORER GENES OF CYTOPLASMIC MALE STERILE RICE LINES USING SSR." Indonesian Journal of Agricultural Science 18, no. 2 (January 30, 2018): 43. http://dx.doi.org/10.21082/ijas.v18n2.2017.p43-50.
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<p class="abstrakinggris">Development of hybrid rice depends on the effectivity of cytoplasmic male sterility (CMS) and restorer (R) lines. The molecular genetic approach is expected to help the breeder in identification of suitable parental lines to hybrid rice improvement. The study aimed to assess genetic relationship among three types of CMS systems (wild abbortive/WA Kalinga and Gambiaca) as female parents and to identify diversity of genes controlling fertility restoration in rice. The study used nine F<sub>1</sub> hybrids and F<sub>2</sub> populations obtained from the hybridization of three different CMS lines (IR58025A-WA, IR80156A-Kalinga and IR80154A-Gambiaca) with three restorer lines (PK90, PK12 and BP11). Fifteen SSR markers were used to select genomic regions of chromosome 1 and 10 on which <em>Rf3</em> and <em>Rf4</em> genes located in the hybrids. The results showed that fertility restoration in CMS-WA and CMS-Gambiaca was governed by two independent and dominant genes (<em>Rf3</em> and <em>Rf4</em>), while in CMS-Kalinga the fertility restoration was controlled by one single dominant gene. Biological processes occurred in the fertility restoration of the hybrids were the same based on the pollen and spikelet fertilities of F<sub>1</sub> hybrids derived from three CMS and R lines, i.e. 76.1–78.3% and 69.1–76.6%, respectively. A restorer line PK12 had a higher capability in fertility restoration than PK90 and BP11. The SSR primers RM490 and RM258 were capable of identifying the <em>Rf3</em> and <em>Rf4</em> genes controlled fertility restoration in CMS-WA. The study supports the use of male sterile WA in rice hybridization. </p><p class="keyword"> </p>
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Shemesh-Mayer, Einat, Adi Faigenboim, Tomer E. Ben Michael, and Rina Kamenetsky-Goldstein. "Integrated Genomic and Transcriptomic Elucidation of Flowering in Garlic." International Journal of Molecular Sciences 23, no. 22 (November 10, 2022): 13876. http://dx.doi.org/10.3390/ijms232213876.
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Commercial cultivars of garlic are sterile, and therefore efficient breeding of this crop is impossible. Recent restoration of garlic fertility has opened new options for seed production and hybridization. Transcriptome catalogs were employed as a basis for garlic genetic studies, and in 2020 the huge genome of garlic was fully sequenced. We provide conjoint genomic and transcriptome analysis of the regulatory network in flowering garlic genotypes. The genome analysis revealed phosphatidylethanolamine-binding proteins (PEBP) and LEAFY (LFY) genes that were not found at the transcriptome level. Functions of TFL-like genes were reduced and replaced by FT-like homologs, whereas homologs of MFT-like genes were not found. The discovery of three sequences of LFY-like genes in the garlic genome and confirmation of their alternative splicing suggest their role in garlic florogenesis. It is not yet clear whether AsLFY1 acts alone as the “pioneer transcription factor” or AsLFY2 also provides these functions. The presence of several orthologs of flowering genes that differ in their expression and co-expression network advocates ongoing evolution in the garlic genome and diversification of gene functions. We propose that the process of fertility deprivation in garlic cultivars is based on the loss of transcriptional functions of the specific genes.
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Leonardi, D. P., and A. R. Vieira. "From Caries Progression and Restoration Failures to Periapical Lesions in the Era of Precision." JDR Clinical & Translational Research 5, no. 1 (April 26, 2019): 10–12. http://dx.doi.org/10.1177/2380084419846436.
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Knowledge Transfer Statement: Dental research can be thought of as a continuum of clinical observations that are dissected in the laboratory with answers that can be brought back to the clinic to change patient management. We believe this is the case for the use of adhesive systems and outcomes of dental treatment. Clinical observations related to negative outcomes have been tested in the laboratory and solutions have been proposed, with more precise implementation of these solutions possible when genomic approaches are added. Here we elaborate on this process based on the observations that lead to an attempt to inactivate metalloproteinase activity by dentin crosslinking.
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Shoshan, Yoav, Noa Liscovitch-Brauer, Joshua J. C. Rosenthal, and Eli Eisenberg. "Adaptive Proteome Diversification by Nonsynonymous A-to-I RNA Editing in Coleoid Cephalopods." Molecular Biology and Evolution 38, no. 9 (May 22, 2021): 3775–88. http://dx.doi.org/10.1093/molbev/msab154.
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Abstract RNA editing by the ADAR enzymes converts selected adenosines into inosines, biological mimics for guanosines. By doing so, it alters protein-coding sequences, resulting in novel protein products that diversify the proteome beyond its genomic blueprint. Recoding is exceptionally abundant in the neural tissues of coleoid cephalopods (octopuses, squids, and cuttlefishes), with an over-representation of nonsynonymous edits suggesting positive selection. However, the extent to which proteome diversification by recoding provides an adaptive advantage is not known. It was recently suggested that the role of evolutionarily conserved edits is to compensate for harmful genomic substitutions, and that there is no added value in having an editable codon as compared with a restoration of the preferred genomic allele. Here, we show that this hypothesis fails to explain the evolutionary dynamics of recoding sites in coleoids. Instead, our results indicate that a large fraction of the shared, strongly recoded, sites in coleoids have been selected for proteome diversification, meaning that the fitness of an editable A is higher than an uneditable A or a genomically encoded G.