Journal articles: 'Gene coregulation'

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Reja, Rohit, Vinesh Vinayachandran, Sujana Ghosh, and B. Franklin Pugh. "Molecular mechanisms of ribosomal protein gene coregulation." Genes & Development 29, no. 18 (September 15, 2015): 1942–54. http://dx.doi.org/10.1101/gad.268896.115.

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Györy, Ildikó, and Janos Minarovits. "Epigenetic regulation of lymphoid specific gene sets." Biochemistry and Cell Biology 83, no. 3 (June 1, 2005): 286–95. http://dx.doi.org/10.1139/o05-020.

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Coregulation of lymphoid-specific gene sets is achieved by a series of epigenetic mechanisms. Association with higher-order chromosomal structures (nuclear subcompartments repressing or favouring gene expression) and locus control regions affects recombination and transcription of clonotypic antigen receptors and expression of a series of other lymphoid-specific genes. Locus control regions can regulate DNA methylation patterns in their vicinity. They may induce tissue- and site-specific DNA demethylation and affect, thereby, accessibility to recombination-activating proteins, transcription factors, and enzymes involved in histone modifications. Both DNA methylation and the Polycomb group of proteins (PcG) function as alternative systems of epigenetic memory in lymphoid cells. Complexes of PcG proteins mark their target genes by covalent histone tail modifications and influence lymphoid development and rearrangement of IgH genes. Ectopic expression of protein noncoding microRNAs may affect the generation of B-lineage cells, too, by guiding effector complexes to sites of heterochromatin assembly. Coregulation of lymphoid and viral promoters is also possible. EBNA 2, a nuclear protein encoded by episomal Epstein-Barr virus genomes, binds to the cellular protein CBF1 (C promoter binding factor 1) and operates, thereby, a regulatory network to activate latent viral promoters and cellular promoters associated with CBF1 binding sites.Key words : lymphoid cells, coregulation of gene batteries, epigenetic regulation, nuclear subcompartment switch, locus control region, DNA methylation, Polycomb group of proteins, histone modifications, microRNA, Epstein-Barr virus, EBNA 2, regulatory network.

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Isaac, R. Stefan, Erik McShane, and L. Stirling Churchman. "The Multiple Levels of Mitonuclear Coregulation." Annual Review of Genetics 52, no. 1 (November 23, 2018): 511–33. http://dx.doi.org/10.1146/annurev-genet-120417-031709.

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Together, the nuclear and mitochondrial genomes encode the oxidative phosphorylation (OXPHOS) complexes that reside in the mitochondrial inner membrane and enable aerobic life. Mitochondria maintain their own genome that is expressed and regulated by factors distinct from their nuclear counterparts. For optimal function, the cell must ensure proper stoichiometric production of OXPHOS subunits by coordinating two physically separated and evolutionarily distinct gene expression systems. Here, we review our current understanding of mitonuclear coregulation primarily at the levels of transcription and translation. Additionally, we discuss other levels of coregulation that may exist but remain largely unexplored, including mRNA modification and stability and posttranslational protein degradation.

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Perco, Paul, Alexander Kainz, Gert Mayer, Arno Lukas, Rainer Oberbauer, and Bernd Mayer. "Detection of coregulation in differential gene expression profiles." Biosystems 82, no. 3 (December 2005): 235–47. http://dx.doi.org/10.1016/j.biosystems.2005.08.001.

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Arnone, James T., Jeffrey R. Arace, Anand R. Soorneedi, Teryn T. Citino, Tadashi L. Kamitaki, and Michael A. McAlear. "Dissecting thecisandtransElements That Regulate Adjacent-Gene Coregulation in Saccharomyces cerevisiae." Eukaryotic Cell 13, no. 6 (April 4, 2014): 738–48. http://dx.doi.org/10.1128/ec.00317-13.

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ABSTRACTThe relative positions that genes occupy on their respective chromosomes can play a critical role in determining how they are regulated at the transcriptional level. For example, a significant fraction of the genes from a variety of coregulated gene sets, including the ribosomal protein (RP) and the rRNA and ribosome biogenesis (RRB) regulons, exist as immediate, adjacent gene pairs. These gene pairs occur in all possible divergent, tandem, and convergent orientations. Adjacent-gene pairing in these regulons is associated with a tighter transcriptional coregulation than is observed for nonpaired genes of the same regulons. In order to define thecisandtransfactors that regulate adjacent-gene coregulation (AGC), we conducted a mutational analysis of the convergently oriented RRB gene pairMPP10-YJR003C. We observed that coupled corepression of the gene pair under heat shock was abrogated when the two genes were separated by an actively expressed RNA polymerase (Pol) II transcription unit (theLEU2gene) but not when the insertedLEU2gene was repressed. In contrast, the insertion of an RNA Pol III-transcribed tRNA (Thr) gene did not disrupt the coregulated repression ofMPP10andYJR003C. A targeted screen of mutants defective in regulating chromosome architecture revealed that the Spt20, Snf2, and Chd1 proteins were required for coupling the repression ofYJR003Cto that ofMPP10. Nucleosome occupancy assays performed across theMPP10andYJR003Cpromoter regions revealed that the mechanism of corepression of the gene pair was not related to the repositioning of nucleosomes across the respective gene promoters.

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Zuo, Yu-Ling, Di-Ping Gong, Bi-Ze Li, Juan Zhao, Ling-Yue Zhou, Fang-Yang Shao, Zhao Jin, and Yuan He. "The TF-miRNA Coregulation Network in Oral Lichen Planus." BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/731264.

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Oral lichen planus (OLP) is a chronic inflammatory disease that affects oral mucosa, some of which may finally develop into oral squamous cell carcinoma. Therefore, pinpointing the molecular mechanisms underlying the pathogenesis of OLP is important to develop efficient treatments for OLP. Recently, the accumulation of the large amount of omics data, especially transcriptome data, provides opportunities to investigate OLPs from a systematic perspective. In this paper, assuming that the OLP associated genes have functional relationships, we present a new approach to identify OLP related gene modules from gene regulatory networks. In particular, we find that the gene modules regulated by both transcription factors (TFs) and microRNAs (miRNAs) play important roles in the pathogenesis of OLP and many genes in the modules have been reported to be related to OLP in the literature.

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Medini, Hadar, Tal Cohen, and Dan Mishmar. "Mitochondria Are Fundamental for the Emergence of Metazoans: On Metabolism, Genomic Regulation, and the Birth of Complex Organisms." Annual Review of Genetics 54, no. 1 (November 23, 2020): 151–66. http://dx.doi.org/10.1146/annurev-genet-021920-105545.

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Out of many intracellular bacteria, only the mitochondria and chloroplasts abandoned their independence billions of years ago and became endosymbionts within the host eukaryotic cell. Consequently, one cannot grow eukaryotic cells without their mitochondria, and the mitochondria cannot divide outside of the cell, thus reflecting interdependence. Here, we argue that such interdependence underlies the fundamental role of mitochondrial activities in the emergence of metazoans. Several lines of evidence support our hypothesis: ( a) Differentiation and embryogenesis rely on mitochondrial function; ( b) mitochondrial metabolites are primary precursors for epigenetic modifications (such as methyl and acetyl), which are critical for chromatin remodeling and gene expression, particularly during differentiation and embryogenesis; and ( c) mitonuclear coregulation adapted to accommodate both housekeeping and tissue-dependent metabolic needs. We discuss the evolution of the unique mitochondrial genetic system, mitochondrial metabolites, mitonuclear coregulation, and their critical roles in the emergence of metazoans and in human disorders.

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Warrell, Jonathan, and Musa Mhlanga. "Stability and structural properties of gene regulation networks with coregulation rules." Journal of Theoretical Biology 420 (May 2017): 304–17. http://dx.doi.org/10.1016/j.jtbi.2016.10.020.

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Anda-Jáuregui, Guillermo de, Cristobal Fresno, Diana García-Cortés, Jesús Espinal Enríquez, and Enrique Hernández-Lemus. "Intrachromosomal regulation decay in breast cancer." Applied Mathematics and Nonlinear Sciences 4, no. 1 (June 28, 2019): 223–30. http://dx.doi.org/10.2478/amns.2019.1.00020.

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AbstractBiological systems exhibit unique phenotypes as the result of the expression of a genomic program. The regulation of this program is a complex phenomenon, wherein different regulatory mechanisms are involved. The deregulation of this program is at the centre of the emergence of diseases such as breast cancer. In particular, it has been observed that coregulation patterns between physically distant genes are lost in breast cancer.In this work, we present a systematic study of chromosome-wide gene coregulation patterns in breast cancer as inferred by information theoretical measures over large (whole-genome expression in several hundred transcriptomes) experimental data corpora. We analyzed the chromosomal distance decay of correlations and found it to be with fat-tail distribution in breast cancer while being fundamentally constant in nontumour samples.After model discrimination analyses, we concluded that the behaviour of the breast cancer distributions belongs to an intermediate regime between power law and Weibull distributions, with distinctive contributions corresponding to different chromosomes. This behaviour may have biological implications in terms of the organization of the gene regulatory program, and the changes found in this program between health and disease.

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Brych, Annika, Fabian B. Haas, Katharina Parzefall, Sabine Panzer, Jeanette Schermuly, Janine Altmüller, Timo Engelsdorf, et al. "Coregulation of gene expression by White collar 1 and phytochrome in Ustilago maydis." Fungal Genetics and Biology 152 (July 2021): 103570. http://dx.doi.org/10.1016/j.fgb.2021.103570.

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Berrard, Sylvie, Hélène Varoqui, Riccardo Cervini, Maurice Israël, Jacques Mallet, and Marie-Françoise Diebler. "Coregulation of Two Embedded Gene Products, Choline Acetyltransferase and the Vesicular Acetylcholine Transporter." Journal of Neurochemistry 65, no. 2 (November 23, 2002): 939–42. http://dx.doi.org/10.1046/j.1471-4159.1995.65020939.x.

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Hall, Daniel P., and Rhett A. Kovall. "Structurally conserved binding motifs of transcriptional regulators to notch nuclear effector CSL." Experimental Biology and Medicine 244, no. 17 (September 22, 2019): 1520–29. http://dx.doi.org/10.1177/1535370219877818.

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This mini review discusses the protein complexes comprised of the universal Notch signaling transcription factor, CSL (CBF1/Su(H)/Lag-1), and its activating or repressing transcriptional coregulation partners. Many of these complex structures have been solved crystallographically as well as undergoing extensive binding studies with wild-type and mutant variants. Notch signaling is critically important in a large variety of basic biological processes: cell proliferation, differentiation, cell cycle control to name a few. Aberrant Notch thus remains a coveted target for pharmaceutical intervention. To that end, we provide a molecular-level summary of the similarities and differences in the Notch coregulator complexes that ultimately govern these processes. We highlight a conserved binding motif that multiple superficially unrelated proteins have adopted to become involved in Notch target gene regulation. As CSL-interacting small molecules begin to be characterized, this review will provide insight to potential binding sites and differential complex disruption. Impact statement Proper Notch signaling regulation is informed by many distinct protein complexes involving a single nuclear effector. A decade of research into these protein complexes yields multiple crystal structures and a wealth of binding data to guide drug development for Notch-related diseases – cancer, cardiovascular, development disorders.

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Hu, Zhen, and Raj Bhatnagar. "Mining Low-Variance Biclusters to Discover Coregulation Modules in Sequencing Datasets." Scientific Programming 20, no. 1 (2012): 15–27. http://dx.doi.org/10.1155/2012/953863.

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High-throughput sequencing (CHIP-Seq) data exhibit binding events with possible binding locations and their strengths, followed by interpretation of the locations of peaks. Recent methods tend to summarize all CHIP-Seq peaks detected within a limited up and down region of each gene into one real-valued score in order to quantify the probability of regulation in a region. Applying subspace clustering techniques on these scores can help discover important knowledge such as the potential co-regulation or co-factor mechanisms. The ideal biclusters generated would contain subsets of genes and transcription factors (TF) such that the cell-values in biclusters are distributed around a mean value with very low variance. Such biclusters would indicate TF sets regulating gene sets with very similar probability values. However, most existing biclustering algorithms neither enforce low variance as the desired property of a bicluster, nor use variance as a guiding metric while searching for the desirable biclusters. In this paper we present an algorithm that searches a space of all overlapping biclusters organized in a lattice, and uses an upper bound on variance values of biclusters as the guiding metric. We show the algorithm to be an efficient and effective method for discovering the possibly overlapping biclusters under pre-defined variance bounds. We present in this paper our algorithm, its results with synthetic, CHIP-Seq and motif datasets, and compare them with the results obtained by other algorithms to demonstrate the power and effectiveness of our algorithm.

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Hallauer, Patricia L., and Kenneth E. M. Hastings. "Coregulation of fast contractile protein transgene and glycolytic enzyme expression in mouse skeletal muscle." American Journal of Physiology-Cell Physiology 282, no. 1 (January 1, 2002): C113—C124. http://dx.doi.org/10.1152/ajpcell.00294.2001.

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Little is known of the gene regulatory mechanisms that coordinate the contractile and metabolic specializations of skeletal muscle fibers. Here we report a novel connection between fast isoform contractile protein transgene and glycolytic enzyme expression. In quantitative histochemical studies of transgenic mouse muscle fibers, we found extensive coregulation of the glycolytic enzyme glycerol-3-phosphate dehydrogenase (GPDH) and transgene constructs based on the fast skeletal muscle troponin I (TnIfast) gene. In addition to a common IIB > IIX > IIA fiber type pattern, TnIfast transgenes and GPDH showed correlated fiber-to-fiber variation within each fast fiber type, concerted emergence of high-level expression during early postnatal muscle maturation, and parallel responses to muscle under- or overloading. Regulatory information for GPDH-coregulated expression is carried by the TnIfast first-intron enhancer (IRE). These results identify an unexpected contractile/metabolic gene regulatory link that is amenable to further molecular characterization. They also raise the possibility that the equal expression in all fast fiber types observed for the endogenous TnIfast gene may be driven by different metabolically coordinated mechanisms in glycolytic (IIB) vs. oxidative (IIA) fast fibers.

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Wang, Juan, Yan Liang, Hui Yang, and Jian-Huang Wu. "Identification of a Transcription Factor-microRNA-Gene Coregulation Network in Meningioma through a Bioinformatic Analysis." BioMed Research International 2020 (August 7, 2020): 1–13. http://dx.doi.org/10.1155/2020/6353814.

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Background. Meningioma is a prevalent type of brain tumor. However, the initiation and progression mechanisms involved in the meningioma are mostly unknown. This study aimed at exploring the potential transcription factors/micro(mi)RNAs/genes and biological pathways associated with meningioma. Methods. mRNA expressions from GSE88720, GSE43290, and GSE54934 datasets, containing data from 83 meningioma samples and eight control samples, along with miRNA expression dataset GSE88721, which had 14 meningioma samples and one control sample, were integrated analyzed. The bioinformatics approaches were used for identifying differentially expressed genes and miRNAs, as well as predicting transcription factor targets related to the differentially expressed genes. The approaches were also used for gene ontology term analysis and biological pathway enrichment analysis, construction, and analysis of protein-protein interaction network, and transcription factor-miRNA-gene coregulation network construction. Results. Fifty-six upregulated and 179 downregulated genes were identified. Thirty transcription factors able to target the differentially expressed genes were predicted and selected based on public databases. One hundred seventeen overlapping genes were identified from the differentially expressed genes and the miRNAs predicted by miRWalk. Furthermore, NF-κB/IL6, PTGS2, MYC/hsa-miR-574-5p, hsa-miR-26b-5p, hsa-miR-335-5p, and hsa-miR-98-5p, which are involved in the transcription factor-miRNA-mRNA coregulation network, were found to be associated with meningioma. Conclusion. The bioinformatics analysis identified several potential molecules and relevant pathways that may represent critical mechanisms involved in the progression and development of meningioma. This work provides new insights into meningioma pathogenesis and treatments.

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Homuth, Georg, Alexandra Rompf, Wolfgang Schumann, and Dieter Jahn. "Transcriptional Control of Bacillus subtilis hemN and hemZ." Journal of Bacteriology 181, no. 19 (October 1, 1999): 5922–29. http://dx.doi.org/10.1128/jb.181.19.5922-5929.1999.

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ABSTRACT Previous characterization of Bacillus subtilis hemN, encoding a protein involved in oxygen-independent coproporphyrinogen III decarboxylation, indicated the presence of a secondhemN-like gene (B. Hippler, G. Homuth, T. Hoffmann, C. Hungerer, W. Schumann, and D. Jahn, J. Bacteriol. 179:7181–7185, 1997). The corresponding hemZ gene was found to be split into the two potential open reading frames yhaV andyhaW by a sequencing error of the genome sequencing project. The hemZ gene, encoding a 501-amino-acid protein with a calculated molecular mass of 57,533 Da, complemented aSalmonella typhimurium hemF hemN double mutant under aerobic and anaerobic growth conditions. A B. subtilis hemZmutant accumulated coproporphyrinogen III under anaerobic growth conditions. A hemN hemZ double mutant exhibited normal aerobic and anaerobic growth, indicating the presence of a third alternative oxygen-independent enzymatic system for coproporphyrinogen III oxidation. The hemY gene, encoding oxygen-dependent protoporphyrinogen IX oxidase with coproporphyrinogen III oxidase side activity, did not significantly contribute to this newly identified system. Growth behavior of hemY mutants revealed the presence of an oxygen-independent protoporphyrinogen IX oxidase inB. subtilis. A monocistronic hemZ mRNA, starting 31 bp upstream of the translational start codon, was detected. Reporter gene fusions of hemZ and hemNdemonstrated a fivefold anaerobic induction of both genes under nitrate ammonifying growth conditions. No anaerobic induction was observed for fermentatively growing B. subtilis. The B. subtilis redox regulatory systems encoded by resDE,fnr, and ywiD were indispensable for the observed transcriptional induction. A redox regulation cascade proceeding from an unknown sensor via resDE, throughfnr and ywiD to hemN/hemZ, is suggested for the observed coregulation of heme biosynthesis and the anaerobic respiratory energy metabolism. Finally, only hemZwas found to be fivefold induced by the presence of H2O2, indicating further coregulation of heme biosynthesis with the formation of the tetrapyrrole enzyme catalase.

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de Nys, Rebekah, Raman Kumar, and Jozef Gecz. "Protocadherin 19 Clustering Epilepsy and Neurosteroids: Opportunities for Intervention." International Journal of Molecular Sciences 22, no. 18 (September 9, 2021): 9769. http://dx.doi.org/10.3390/ijms22189769.

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Steroids yield great influence on neurological development through nuclear hormone receptor (NHR)-mediated gene regulation. We recently reported that cell adhesion molecule protocadherin 19 (encoded by the PCDH19 gene) is involved in the coregulation of steroid receptor activity on gene expression. PCDH19 variants cause early-onset developmental epileptic encephalopathy clustering epilepsy (CE), with altered steroidogenesis and NHR-related gene expression being identified in these individuals. The implication of hormonal pathways in CE pathogenesis has led to the investigation of various steroid-based antiepileptic drugs in the treatment of this disorder, with mixed results so far. Therefore, there are many unmet challenges in assessing the antiseizure targets and efficiency of steroid-based therapeutics for CE. We review and assess the evidence for and against the implication of neurosteroids in the pathogenesis of CE and in view of their possible clinical benefit.

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Mason, Hugh S., Daryll B. DeWald, Robert A. Creelman, and John E. Mullet. "Coregulation of Soybean Vegetative Storage Protein Gene Expression by Methyl Jasmonate and Soluble Sugars." Plant Physiology 98, no. 3 (March 1, 1992): 859–67. http://dx.doi.org/10.1104/pp.98.3.859.

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Pennings, Jeroen L. A., Dorien A. M. van Dartel, Tessa E. Pronk, Peter J. M. Hendriksen, and Aldert H. Piersma. "Identification by Gene Coregulation Mapping of Novel Genes Involved in Embryonic Stem Cell Differentiation." Stem Cells and Development 20, no. 1 (January 2011): 115–26. http://dx.doi.org/10.1089/scd.2010.0181.

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Mura, Catherine, Gérald Le Gac, Sandrine Jacolot, and Claude Férec. "Transcriptional regulation of the human HFE gene indicates high liver expression and erythropoiesis coregulation." FASEB Journal 18, no. 15 (October 5, 2004): 1922–24. http://dx.doi.org/10.1096/fj.04-2520fje.

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Schuster, André, Christian P. Kubicek, and Monika Schmoll. "Dehydrogenase GRD1 Represents a Novel Component of the Cellulase Regulon in Trichoderma reesei (Hypocrea jecorina)." Applied and Environmental Microbiology 77, no. 13 (May 20, 2011): 4553–63. http://dx.doi.org/10.1128/aem.00513-11.

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ABSTRACTTrichoderma reesei(Hypocrea jecorina) is nowadays the most important industrial producer of cellulase and hemicellulase enzymes, which are used for pretreatment of cellulosic biomass for biofuel production. In this study, we introduce a novel component, GRD1 (glucose-ribitol dehydrogenase 1), which shows enzymatic activity on cellobiose and positively influences cellulase gene transcription, expression, and extracellular endo-1,4-β-d-glucanase activity.grd1is differentially transcribed upon growth on cellulose and the induction of cellulase gene expression by sophorose. The transcription ofgrd1is coregulated with that ofcel7a(cbh1) under inducing conditions. GRD1 is further involved in carbon source utilization on several carbon sources, such as those involved in lactose andd-galactose catabolism, in several cases in a light-dependent manner. We conclude that GRD1 represents a novel enhancer of cellulase gene expression, which by coregulation with the major cellulase may act via optimization of inducing mechanisms.

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Chen, Haiming, Jie Chen, Lindsey A. Muir, Scott Ronquist, Walter Meixner, Mats Ljungman, Thomas Ried, Stephen Smale, and Indika Rajapakse. "Functional organization of the human 4D Nucleome." Proceedings of the National Academy of Sciences 112, no. 26 (June 15, 2015): 8002–7. http://dx.doi.org/10.1073/pnas.1505822112.

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The 4D organization of the interphase nucleus, or the 4D Nucleome (4DN), reflects a dynamical interaction between 3D genome structure and function and its relationship to phenotype. We present initial analyses of the human 4DN, capturing genome-wide structure using chromosome conformation capture and 3D imaging, and function using RNA-sequencing. We introduce a quantitative index that measures underlying topological stability of a genomic region. Our results show that structural features of genomic regions correlate with function with surprising persistence over time. Furthermore, constructing genome-wide gene-level contact maps aided in identifying gene pairs with high potential for coregulation and colocalization in a manner consistent with expression via transcription factories. We additionally use 2D phase planes to visualize patterns in 4DN data. Finally, we evaluated gene pairs within a circadian gene module using 3D imaging, and found periodicity in the movement of clock circadian regulator and period circadian clock 2 relative to each other that followed a circadian rhythm and entrained with their expression.

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Chang, Hun Soo, Shin-Hwa Lee, Jong-Uk Lee, Jong Sook Park, Il Yup Chung, and Choon-Sik Park. "Functional Characterization of Exonic Variants of the PPARGC1B Gene in Coregulation of Estrogen Receptor Alpha." DNA and Cell Biology 35, no. 7 (July 2016): 314–21. http://dx.doi.org/10.1089/dna.2015.3195.

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Ku, Wai Lim, Geet Duggal, Yuan Li, Michelle Girvan, and Edward Ott. "Interpreting Patterns of Gene Expression: Signatures of Coregulation, the Data Processing Inequality, and Triplet Motifs." PLoS ONE 7, no. 2 (February 29, 2012): e31969. http://dx.doi.org/10.1371/journal.pone.0031969.

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Putt, Mary E., Sridhar Hannenhalli, Yun Lu, Philip Haines, Hareesh R. Chandrupatla, Edward E. Morrisey, Kenneth B. Margulies, and Thomas P. Cappola. "Evidence for Coregulation of Myocardial Gene Expression by MEF2 and NFAT in Human Heart Failure." Circulation: Cardiovascular Genetics 2, no. 3 (June 2009): 212–19. http://dx.doi.org/10.1161/circgenetics.108.816686.

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Vecellio Rogers, Patricia, Joseph F. Sucic, Yizhong Yin, and Charles L. Rutherford. "Disruption of glycogen phosphorylase gene expression in Dictyostelium: Evidence for altered glycogen metabolism and developmental coregulation of the gene products." Differentiation 56, no. 1-2 (March 1994): 1–12. http://dx.doi.org/10.1046/j.1432-0436.1994.56120001.x.

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Nagel, Stefan, Christof Burek, Letizia Venturini, Michaela Scherr, Hilmar Quentmeier, Corinna Meyer, Andreas Rosenwald, Hans G. Drexler, and Roderick A. F. MacLeod. "Comprehensive analysis of homeobox genes in Hodgkin lymphoma cell lines identifies dysregulated expression of HOXB9 mediated via ERK5 signaling and BMI1." Blood 109, no. 7 (December 5, 2006): 3015–23. http://dx.doi.org/10.1182/blood-2006-08-044347.

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Abstract Many members of the nearly 200-strong homeobox gene family have been implicated in cancer, mostly following ectopic expression. In this study we analyzed homeobox gene expression in Hodgkin lymphoma (HL) cell lines. Both reverse transcription–polymerase chain reaction (RT-PCR) using degenerate primers and microarray profiling identified consistently up-regulated HOXB9 expression. Analysis of HOXB9 regulation in HL cells revealed E2F3A and BMI1 as activator and repressor, respectively. Furthermore, a constitutively active ERK5 pathway was identified in all HL cell lines analyzed as well as primary HL cells. Our data show that ERK5 probably mediates HOXB9 expression by repressing BMI1. In addition, expression analysis of the neighboring microRNA gene mir-196a1 revealed coregulation with HOXB9. Functional analysis of HOXB9 by knockdown and overexpression assays indicated their influence on both proliferation and apoptosis in HL cells. In summary, we identified up-regulation of HOXB9 in HL mediated by constitutively active ERK5 signaling which may represent novel therapeutic targets in HL.

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Man, Joyce C. K., Karel van Duijvenboden, Peter H. L. Krijger, Ingeborg B. Hooijkaas, Ingeborg van der Made, Corrie de Gier-de Vries, Vincent Wakker, et al. "Genetic Dissection of a Super Enhancer Controlling the Nppa-Nppb Cluster in the Heart." Circulation Research 128, no. 1 (January 8, 2021): 115–29. http://dx.doi.org/10.1161/circresaha.120.317045.

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Rationale: ANP (atrial natriuretic peptide) and BNP (B-type natriuretic peptide), encoded by the clustered genes Nppa and Nppb , are important prognostic, diagnostic, and therapeutic proteins in cardiac disease. The spatiotemporal expression pattern and stress-induction of the Nppa and Nppb are tightly regulated, possibly involving their coregulation by an evolutionary conserved enhancer cluster. Objective: To explore the physiological functions of the enhancer cluster and elucidate the genomic mechanism underlying Nppa-Nppb coregulation in vivo. Methods and Results: By analyzing epigenetic data we uncovered an enhancer cluster with super enhancer characteristics upstream of Nppb . Using CRISPR/Cas9 genome editing, the enhancer cluster or parts thereof, Nppb and flanking regions or the entire genomic block spanning Nppa-Nppb , respectively, were deleted from the mouse genome. The impact on gene regulation and phenotype of the respective mouse lines was investigated by transcriptomic, epigenomic, and phenotypic analyses. The enhancer cluster was essential for prenatal and postnatal ventricular expression of Nppa and Nppb but not of any other gene. Enhancer cluster–deficient mice showed enlarged hearts before and after birth, similar to Nppa-Nppb compound knockout mice we generated. Analysis of the other deletion alleles indicated the enhancer cluster engages the promoters of Nppa and Nppb in a competitive rather than a cooperative mode, resulting in increased Nppa expression when Nppb and flanking sequences were deleted. The enhancer cluster maintained its active epigenetic state and selectivity when its target genes are absent. In enhancer cluster–deficient animals, Nppa was induced but remained low in the postmyocardial infarction border zone and in the hypertrophic ventricle, involving regulatory sequences proximal to Nppa . Conclusions: Coordinated ventricular expression of Nppa and Nppb is controlled in a competitive manner by a shared super enhancer, which is also required to augment stress-induced expression and to prevent premature hypertrophy.

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Kobayashi, Takeshi, and Ko Fujimori. "Very long-chain-fatty acids enhance adipogenesis through coregulation of Elovl3 and PPARγ in 3T3-L1 cells." American Journal of Physiology-Endocrinology and Metabolism 302, no. 12 (June 15, 2012): E1461—E1471. http://dx.doi.org/10.1152/ajpendo.00623.2011.

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Here, we show that Elovl3 (elongation of very long-chain fatty acids 3) was involved in the regulation of the progression of adipogenesis through activation of peroxisome proliferator-activated receptor (PPAR)γ in mouse adipocytic 3T3-L1 cells. The expression of the Elovl3 gene increased during adipogenesis, the expression pattern of which was similar to that of the PPARγ gene. Troglitazone, a PPARγ agonist, enhanced Elovl3 expression in adipocytes, as it did that of other PPARγ target genes. Promoter-reporter analysis demonstrated that three PPAR-responsive elements in the Elovl3 gene promoter had the potential to activate its expression in 3T3-L1 cells. Moreover, a chromatin immunoprecipitation assay revealed that PPARγ bound these PPAR-responsive elements of the Elovl3 promoter. When the Elovl3 mRNA level was suppressed by its siRNAs, the level of intracellular triglycerides was significantly decreased, and the expression levels of adipogenic, lipolytic, and lipogenic genes were also repressed. In a mammalian two-hybrid assay, C18:1 and C20:1 very long-chain fatty acids (VLCFAs), which are the products of Elovl3 and activated PPARγ function. In addition, these same VLCFAs could prevent the Elovl3 siRNA-mediated suppression of adipogenesis by enhancing the expression of adipogenic, lipolytic, and lipogenic genes in adipocytes. Moreover, this VLCFAs-mediated activation was repressed by a PPARγ antagonist. These results indicate that the expression of the Elovl3 gene was activated by PPARγ during adipogenesis. Elovl3-produced C18:1 and C20:1 VLCFAs acted as agonists of PPARγ in 3T3-L1 cells. Thus, the Elovl3-PPARγ cascade is a novel regulatory circuit for the regulation of adipogenesis through improvement of PPARγ function in adipocytes.

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Rouault, H., K. Mazouni, L. Couturier, V. Hakim, and F. Schweisguth. "Genome-wide identification of cis-regulatory motifs and modules underlying gene coregulation using statistics and phylogeny." Proceedings of the National Academy of Sciences 107, no. 33 (July 29, 2010): 14615–20. http://dx.doi.org/10.1073/pnas.1002876107.

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Fouchet, Claude, Pierre Gane, Martine Huet, Marc Fellous, Philippe Rouger, George Banting, Jean-Pierre Cartron, and Claude Lopez. "A study of the coregulation and tissue specificity of XGand MIC2 gene expression in eukaryotic cells." Blood 95, no. 5 (March 1, 2000): 1819–26. http://dx.doi.org/10.1182/blood.v95.5.1819.005k05_1819_1826.

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CD99, the product of the MIC2 gene, exhibits an erythroid-specific quantitative polymorphism coregulated with the polymorphism of the XG blood group gene. As a preliminary study of this phenomenon, human XG and CD99 recombinant proteins were expressed in murine RAG cells and analyzed by flow cytometry. Both proteins were expressed independently and at a similar level in single and double transfectants. Immunoprecipitation and Western blot analysis, using the murine monoclonal antibodies NBL-1 and 12E7, revealed species of 26 kd (XG) and 32 kd (CD99), respectively. A putative 28-kd intracellular precursor of CD99 was also detected, as was a 26-kd species after neuraminidase treatment of CD99-expressing cells. No evidence of association or complex formation between XG and CD99 proteins could be proven, either on transfected RAG cells or on human erythrocytes. These results were confirmed using somatic hybrids between single transfectants. These findings suggest that the phenotypic relationship between XG and CD99 is mostly regulated at the transcriptional level, but they do not formally exclude some posttranscriptional effect. Studies on the tissue specificity of XG expression showed that surface expression of the XG protein could not be restored in somatic hybrids between B-lymphoblastoid cell lines from Xg(a+) persons and fibroblasts (RAG) or erythroid (MEL) cells. RT-PCR analysis of the transcripts revealed the existence of an XG mRNA in each cell line, suggesting that the tissue-specific regulation of cell surface XG expression occurs either at a quantitative transcriptional level or is a posttranscriptional event. By Northern blot analysis,XG transcripts were detected in erythroid tissues and several nonerythroid tissues.

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MacLean, Jason N., Ying Zhang, Marie L. Goeritz, Richard Casey, Ricardo Oliva, John Guckenheimer, and Ronald M. Harris-Warrick. "Activity-Independent Coregulation of IA and Ih in Rhythmically Active Neurons." Journal of Neurophysiology 94, no. 5 (November 2005): 3601–17. http://dx.doi.org/10.1152/jn.00281.2005.

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The fast transient potassium or A current ( IA) plays an important role in determining the activity of central pattern generator neurons. We have previously shown that the shal K+ channel gene encodes IA in neurons of the pyloric network in the spiny lobster. To further study how IA shapes pyloric neuron and network activity, we microinjected RNA for a shal-GFP fusion protein into four identified pyloric neuron types. Neurons expressing shal-GFP had a constant increase in IA amplitude, regardless of cell type. This increase in IA was paralleled by a concomitant increase in the hyperpolarization-activated cation current Ih in all pyloric neurons. Despite significant increases in these currents, only modest changes in cell firing properties were observed. We used models to test two hypotheses to explain this failure to change firing properties. First, this may reflect the mislocalization of the expressed shal protein solely to the somata and initial neurites of injected neurons, rendering it electrically remote from the integrating region in the neuropil. To test this hypothesis, we generated a multicompartment model where increases in IA could be localized to the soma, initial neurite, or neuropil/axon compartments. Although spike activity was somewhat more sensitive to increases in neuropil/axon versus somatic/primary neurite IA, increases in IA limited to the soma and primary neurite still evoked much more dramatic changes than were seen in the shal-GFP–injected neurons. Second, the effect of the increased IA could be compensated by the endogenous increase in Ih. To test this, we modeled the compensatory increases of IA and Ih with a cycling two-cell model. We found that the increase in Ih was sufficient to compensate the effects of increased IA, provided that they increase in a constant ratio, as we observed experimentally in both shal-injected and noninjected neurons. Thus an activity-independent homeostatic mechanism maintains constant neuronal activity in the face of dramatic increases in IA.

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Bally-Cuif, Laure, Carole Goutel, Marion Wassef, Wolfgang Wurst, and Frédéric Rosa. "Coregulation of anterior and posterior mesendodermal development by a hairy-related transcriptional repressor." Genes & Development 14, no. 13 (July 1, 2000): 1664–77. http://dx.doi.org/10.1101/gad.14.13.1664.

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During embryonic development in vertebrates, the endoderm becomes patterned along the anteroposterior axis to produce distinct derivatives. How this regulation is controlled is not well understood. We report that the zebrafish hairy/enhancer of split [E(spl)]-related gene her5 plays a critical role in this process. At gastrulation, following endoderm induction and further cell interaction processes including a local release of Notch/Delta signaling, her5 expression is progressively excluded from the presumptive anterior- and posteriormost mesendodermal territories to become restricted to an adjacent subpopulation of dorsal endodermal precursors. Ectopic misexpressions of wild-type and mutant forms of her5 reveal that her5functions primarily within the endodermal/endmost mesendodermal germ layer to inhibit cell participation to the endmost-fated mesendoderm. In this process, her5 acts as an active transcriptional repressor. These features are strikingly reminiscent of the function of Drosophila Hairy/E(spl) factors in cell fate decisions. Our results provide the first model for vertebrate endoderm patterning where an early regulatory step at gastrulation, mediated by her5 controls cell contribution jointly to the anterior- and posteriormost mesendodermal regions.

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Baetz, Kristin, Jason Moffat, Jennifer Haynes, Michael Chang, and Brenda Andrews. "Transcriptional Coregulation by the Cell Integrity Mitogen-Activated Protein Kinase Slt2 and the Cell Cycle Regulator Swi4." Molecular and Cellular Biology 21, no. 19 (October 1, 2001): 6515–28. http://dx.doi.org/10.1128/mcb.21.19.6515-6528.2001.

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ABSTRACT In Saccharomyces cerevisiae, the heterodimeric transcription factor SBF (for SCB binding factor) is composed of Swi4 and Swi6 and activates gene expression at the G1/S-phase transition of the mitotic cell cycle. Cell cycle commitment is associated not only with major alterations in gene expression but also with highly polarized cell growth; the mitogen-activated protein kinase (MAPK) Slt2 is required to maintain cell wall integrity during periods of polarized growth and cell wall stress. We describe experiments aimed at defining the regulatory pathway involving the cell cycle transcription factor SBF and Slt2-MAPK. Gene expression assays and chromatin immunoprecipitation experiments revealed Slt2-dependent recruitment of SBF to the promoters of the G1 cyclinsPCL1 and PCL2 after activation of the Slt2-MAPK pathway. We performed DNA microarray analysis and identified other genes whose expression was reduced in both SLT2and SWI4 deletion strains. Genes that are sensitive to both Slt2 and Swi4 appear to be uniquely regulated and reveal a role for Swi4, the DNA-binding component of SBF, which is independent of the regulatory subunit Swi6. Some of the Swi4- and Slt2-dependent genes do not require Swi6 for either their expression or for Swi4 localization to their promoters. Consistent with these results, we found a direct interaction between Swi4 and Slt2. Our results establish a new Slt2-dependent mode of Swi4 regulation and suggest roles for Swi4 beyond its prominent role in controlling cell cycle transcription.

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Peng, Chien-Hua, Shu-Hsi Lin, Shih-Chi Peng, Ping-Chiang Lyu, Masanori Arita, and Chuan-Yi Tang. "Feature Identification of Compensatory Gene Pairs without Sequence Homology in Yeast." Comparative and Functional Genomics 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/653174.

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Genetic robustness refers to a compensatory mechanism for buffering deleterious mutations or environmental variations. Gene duplication has been shown to provide such functional backups. However, the overall contribution of duplication-based buffering for genetic robustness is rather small. In this study, we investigated whether transcriptional compensation also exists among genes that share similar functions without sequence homology. A set of nonhomologous synthetic-lethal gene pairs was assessed by using a coexpression network, protein-protein interactions, and other types of genetic interactions in yeast. Our results are notably different from those of previous studies on buffering paralogs. The low expression similarity and the conditional coexpression alone do not play roles in identifying the functionally compensatory genes. Additional properties such as synthetic-lethal interaction, the ratio of shared common interacting partners, and the degree of coregulation were, at least in part, necessary to extract functional compensatory genes. Our network-based approach is applicable to select several well-documented cases of compensatory gene pairs and a set of new pairs. The results suggest that transcriptional reprogramming plays a limited role in functional compensation among nonhomologous genes. Our study aids in understanding the mechanism and features of functional compensation more in detail.

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Wang, Siwen, Zheng Xing, Pete E. Pascuzzi, and Elizabeth J. Tran. "Metabolic Adaptation to Nutrients Involves Coregulation of Gene Expression by the RNA Helicase Dbp2 and the Cyc8 Corepressor in Saccharomyces cerevisiae." G3 Genes|Genomes|Genetics 7, no. 7 (July 1, 2017): 2235–47. http://dx.doi.org/10.1534/g3.117.041814.

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Abstract Cells fine-tune their metabolic programs according to nutrient availability in order to maintain homeostasis. This is achieved largely through integrating signaling pathways and the gene expression program, allowing cells to adapt to nutritional change. Dbp2, a member of the DEAD-box RNA helicase family in Saccharomyces cerevisiae, has been proposed to integrate gene expression with cellular metabolism. Prior work from our laboratory has reported the necessity of DBP2 in proper gene expression, particularly for genes involved in glucose-dependent regulation. Here, by comparing differentially expressed genes in dbp2∆ to those of 700 other deletion strains from other studies, we find that CYC8 and TUP1, which form a complex and inhibit transcription of numerous genes, corepress a common set of genes with DBP2. Gene ontology (GO) annotations reveal that these corepressed genes are related to cellular metabolism, including respiration, gluconeogenesis, and alternative carbon-source utilization genes. Consistent with a direct role in metabolic gene regulation, loss of either DBP2 or CYC8 results in increased cellular respiration rates. Furthermore, we find that corepressed genes have a propensity to be associated with overlapping long noncoding RNAs and that upregulation of these genes in the absence of DBP2 correlates with decreased binding of Cyc8 to these gene promoters. Taken together, this suggests that Dbp2 integrates nutrient availability with energy homeostasis by maintaining repression of glucose-repressed, Cyc8-targeted genes across the genome.

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Salameh, Ahmad, Alessandro K. Lee, Marina Cardó-Vila, Diana N. Nunes, Eleni Efstathiou, Fernanda I. Staquicini, Andrey S. Dobroff, et al. "PRUNE2 is a human prostate cancer suppressor regulated by the intronic long noncoding RNA PCA3." Proceedings of the National Academy of Sciences 112, no. 27 (June 15, 2015): 8403–8. http://dx.doi.org/10.1073/pnas.1507882112.

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Prostate cancer antigen 3 (PCA3) is the most specific prostate cancer biomarker but its function remains unknown. Here we identify PRUNE2, a target protein-coding gene variant, which harbors the PCA3 locus, thereby classifying PCA3 as an antisense intronic long noncoding (lnc)RNA. We show that PCA3 controls PRUNE2 levels via a unique regulatory mechanism involving formation of a PRUNE2/PCA3 double-stranded RNA that undergoes adenosine deaminase acting on RNA (ADAR)-dependent adenosine-to-inosine RNA editing. PRUNE2 expression or silencing in prostate cancer cells decreased and increased cell proliferation, respectively. Moreover, PRUNE2 and PCA3 elicited opposite effects on tumor growth in immunodeficient tumor-bearing mice. Coregulation and RNA editing of PRUNE2 and PCA3 were confirmed in human prostate cancer specimens, supporting the medical relevance of our findings. These results establish PCA3 as a dominant-negative oncogene and PRUNE2 as an unrecognized tumor suppressor gene in human prostate cancer, and their regulatory axis represents a unique molecular target for diagnostic and therapeutic intervention.

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Willscher, Edith, Lydia Hopp, Markus Kreuz, Maria Schmidt, Siras Hakobyan, Arsen Arakelyan, Bettina Hentschel, et al. "High-Resolution Cartography of the Transcriptome and Methylome Landscapes of Diffuse Gliomas." Cancers 13, no. 13 (June 26, 2021): 3198. http://dx.doi.org/10.3390/cancers13133198.

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Molecular mechanisms of lower-grade (II–III) diffuse gliomas (LGG) are still poorly understood, mainly because of their heterogeneity. They split into astrocytoma- (IDH-A) and oligodendroglioma-like (IDH-O) tumors both carrying mutations(s) at the isocitrate dehydrogenase (IDH) gene and into IDH wild type (IDH-wt) gliomas of glioblastoma resemblance. We generated detailed maps of the transcriptomes and DNA methylomes, revealing that cell functions divided into three major archetypic hallmarks: (i) increased proliferation in IDH-wt and, to a lesser degree, IDH-O; (ii) increased inflammation in IDH-A and IDH-wt; and (iii) the loss of synaptic transmission in all subtypes. Immunogenic properties of IDH-A are diverse, partly resembling signatures observed in grade IV mesenchymal glioblastomas or in grade I pilocytic astrocytomas. We analyzed details of coregulation between gene expression and DNA methylation and of the immunogenic micro-environment presumably driving tumor development and treatment resistance. Our transcriptome and methylome maps support personalized, case-by-case views to decipher the heterogeneity of glioma states in terms of data portraits. Thereby, molecular cartography provides a graphical coordinate system that links gene-level information with glioma subtypes, their phenotypes, and clinical context.

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Hwang, Junghyun, and Heenam Stanley Kim. "Cell Wall Recycling-Linked Coregulation of AmpC and PenB β-Lactamases throughampDMutations in Burkholderia cenocepacia." Antimicrobial Agents and Chemotherapy 59, no. 12 (September 28, 2015): 7602–10. http://dx.doi.org/10.1128/aac.01068-15.

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ABSTRACTIn many Gram-negative pathogens, mutations in the key cell wall-recycling enzyme AmpD (N-acetyl-anhydromuramyl-l-alanine amidase) affect the activity of the regulator AmpR, which leads to the expression of AmpC β-lactamase, conferring resistance to expanded-spectrum cephalosporin antibiotics.Burkholderia cepaciacomplex (Bcc) species also have these Amp homologs; however, the regulatory circuitry and the nature of causalampDmutations remain to be explored. A total of 92ampDmutants were obtained, representing four types of mutations: single nucleotide substitution (causing an amino acid substitution or antitermination of the enzyme), duplication, deletion, and IS element insertion. Duplication, which can go through reversion, was the most frequent type. Intriguingly, mutations inampDled to the induction of two β-lactamases, AmpC and PenB. Coregulation of AmpC and PenB inB. cenocepacia, and likely also in many Bcc species with the same gene organization, poses a serious threat to human health. This resistance mechanism is of evolutionary optimization in thatampDis highly prone to mutations allowing rapid response to antibiotic challenge, and many of the mutations are reversible in order to resume cell wall recycling when the antibiotic challenge is relieved.

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Rose, Samuel J., Marvin J. Rosenberg, Roy J. Britten, and Eric H. Davidson. "Expression of myosin heavy chain gene in the sea urchin: Coregulation with muscle actin transcription in early development." Developmental Biology 123, no. 1 (September 1987): 115–24. http://dx.doi.org/10.1016/0012-1606(87)90433-7.

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Du, Hong, Min Wang, Zhe Luo, Bin Ni, Fei Wang, Yanchen Meng, Shungao Xu, and Xinxiang Huang. "Coregulation of Gene Expression by Sigma Factors RpoE and RpoS in Salmonella enterica Serovar Typhi During Hyperosmotic Stress." Current Microbiology 62, no. 5 (February 11, 2011): 1483–89. http://dx.doi.org/10.1007/s00284-011-9890-8.

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Xin, Haiyan, Ziyan Feng, and Chao Yao. "SNHG1/miR-145-5p/KLF5 Axis Participates in Regulating the Proliferation and Migration of Oral Squamous Cell Cancer." Journal of Healthcare Engineering 2022 (March 3, 2022): 1–8. http://dx.doi.org/10.1155/2022/2053271.

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We aimed to clarify the molecular mechanism of lncRNA SNHG1 in regulating the OSCC process. Clinical samples of OSCC were collected for detecting the differential level of SNHG1 by qRT-PCR. Pathological indexes of OSCC patients were analyzed for uncovering the prognostic value of SNHG1. The interaction between SNHG1 and miR-145-5p was assessed through the bioinformatics method and dual-luciferase reporter assay. Their coregulation on proliferative and migratory functions of Tca8113 and CAL-27 cells was explored by the CCK-8, EdU, and Transwell assay. Finally, the regulatory effect of miR-145-5p on its downstream gene KLF5 was evaluated. SNHG1 was abnormally upregulated in OSCC samples and linked to a poor prognosis of OSCC patients. Serving as an oncogene, SNHG1 strengthened proliferative and migratory functions of Tca8113 and CAL-27 cells. miR-145-5p was a key downstream target inducing the oncogenic role of SNHG1 in the OSCC process with KLF5 as its downstream gene. SNHG1/miR-145-5p/KLF1 axis is responsible for driving the malignant process of OSCC.

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Lund, Caren V., Mikhail Popkov, Laurent Magnenat, and Carlos F. Barbas. "Zinc Finger Transcription Factors Designed for Bispecific Coregulation of ErbB2 and ErbB3 Receptors: Insights into ErbB Receptor Biology." Molecular and Cellular Biology 25, no. 20 (October 15, 2005): 9082–91. http://dx.doi.org/10.1128/mcb.25.20.9082-9091.2005.

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ABSTRACT Signaling through the ErbB family of tyrosine kinase receptors in normal and cancer-derived cell lines contributes to cell growth and differentiation. In this work, we altered the levels of ErbB2 and ErbB3 receptors, individually and in combination, by using 6-finger and 12-finger synthetic zinc finger protein artificial transcription factors (ATFs) in an epidermoid squamous cell carcinoma line, A431. We successfully designed 12-finger ATFs capable of coregulating ErbB3 and ICAM-1 or ErbB2 and ErbB3. With ATFs, the effects of changes in ErbB2 and ErbB3 receptor levels were evaluated by using cell proliferation, cell migration, and cell signaling assays. Cell proliferation was increased when ErbB2 and ErbB3 were both overexpressed. Cell migration on collagen was decreased when ErbB2 was down-regulated, yet migration on laminin was significantly increased with ErbB3 overexpression. ErbB2 and ErbB3 overexpression also stimulated the phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways. Our ATF approach has elucidated differences in ErbB receptor-mediated proliferation, migration, and intracellular signaling that cannot be explained merely by the presence or absence of particular ErbB receptors and emphasizes the dynamic nature of the ErbB signaling system. The transcription factor approach developed here provides a gene-economical route to the regulation of multiple genes and may be important for complex gene therapies.

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Cockman, Eric, Paul Anderson, and Pavel Ivanov. "TOP mRNPs: Molecular Mechanisms and Principles of Regulation." Biomolecules 10, no. 7 (June 27, 2020): 969. http://dx.doi.org/10.3390/biom10070969.

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The cellular response to changes in the surrounding environment and to stress requires the coregulation of gene networks aiming to conserve energy and resources. This is often achieved by downregulating protein synthesis. The 5’ Terminal OligoPyrimidine (5’ TOP) motif-containing mRNAs, which encode proteins that are essential for protein synthesis, are the primary targets of translational control under stress. The TOP motif is a cis-regulatory RNA element that begins directly after the m7G cap structure and contains the hallmark invariant 5’-cytidine followed by an uninterrupted tract of 4–15 pyrimidines. Regulation of translation via the TOP motif coordinates global protein synthesis with simultaneous co-expression of the protein components required for ribosome biogenesis. In this review, we discuss architecture of TOP mRNA-containing ribonucleoprotein complexes, the principles of their assembly, and the modes of regulation of TOP mRNA translation.

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Chavrier, P., U. Janssen-Timmen, M. G. Mattéi, M. Zerial, R. Bravo, and P. Charnay. "Structure, chromosome location, and expression of the mouse zinc finger gene Krox-20: multiple gene products and coregulation with the proto-oncogene c-fos." Molecular and Cellular Biology 9, no. 2 (February 1989): 787–97. http://dx.doi.org/10.1128/mcb.9.2.787-797.1989.

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We have analyzed the structure and the regulation of Krox-20, a mouse zinc finger-encoding gene which is transiently activated following serum stimulation of quiescent fibroblast cells in culture. The gene is localized on chromosome 10, band B5, in the mouse, and the homologous human gene also maps to chromosome 10 (region q21.1 to q22.1). Alternative splicing of the 5'-most intron of the Krox-20 gene gives rise to mRNAs encoding putative zinc finger proteins with different N termini. The first exon contains a sequence element with strong similarity to the c-fos proto-oncogene serum response element (SRE). This element can functionally substitute for the c-fos SRE, and it binds the same nuclear protein. It is probably responsible for the serum induction of Krox-20, possibly in combination with a weaker SRE located in the 5'-flanking region of the gene. Our findings suggest that c-fos, Krox-20, and a number of immediate-early serum response genes are coregulated and that the SRE and its cognate protein are essential components of this regulatory pathway.

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Chavrier, P., U. Janssen-Timmen, M. G. Mattéi, M. Zerial, R. Bravo, and P. Charnay. "Structure, chromosome location, and expression of the mouse zinc finger gene Krox-20: multiple gene products and coregulation with the proto-oncogene c-fos." Molecular and Cellular Biology 9, no. 2 (February 1989): 787–97. http://dx.doi.org/10.1128/mcb.9.2.787.

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We have analyzed the structure and the regulation of Krox-20, a mouse zinc finger-encoding gene which is transiently activated following serum stimulation of quiescent fibroblast cells in culture. The gene is localized on chromosome 10, band B5, in the mouse, and the homologous human gene also maps to chromosome 10 (region q21.1 to q22.1). Alternative splicing of the 5'-most intron of the Krox-20 gene gives rise to mRNAs encoding putative zinc finger proteins with different N termini. The first exon contains a sequence element with strong similarity to the c-fos proto-oncogene serum response element (SRE). This element can functionally substitute for the c-fos SRE, and it binds the same nuclear protein. It is probably responsible for the serum induction of Krox-20, possibly in combination with a weaker SRE located in the 5'-flanking region of the gene. Our findings suggest that c-fos, Krox-20, and a number of immediate-early serum response genes are coregulated and that the SRE and its cognate protein are essential components of this regulatory pathway.

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Lawson, Rebecca, Wolfgang Maret, and Christer Hogstrand. "ZnT8 Haploinsufficiency Impacts MIN6 Cell Zinc Content and β-Cell Phenotype via ZIP-ZnT8 Coregulation." International Journal of Molecular Sciences 20, no. 21 (November 4, 2019): 5485. http://dx.doi.org/10.3390/ijms20215485.

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The zinc transporter ZnT8 (SLC30A8) localises to insulin secretory granules of β-cells where it facilitates zinc uptake for insulin crystallisation. ZnT8 abundance has been linked to β-cell survival and functional phenotype. However, the consequences of ZnT8 haploinsufficiency for β-cell zinc trafficking and function remain unclear. Since investigations in human populations have shown SLC30A8 truncating polymorphisms to decrease the risk of developing Type 2 Diabetes, we hypothesised that ZnT8 haploinsufficiency would improve β-cell function and maintain the endocrine phenotype. We used CRISPR/Cas9 technology to generate ZnT8 haploinsufficient mouse MIN6 β-cells and showed that ZnT8 haploinsufficiency is associated with downregulation of mRNAs for Slc39a8 and Slc39a14, which encode for the zinc importers, Znt- and Irt-related proteins 8 (ZIP8) and 14 (ZIP14), and with lowered total cellular zinc content. ZnT8 haploinsufficiency disrupts expression of a distinct array of important β-cell markers, decreases cellular proliferation via mitogen-activated protein (MAP) kinase cascades and downregulates insulin gene expression. Thus, ZnT8 cooperates with zinc importers of the ZIP family to maintain β-cell zinc homeostasis. In contrast to the hypothesis, lowered ZnT8 expression reduces MIN6 cell survival by affecting zinc-dependent transcription factors that control the β-cell phenotype.

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Tohge, Takayuki, Keiko Yonekura-Sakakibara, Rie Niida, Akiko Watanabe-Takahashi, and Kazuki Saito. "Phytochemical genomics in Arabidopsis thaliana: A case study for functional identification of flavonoid biosynthesis genes." Pure and Applied Chemistry 79, no. 4 (January 1, 2007): 811–23. http://dx.doi.org/10.1351/pac200779040811.

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The completion of the whole genome sequence of Arabidopsis thaliana has made it possible to explore the phytochemical genomics in this species by determining gene-to-metabolite correlation through the comprehensive analysis of metabolite accumulation and gene expression. In this study, flavonoid profiling of wild-type plants and T-DNA insertion mutants was analyzed using ultra-performance liquid chromatography (UPLC)/photodiode array detection (PDA)/electrospray ionization (ESI)/multiple-stage mass spectrometry (MSn). Detailed analysis of the metabolite changes in the mutants suggested the functions of genes that have been mutated. In silico coexpression analysis of genes involved in flavonoid metabolism in Arabidopsis was performed using a publicly available transcriptome database of DNA microarrays. We inferred a coexpression framework model of the genes involved in the pathways of flavonol, anthocyanin, and proanthocyanidin synthesis, suggesting specific functions and coregulation of the genes of pathway enzymes and transcription factors. The metabolic profiling of the omt1 mutant lacking a methyltransferase gene narrowed down by the coexpression analysis showed that AtOMT1 (At5g54160) is involved not only in the production of lignins and sinapoyl esters but also in the methylation of flavonols forming isorhamnetin. These results suggest that the functional genomics approach by detailed target-metabolite profiling with transcriptome coexpression analysis provides an efficient way of identifying novel gene functions involved in plant metabolism.

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Stein, I., M. Neeman, D. Shweiki, A. Itin, and E. Keshet. "Stabilization of vascular endothelial growth factor mRNA by hypoxia and hypoglycemia and coregulation with other ischemia-induced genes." Molecular and Cellular Biology 15, no. 10 (October 1995): 5363–68. http://dx.doi.org/10.1128/mcb.15.10.5363.

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Expression of vascular endothelial growth factor (VEGF), an endothelial cell-specific mitogen and a potent angiogenic factor, is upregulated in response to a hypoxic or hypoglycemic stress. Here we show that the increase in steady-state levels of VEGF mRNA is partly due to transcriptional activation but mostly due to increase in mRNA stability. Both oxygen and glucose deficiencies result in extension of the VEGF mRNA half-life in a protein synthesis-dependent manner. Viewing VEGF as a stress-induced gene, we compared its mode of regulation with that of other stress-induced genes. Results showed that under nonstressed conditions, VEGF shares with the glucose transporter GLUT-1 a relatively short half-life (0.64 and 0.52 h, respectively), which is extended fourfold and more than eightfold, respectively, when cells are deprived of either oxygen or glucose. In contrast, the mRNAs of another hypoxia-inducible and hypoglycemia-inducible gene, grp78, as well as that of HSP70, were not stabilized by these metabolic insults. To show that VEGF and GLUT-1 are coinduced in differentially stressed microenvironments, multicell spheroids representing a clonal population of glioma cells in which each cell layer is differentially stressed were analyzed by in situ hybridization. Cellular microenvironments conducive to induction of VEGF and GLUT-1 were completely coincidental. These findings show that two different consequences of tissue ischemia, namely, hypoxia and glucose deprivation, induce VEGF and GLUT-1 expression by similar mechanisms. These proteins function, in turn, to satisfy the tissue needs through expanding its vasculature and improving its glucose utilization, respectively.

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Deveaux, S., A. Filipe, V. Lemarchandel, J. Ghysdael, PH Romeo, and V. Mignotte. "Analysis of the thrombopoietin receptor (MPL) promoter implicates GATA and Ets proteins in the coregulation of megakaryocyte-specific genes." Blood 87, no. 11 (June 1, 1996): 4678–85. http://dx.doi.org/10.1182/blood.v87.11.4678.bloodjournal87114678.

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he MPL gene codes for the thrombopoietin receptor, whose ligand specifically controls megakaryocytic differentiation. To understand the molecular basis for the megakaryocyte-specific expression of MPL, we analyzed the promoter of this gene. A 200 bp fragment is sufficient for high-level specific expression. This fragment can bind several trans- acting factors in vitro, including GATA-1 and members of the Ets family. GATA-1 binds with low affinity to a unique GATA motif at -70 in the MPL promoter, and destruction of this site yields only a modest decrease in expression level in HEL cells. Ets proteins also bind with low affinity to two sites. One is located at position -15 and its destruction reduces expression to 50%; the other is located immediately downstream of the GATA motif and plays a crucial role in expression of the promoter in HEL cells, as its inactivation reduces expression to 15%. Furthermore, GATA-1 and two Ets proteins, Ets-1 and Fli-1, can trans-activate the MPL promoter in heterologous cells. The effects of GATA-1 and these two Ets proteins are additive. Together with our previous results on the glycoprotein IIb (GpIIb) promoter, this study indicates a molecular basis for the coregulation of early markers of megakaryocyte differentiation.

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Journal articles on the topic 'Gene coregulation'

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