Relevant bibliographies by topics / Transcription; gene regulation; obesity

Academic literature on the topic 'Transcription; gene regulation; obesity'

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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Journal articles on the topic "Transcription; gene regulation; obesity"

He, Qing, Zhanguo Gao, Jun Yin, Jin Zhang, Zhong Yun, and Jianping Ye. "Regulation of HIF-1α activity in adipose tissue by obesity-associated factors: adipogenesis, insulin, and hypoxia." American Journal of Physiology-Endocrinology and Metabolism 300, no. 5 (May 2011): E877—E885. http://dx.doi.org/10.1152/ajpendo.00626.2010.

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The transcription factor HIF-1α activity is increased in adipose tissue to contribute to chronic inflammation in obesity. However, its upstream and downstream events remain to be characterized in adipose tissue in obesity. We addressed this issue by investigating adipocyte HIF-1α activity in response to obesity-associated factors, such as adipogenesis, insulin, and hypoxia. In adipose tissue, both HIF-1α mRNA and protein were increased by obesity. The underlying mechanism was investigated in 3T3-L1 adipocytes. HIF-1α mRNA and protein were augmented by adipocyte differentiation. In differentiated adipocytes, insulin further enhanced HIF-1α in both levels. Hypoxia enhanced only HIF-1α protein, not mRNA. PI3K and mTOR activities are required for the HIF-1α expression. Function of HIF-1α protein was investigated in the regulation of VEGF gene transcription. ChIP assay shows that HIF-1α binds to the proximal hypoxia response element in the VEGF gene promoter, and its function is inhibited by a corepressor composed of HDAC3 and SMRT. These observations suggest that of the three obesity-associated factors, all of them are able to augment HIF-1α protein levels, but only two (adipogenesis and insulin) are able to enhance HIF-1α mRNA activity. Adipose tissue HIF-1α activity is influenced by multiple signals, including adipogenesis, insulin, and hypoxia in obesity. The transcriptional activity of HIF-1α is inhibited by HDAC3-SMRT corepressor in the VEGF gene promoter.

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Ren, Wei, Jianjin Guo, Feng Jiang, Jun Lu, Ying Ding, Aimei Li, Xiubin Liang, and Weiping Jia. "CCAAT/Enhancer-Binding ProteinαIs a Crucial Regulator of Human Fat Mass and Obesity Associated Gene Transcription and Expression." BioMed Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/406909.

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Several susceptibility loci have been reported associated with obesity and T2DM in GWAS. Fat mass and obesity associated gene (FTO) is the first gene associated with body mass index (BMI) and risk for diabetes in diverse patient populations. FTO is highly expressed in the brain and pancreas, and is involved in regulating dietary intake and energy expenditure. While much is known about the epigenetic mutations contributing to obesity and T2DM, less is certain with the expression regulation of FTO gene. In this study, a highly conserved canonical C/EBPαbinding site was located around position −45~−54 bp relative to the human FTO gene transcriptional start site. Site-directed mutagenesis of the putative C/EBPαbinding sites decreased FTO promoter activity. Overexpression and RNAi studies also indicated that C/EBPαwas required for the expression of FTO. Chromatin immunoprecipitation (ChIP) experiment was carried out and the result shows direct binding of C/EBPαto the putative binding regions in the FTO promoter. Collectively, our data suggest that C/EBPαmay act as a positive regulator binding to FTO promoter and consequently, activates the gene transcription.

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Martínez-Hernández, Alfredo, Luís Enríquez, María Jesús Moreno-Moreno, and Amelia Martí. "Genetics of obesity." Public Health Nutrition 10, no. 10A (October 2007): 1138–44. http://dx.doi.org/10.1017/s1368980007000626.

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AbstractObjectiveThe aim was to review and update advances in genetics of obesity.DesignAnalysis and interpretation of recent investigations about regulating the energy balance as well as about gene-nutrient interactions and current nutrigenomic research methods.Background and main statementsObesity results from a long-term positive energy balance. However, its rising prevalence in developed and developing societies must reflect lifestyle changes, since genetic susceptibility remains stable over many generations. Like most complex diseases, obesity derives from a failure of adequate homoeostasis within the physiological system controlling body weight. The identification of genes that are involved in syndromic, monogenic and polygenic obesity has seriously improved our knowledge of body weight regulation. This disorder may arise from a deregulation at the genetic level (e.g. gene transcription or altered protein function) or environmental exposure (e.g. diet, physical activity, etc.).ConclusionsIn practice, obesity involves the interaction between genetic and environmental factors.

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Liu, Meilian, and Feng Liu. "Transcriptional and post-translational regulation of adiponectin." Biochemical Journal 425, no. 1 (December 14, 2009): 41–52. http://dx.doi.org/10.1042/bj20091045.

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Adiponectin is an adipose-tissue-derived hormone with anti-diabetic, anti-atherogenic and anti-inflammatory functions. Adiponectin circulates in the bloodstream in trimeric, hexameric and high-molecular-mass species, and different forms of adiponectin have been found to play distinct roles in the regulation of energy homoeostasis. The serum levels of adiponectin are negatively correlated with obesity and insulin resistance, yet the underlying mechanisms remain elusive. In the present review, we summarize recent progress made on the mechanisms regulating adiponectin gene transcription, multimerization and secretion. We also discuss the potential relevance of these studies to the development of new clinical therapy for insulin resistance, Type 2 diabetes and other obesity-related metabolic disorders.

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Miroshnikova, V. V., A. A. Panteleeva, E. A. Bazhenova, E. P. Demina, T. S. Usenko, M. A. Nikolaev, I. A. Semenova, et al. "Regulation of ABCA1 and ABCG1 gene expression in the intraabdominal adipose tissue." Biomeditsinskaya Khimiya 62, no. 3 (2016): 283–89. http://dx.doi.org/10.18097/pbmc20166203283.

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Tissue specific expression of genes encoding cholesterol transporters ABCA1 and ABCG1 as well as genes encoding the most important transcriptional regulators of adipogenesis – LXRa, LXRb, PPARg and RORa has been investigated in intraabdominal adipose tissue (IAT) samples.A direct correlation between the content of ABCA1 and ABCG1 proteins with RORa protein level (r=0.480, p<0.05; r=0.435, p<0.05, respectively) suggests the role of the transcription factor RORa in the regulation of IAT ABCA1 and ABCG1 protein levels. ABCA1 and ABCG1 gene expression positively correlated with obesity indicators such as body mass index (BMI) (r=0.522, p=0.004; r=0.594, p=0.001, respectively) and waist circumference (r=0.403, p=0.033; r=0.474, p=0.013, respectively). The development of obesity is associated with decreased IAT levels of RORa and LXRb mRNA (p=0.016 and p=0.002, respectively). These data suggest that the nuclear factor RORa can play a significant role in the regulation of cholesterol metabolism and control IAT expression of ABCA1 and ABCG1, while the level of IAT LXRb gene expression may be an important factor associated with the development of obesity.

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Yuxin, Liu, Lin Chen, Luo Xiaoxia, Luo Yue, Lai Junjie, Li Youzhu, Zhou Huiliang, and Liu Qicai. "Research Progress on the Relationship between Obesity-Inflammation-Aromatase Axis and Male Infertility." Oxidative Medicine and Cellular Longevity 2021 (February 8, 2021): 1–7. http://dx.doi.org/10.1155/2021/6612796.

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Aromatase is a key enzyme in the transformation of androgen into estrogen. Its high expression will destroy the hormonal balance in the male body, and the excessive transformation of androgen into estrogen in the body will further damage the spermatogenic function of the testis, affect the normal development of the sperm, and cause spermatogenic disturbance. Adipose tissue has a high expression of aromatase and shows high enzymatic activity and ability to convert estrogen. Adipose tissue is the most estrogen-producing nongonadal tissue in the body because of its large size, accounting for about 20% of the body mass in healthy adults. PPARγ is recognized as the key adipose differentiation in the transcriptional regulation of the transcription factor. In the process of adipocyte differentiation, PPARγ regulate the expression of aromatase. The increase of aromatase is associated with the inflammatory response in adipose tissue caused by obesity. After obesity, the increase of proinflammatory factors in adipocytes will lead to enhanced transcription of the CYP19 gene encoding aromatase in adipocytes, which in turn will lead to increased expression of aromatase in adipocytes. This article reviews the regulation of male sterility from the angle of the “obesity-inflammation-aromatase” axis.

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Fan, Ji-lin, Ting-ting Zhu, Xiao-ling Tian, Zhen-yu Xue, Jing-qi Guo, Wen-qing Ren, and Shi-liang Zhang. "Relationship Between Obesity and Hypertension From Bioinformatics Analysis." American Journal of Hypertension 36, no. 1 (January 1, 2023): 72. http://dx.doi.org/10.1093/ajh/hpac090.

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Abstract Background To explore the relationship between obesity and hypertension using bioinformatics analyses. Methods Disease databases (GeneCards, OMIM, CTD, TTD, DisGeNET, and Drugbank) were used to obtain hypertension and obesity-related targets. The intersection targets of obesity and hypertension were constructed using Venn diagrams. STRING online platform was used to obtain protein–protein interaction networks of common targets, and Cytohubba plug-in was used to screen the core targets. Gene ontology (GO) analysis and the enrichment analysis of Kyoto encyclopedia of genes and genomes (KEGG) were carried out using DAVID database. Results A total of 459 and 551 targets were obtained for obesity and hypertension, respectively. Among them, 135 were targets for both obesity and hypertension in which tumor necrosis factor (TNF), cell tumor antigen p53 (TP53), chemokine 2 (CCL2), Toll-like receptor 4 (TLR4), interleukin (IL) 1B, nitric oxide synthase 3 (NOS3), IL-6, and serine/threonine protein kinase 1 (AKT1) were key targets for regulating obesity and hypertension. Enrichment analysis yielded 306 GO entries [P < 0.05, false discovery rate (FDR) <0.05], which were involved in positive regulation of mitogen-activated protein kinase (MAPK) cascade, positive regulation of nitric oxide biosynthetic process, cilium basal body, hormone activity, and RNA polymerase II repeating transcription factor binding. The 86 enriched KEGG entries (P < 0.05, FDR <0.05) included adipocytokine signaling pathway, regulation of lipolysis in adipocytes, PI3K–Akt signaling pathway and forkhead transcription factor O (FoxO) signaling pathway. Conclusions TNF, TP53, CCL2, TLR4, IL-1B, NOS3, IL-6, AKT1, and the key pathways including adipocytokine signaling pathway, regulation of adipocyte lipolysis, PI3K–Akt and FoxO signaling pathway play a regulatory role in interactions between obesity and hypertension. These findings provide new insights into the complex interactions between obesity and hypertension.

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CLAYCOMBE, KATE J., YANXIN WANG, BRYNN H. JONES, SUYEON KIM, WILLIAM O. WILKISON, MICHAEL B. ZEMEL, JOSEPH CHUN, and NAIMA MOUSTAID-MOUSSA. "Transcriptional regulation of the adipocyte fatty acid synthase gene by agouti: interaction with insulin." Physiological Genomics 3, no. 3 (September 8, 2000): 157–62. http://dx.doi.org/10.1152/physiolgenomics.2000.3.3.157.

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Claycombe, Kate J., Yanxin Wang, Brynn H. Jones, Suyeon Kim, William O. Wilkison, Michael B. Zemel, Joseph Chun, and Naima Moustaid-Moussa. Transcriptional regulation of the adipocyte fatty acid synthase gene by agouti: interaction with insulin. Physiol Genomics 3: 157–162, 2000.—Mice carrying dominant mutations at the agouti locus exhibit ectopic expression of agouti gene transcripts, obesity, and type II diabetes through unknown mechanisms. To gain insight into the role of agouti protein in modulating adiposity, we investigated regulation of a key lipogenic gene, fatty acid synthase (FAS) by agouti alone and in combination with insulin. Both agouti and insulin increase FAS activity in 3T3-L1 and in human adipocytes. Agouti and insulin independently and additively increase FAS activity in 3T3-L1 adipocytes. We further investigated the mechanism responsible for the agouti-induced FAS expression in these cells and demonstrated that both insulin (3-fold increase) and agouti (2-fold) increased FAS gene expression at the transcriptional level. Furthermore, insulin and agouti together exerted additive effects (5-fold increase) on FAS gene transcription. Transfection assays of FAS promoter-luciferase fusion gene constructs into 3T3-L1 adipocytes indicated that the agouti response element(s) is (are) located in the −435 to −415 region (−435/−415) of the FAS promoter. Nuclear proteins binding to this novel sequence are adipocyte specific. Thus the agouti response sequences mapped to a region upstream of the insulin-responsive element (which we previously reported to be located at −67/−52), consistent with additive effects of these two factors on FAS gene transcription.

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Crispim, Daisy, Felipe Mateus Pellenz, and Tais Silveira Assmann. "Identification of Key Genes and Pathways for Childhood Obesity Using System Biology Approach Based on Comprehensive Gene Information." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A49—A50. http://dx.doi.org/10.1210/jendso/bvab048.098.

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Abstract Introduction: Childhood obesity is one of the most important public health issues of the 21st century. Epidemiological studies have suggested that obesity during childhood increases the risk of developing comorbidities, such as type 2 diabetes, later in life. Childhood obesity is a complex disease whose molecular mechanisms are not completely elucidated. In this context, a system biology approach could contribute to the scientific knowledge regarding genetic factors related to childhood obesity onset. Aim: To identify molecular mechanisms involved in childhood obesity by implementing a system biology approach. Methods: Experimentally validated and computationally predicted genes related to Pediatric Obesity (C2362324) were downloaded from the DisGeNET v7.0 database. The protein-protein interaction (PPI) network was constructed using the STRING v11.0 database and analyzed using NetworkAnalyst v3.0 and Cytoscape v3.8.1. The relevance of each node for the network structure and functionality was assessed using the degree method to define hub genes. Functional and pathway enrichment analyses were performed based on Gene Ontology (GO) terms and KEGG Pathways. Results: The search on the DisGeNET database retrieved 191 childhood obesity-related genes. The PPI network of these genes showed 19 hub genes (STAT3, SIRT1, BCL2, IRS1, PPARG, SOCS3, TGFB1, HDAC4, DNMT1, ADCY3, PPARA, NEDD4L, ACACB, NR0B2, VEGFA, APOA1, GHR, CALR, and MKKS). These hub genes were involved in biological processes of lipid storage / kinase activity, regulation of fatty-acid metabolic processes, regulation of pri-miRNA transcription by RNA polymerase II, and negative regulation of small molecules and carbohydrate metabolic processes. In terms of molecular functions, repressing of transcription factors biding was found enriched. Regarding KEGG Pathways, the hub genes are involved with adipocytokine signaling, insulin resistance, longevity regulation, and cytokine signaling pathways. Conclusion: Our approach identified 19 hub genes, which are highly connected and probably have a key role in childhood obesity. Moreover, functional enrichment analyses demonstrated they are enriched in several biological processes and pathways related to the underlying molecular mechanisms of obesity. These findings provide a more comprehensive information regarding genetic and molecular factors behind childhood obesity pathogenesis. Further experimental investigation of our findings may shed light on the pathophysiology of this disease and contribute to the identification of new therapeutic targets.

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Karnieli, Eddy, and Michal Armoni. "Transcriptional regulation of the insulin-responsive glucose transporter GLUT4 gene: from physiology to pathology." American Journal of Physiology-Endocrinology and Metabolism 295, no. 1 (July 2008): E38—E45. http://dx.doi.org/10.1152/ajpendo.90306.2008.

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The insulin-responsive glucose transporter 4 (GLUT4) plays a key role in glucose uptake and metabolism in insulin target tissues. Being a rate-limiting step in glucose metabolism, the expression and function of the GLUT4 isoform has been extensively studied and found to be tightly regulated at both mRNA and protein levels. Adaptation to states of enhanced metabolic demand is associated with increased glucose metabolism and GLUT4 gene expression, whereas states of insulin resistance such as type 2 diabetes mellitus (DM2), obesity, and aging are associated with impaired regulation of GLUT4 gene expression and function. The present review focuses on the interplay among hormonal, nutritional, and transcription factors in the regulation of GLUT4 transcription in health and sickness.

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Dissertations / Theses on the topic "Transcription; gene regulation; obesity"

Grossman, Sharon R. (Sharon Rachel). "Combinatorial gene regulation by transcription factors." Thesis, Massachusetts Institute of Technology, 2019. https://hdl.handle.net/1721.1/128406.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2019
Cataloged from PDF of thesis. "The Table of Contents does not accurately represent the page numbering"--Disclaimer page.
Includes bibliographical references.
Combinatorial gene regulation is encoded in enhancers and promoters in the form of binding sites for transcription factors (TFs), which collaboratively recruit the transcriptional machinery and drive gene expression. Using high-throughput and quantitative technologies developed by our lab and others, we studied TF binding sites in enhancers from numerous different cell types and regulatory systems, shedding light general principles of motif composition and organization in typical cellular regulatory elements. We find extensive synergy between TF binding sites, some with organizational constraints and some with flexible positioning. We demonstrate that different TFs bind at distinct positions within regulatory elements, suggesting a new type of architectural constraint in enhancers. Importantly, our analysis of both TF organization and cooperativity revealed distinctive patterns that separates TFs into potential functional classes. Together, our results suggest a structure of the regulatory code at the level of TF function and generate new hypotheses about regiospecific binding patterns and functions of TF classes within enhancers.
by Sharon R. Grossman.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Biology

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Deavall, Damian Gregory. "The physiological regulation of cholecystokinin gene transcription." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367183.

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Dunham, Lee. "Dynamic regulation of growth hormone gene transcription." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/dynamic-regulation-of-growth-hormone-gene-transcription(62354b9b-c755-43b6-a3f0-d108c32232c9).html.

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Many genes demonstrate highly dynamic pulsatile expression, with characteristic bursts of activity. Dynamic expression of the human prolactin (hPrl) gene in pituitary cells has previously been investigated identifying key temporal characteristics, influenced by the process of chromatin remodelling. Earlier work on the related pituitary human growth hormone (hGH) proximal promoter (-496/+1bp) indicated that it displayed similar dynamic behaviour. The human GH gene contains an extensive long-distance regulatory sequence, including a locus control region (-14/-32kbp) that has been shown to regulate chromatin remodelling and confer tissue-specificity of hGH expression. In this work I aimed to study dynamic regulation of the hGH gene promoter in detail. Initially I investigated the efficiency of several methods to express the luciferase gene in a 180kb hGH genomic fragment using bacterial artificial chromosome recombineering, to allow the investigation of single cell transcription dynamics. Although a functional recombinant BAC was not finalised during the course of the work, I carried out detailed time course studies using shorter hGH-reporter constructs. Using quantitative microscopy to study live single cells, I compared the dynamic characteristics of a 5kb hPrl promoter fragment with those of -840/+1bp and -3348/+1bp hGH-luciferase promoter-reporter constructs. Whilst previous hPrl analysis utilised a binary mathematical model assuming a simplified two-state (ON/OFF) process of gene transcription, I validated and applied a novel stochastic switch model (SSM), assuming instead that transcription rate can switch between any variable states at any time. Through doing so I observed an asymmetry in transcription rate switching, suggesting an all-or-nothing activation of a single UP-switch, with a greater number of rate decreasing DOWN-switches. The -3348/+1bp construct produced double the number of DOWN-switches, whilst the -840/+1bp construct produced 1.5 DOWN-switches in a 48h period. The cycling of transcriptional activity seen by the shorter construct was modified through the addition of forskolin, activating cAMP signalling. However, significant modification of the transcriptionally inactive refractory period seen with the -3348/+1bp construct (reduced from 3h to 1.9h) required histone modification through application of trichostatin A, a HDAC inhibitor. In conclusion, different promoter elements confer different transcriptional timing and dynamics. A subtler transcriptional modelling, such as used here in the SSM, reveals new insights into the phenomena of transcriptional switching, but the mechanisms involved remain to be determined.

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Pang, Ting-kai Ronald. "Transcriptional regulation of the human secretin receptor gene /." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25059324.

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Mastrangelo, Peter. "Transcription regulation of the Saccharomyces cerevisiae actin gene." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ27461.pdf.

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Garnier, France. "Study of transcription regulation of the gene mdr1." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56986.

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In order to characterize cis-acting sequences and trans-acting factors important in regulating the expression of the mouse mdr1 gene, in vitro DNAsel footprinting experiments were carried out on a mdr1 promoter segment between positions $-$245 and +84, using nuclear protein extracts prepared from cell lines expressing different endogenous amounts of mdr1 mRNAs. Three footprinted sequences were detected on the non-coding strand of the $-$245 to +84 mdr1 promoter fragment (between -77 to -56, between -46 to -24, and between +5 and +15) with nuclear extracts from mdr1 expressing cells (CMT-93, LTA, and Y-1 cells). In addition, a specific footprinted sequence ($-$14 to +5) was detected on both strands only with nuclear extracts from the mdr1 non-expressing cell line (RAG cells) suggesting the presence and binding of a putative negative regulatory factor in these cells. However, replacement of this sequence in the mdr1 basal promoter ($-$93 to +84) by a heterologous, although similar positioned SV40 sequence did not restore promoter activity in RAG cells. The basal mdr1 promoter was further characterized in bidirectional deletion mutants, in order to identify cis-acting elements important for general transcriptional regulation. These studies further localized the mdr1 basal promoter between positions $-$74 and +84, and also suggested the presence of possible positive and negative cis-acting sequence elements modulating the activity of this basal promoter.

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Li, Yifan. "Gene regulation by WT1 and related transcription factors." Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509772.

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Jahangiri, Leila. "Combinatorial gene regulation by T-domain transcription factors." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610328.

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Gay, Robert Daniel. "Neuronal gene regulation by POU family transcription factors." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267026.

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Tshuikina, Wiklander Marina. "Epigenetic Regulation of Gene Transcription in Hematopoietic Tumors." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9206.

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Books on the topic "Transcription; gene regulation; obesity"

Gene control. New York: Garland Science, 2010.

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Julian, Burke, ed. Gene structure and transcription. Oxford, England: IRL Press, 1988.

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Julian, Burke, ed. Gene structure and transcription. 2nd ed. Oxford: IRL Press at Oxford University Press, 1992.

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Latchman, David S. Gene control. New York: Garland Science, 2010.

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Gene transcription: Mechanisms and control. London: Blackwell Science, 2001.

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Gene regulation: A eukaryotic perspective. 5th ed. New York: Taylor & Francis, 2006.

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Latchman, David S. Gene regulation: A eukaryotic perspective. London: Unwin Hyman, 1990.

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Gene regulation: A eukaryotic perspective. 4th ed. Cheltenham: Nelson Thornes, 2002.

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Wingender, Edgar. Gene regulation in eukaryotes. Weinheim: VCH, 1993.

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Gene regulation: A eukaryotic perspective. 2nd ed. London: Chapman & Hall, 1995.

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Book chapters on the topic "Transcription; gene regulation; obesity"

Carlberg, Carsten, and Ferdinand Molnár. "Transcription Factors." In Mechanisms of Gene Regulation, 57–73. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-017-7741-4_4.

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Carlberg, Carsten, and Ferdinand Molnár. "Transcription Factors." In Mechanisms of Gene Regulation, 55–70. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7905-1_4.

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Kim, Minkyu, and Stephen Buratowski. "Transcription Termination by RNA Polymerase II." In Posttranscriptional Gene Regulation, 19–40. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2013. http://dx.doi.org/10.1002/9783527665433.ch2.

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Salehi-Ashtiani, Kourosh, and Erwin Goldberg. "Testis-Specific Gene Transcription." In Cellular and Molecular Regulation of Testicular Cells, 127–34. New York, NY: Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4612-2374-0_10.

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Sybers, David, Daniel Charlier, and Eveline Peeters. "In Vitro Transcription Assay for Archaea Belonging to Sulfolobales." In Prokaryotic Gene Regulation, 81–102. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2413-5_6.

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Ledesma, Leonardo, Rafael Hernandez-Guerrero, and Ernesto Perez-Rueda. "Prediction of DNA-Binding Transcription Factors in Bacteria and Archaea Genomes." In Prokaryotic Gene Regulation, 103–12. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2413-5_7.

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Hetherington, Marion M., and Joanne E. Cecil. "Gene-Environment Interactions in Obesity." In Frontiers in Eating and Weight Regulation, 195–203. Basel: KARGER, 2009. http://dx.doi.org/10.1159/000264407.

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Lavender, P., D. Cousins, and T. Lee. "Regulation of Th2 Cytokine Gene Transcription." In Immunological Mechanisms in Asthma and Allergic Diseases, 16–29. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000058813.

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Yeo, Nan Cher, and George M. Church. "Perturbation of Gene Regulation by Genome Editing." In Transcription Factor Regulatory Networks, 59–68. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2815-7_5.

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Hatfield, G. Wesley, and Janice A. Sharp. "Translational Control of Transcription Termination in Prokaryotes." In Translational Regulation of Gene Expression, 447–71. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5365-2_21.

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Conference papers on the topic "Transcription; gene regulation; obesity"

Mohbeddin, Abeer, Nawar Haj Ahmed, and Layla Kamareddine. "The use of Drosophila Melanogaster as a Model Organism to study the effect of Innate Immunity on Metabolism." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0224.

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Apart from its traditional role in disease control, recent body of evidence has implicated a role of the immune system in regulating metabolic homeostasis. Owing to the importance of this “immune-metabolic alignment” in dictating a state of health or disease, a proper mechanistic understanding of this alignment is crucial in opening up for promising therapeutic approaches against a broad range of chronic, metabolic, and inflammatory disorders like obesity, diabetes, and inflammatory bowel syndrome. In this project, we addressed the role of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) innate immune pathway in regulating different metabolic parameters using the Drosophila melanogaster (DM) fruit fly model organism. Mutant JAK/STAT pathway flies with a systemic knockdown of either Domeless (Dome) [domeG0282], the receptor that activates JAK/STAT signaling, or the signal-transducer and activator of transcription protein at 92E (Stat92E) [stat92EEY10528], were used. The results of the study revealed that blocking JAK/STAT signaling alters the metabolic profile of mutant flies. Both domeG0282 and stat92EEY10528 mutants had an increase in body weight, lipid deprivation from their fat body (lipid storage organ in flies), irregular accumulation of lipid droplets in the gut, systemic elevation of glucose and triglyceride levels, and differential down-regulation in the relative gene expression of different peptide hormones (Tachykinin, Allatostatin C, and Diuretic hormone 31) known to regulate metabolic homeostasis in flies. Because the JAK/STAT pathway is evolutionary conserved between invertebrates and vertebrates, our potential findings in the fruit fly serves as a platform for further immune-metabolic translational studies in more complex mammalian systems including humans.

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Docquier, Aurelie, Pierre-Olivier Harmand, Samuel Fritsch, Eric Badia, Lluis Fajas, Patrick Augereau, and Vincent Cavailles. "Abstract 4970: Complex regulation of RIP140 gene expression by E2F transcription factors." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4970.

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Hu, Biao, Zhe Wu, and Sem H. Phan. "Regulation Of Telomerase Reverse Transcriptase Gene Expression By Kruppel-Like Transcription Factor 4." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3516.

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Kuijjer, Marieke Lydia, Kimberly Glass, and John Quackenbush. "Abstract B1-20: Gene regulation by transcription factors and microRNAs in ovarian cancer." In Abstracts: AACR Special Conference: Computational and Systems Biology of Cancer; February 8-11, 2015; San Francisco, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.compsysbio-b1-20.

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Valli, Emanuele, Chengyuan Xue, Leanna Cheung, Laura Gamble, Ruby Pandher, Simone Di Giacomo, Catherine Burkhart, et al. "Abstract 2616: A novel iron-chelating agent reduces MYC transcription via E2F gene family regulation." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2616.

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Kozaki, Akiko. "Gene regulation via the combination of transcription factors in the INDETERMINATE DOMAIN and GRAS families." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1049086.

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Rosanò, Laura, Roberta Cianfrocca, Valeriana Di Castro, Francesca Spinella, Maria Rita Nicotra, Pier Giorgio Natali, and Anna Bagnato. "Abstract 2363: Positive inter-regulation between β-catenin and endothelin signaling in ovarian cancer cells: Epigenetic regulation of gene transcription." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2363.

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Polstein, Lauren R., and Charles A. Gersbach. "Photoregulated Gene Expression in Human Cells With Light-Inducible Engineered Transcription Factors." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80573.

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Systems for controlling gene expression in mammalian cells have a wide range of applications in medicine, biotechnology and basic science. An ideal gene regulatory system would allow for precise and specific control over the magnitude and kinetics of gene expression in space and time, while also exerting minimal influence on other genes and cellular components. Several gene regulatory systems have been developed in which orthogonal transcription machinery from prokaryotes or insects has been imported into mammalian cells and used to control the expression of a specific gene. Despite the transformative impact of these systems in biomedical and biological research, several limitations of these technologies restrict the scope of possible applications. For example, gene expression in these systems is controlled by a freely diffusible small molecule, such as an antibiotic or steroid. Consequently, it is not possible to achieve spatial control over gene expression within cell culture, tissues, or whole organisms. This is in contrast to natural mechanisms of biological regulation in which spatial control is critical, such as developmental patterning and tissue morphogenesis. Second, dynamic gene regulation requires the removal of these small molecules, which may be slow, laborious, and/or impractical for a particular application. To overcome these limitations, we have engineered an optogenetic system in which the magnitude of gene expression in human cells can be finely tuned by photoregulated synthetic transcription factors.

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Fowlkes, P. M., P. K. Lund, M. Blake, and J. Snouwaert. "THE REGULATION OF FIBRINOGEN PRODUCTION INVOLVES AT LEAST ONE OTHER HEPATOCYTE GENE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644317.

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It is currently thought that glucocorticosteriods have a direct effect on the transcription of the alpha, beta and gamma fibrinogen genes. However, our studies indicate that while corticosteriods play a role in fibrinogen production, this role is not due to transcriptional activation via glucocorticosteriod receptors. In initial experiments, we compared the levels of fibrinogen mRNA in hepatocytes isolated from hypophysectomized rats to those from control animals. The levels of mRNA in hypophysectomized rats, which produce little ACTH or corticosteriods, were significantly higher than the levels in control animals. Albumin mRNA levels were unaffected by hypophysectomy. These results are in opposition to those which we had anticipated. Based on previously published data, we had thought that physiologic deprivation of corticosteriods would lead to decreased levels of fibrinogen. We propose that these results are related to the negative feedback that corticosteroids have on Hepatocyte Stimulating Factor (HSF) production through a tightly controlled feedback circuit. To investigate the role of corticosteriods in fibrinogen gene regulation, we have conducted experiments with primary hepatocytes in culture and rat FAZA cells (continuous hepatoma cell line). There is a 4 to 5 fold increase in fibrinogen production when these cells are treated with HSF but no change when these cells are treated with dexamethasone alone. However, there is a marked additional increase in the production of fibrinogen with the combination of dexamethasone and HSF. Data gathered through kinetic analysis of this synergistic interaction suggest that the maximum response to HSF requires another gene product whose production is responsive to dexamethasone. Detailed analysis of the rate of transcription of thegamma fibrinogen gene, its processing and mRNA turnover suggests a specific role for this gene product in regulating fibrinogen synthesis. Characterization of this gene product will lead to greater understanding of the regulation of the Acute Phase Reactants.

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Reports on the topic "Transcription; gene regulation; obesity"

Latchman, David S. Regulation of BRCA-1 Gene Expression and Mammary Tumorigenesis by the Brn-3B POU Family Transcription Factor. Fort Belvoir, VA: Defense Technical Information Center, December 2001. http://dx.doi.org/10.21236/ada403379.

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Latchman, David S. Regulation of BRCA-1 Gene Expression and Mammary Tumorigenesis by the Brn-3b POU Family Transcription Factor. Fort Belvoir, VA: Defense Technical Information Center, December 2002. http://dx.doi.org/10.21236/ada413037.

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Bollig, Aliccia, and Richard J. Miksicek. Role of ERa Splicing Variants in Regulation of AP-1 Directed Gene Transcription in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada391091.

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Paran, Ilan, and Allen Van Deynze. Regulation of pepper fruit color, chloroplasts development and their importance in fruit quality. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598173.bard.

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Pepper exhibits large natural variation in chlorophyll content in the immature fruit. To dissect the genetic and molecular basis of this variation, we conducted QTL mapping for chlorophyll content in a cross between light and dark green-fruited parents, PI 152225 and 1154. Two major QTLs, pc1 and pc10, that control chlorophyll content by modulation of chloroplast compartment size in a fruit-specific manner were detected in chromosomes 1 and 10, respectively. The pepper homolog of GOLDEN2- LIKE transcription factor (CaGLK2) was found as underlying pc10, similar to its effect on tomato fruit chloroplast development. A candidate gene for pc1was found as controlling chlorophyll content in pepper by the modulation of chloroplast size and number. Fine mapping of pc1 aided by bulked DNA and RNA-seq analyses enabled the identification of a zinc finger transcription factor LOL1 (LSD-One-Like 1) as a candidate gene underlying pc1. LOL1 is a positive regulator of oxidative stress- induced cell death in Arabidopsis. However, over expression of the rice ortholog resulted in an increase of chlorophyll content. Interestingly, CaAPRR2 that is linked to the QTL and was found to affect immature pepper fruit color in a previous study, did not have a significant effect on chlorophyll content in the present study. Verification of the candidate's function was done by generating CRISPR/Cas9 knockout mutants of the orthologues tomato gene, while its knockout experiment in pepper by genome editing is under progress. Phenotypic similarity as a consequence of disrupting the transcription factor in both pepper and tomato indicated its functional conservation in controlling chlorophyll content in the Solanaceae. A limited sequence diversity study indicated that null mutations in CaLOL1 and its putative interactorCaMIP1 are present in C. chinensebut not in C. annuum. Combinations of mutations in CaLOL1, CaMIP1, CaGLK2 and CaAPRR2 are required for the creation of the extreme variation in chlorophyll content in Capsicum.

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Arazi, Tzahi, Vivian Irish, and Asaph Aharoni. Micro RNA Targeted Transcription Factors for Fruit Quality Improvement. United States Department of Agriculture, July 2008. http://dx.doi.org/10.32747/2008.7592651.bard.

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Fruits are unique to flowering plants and represent an important component of human and animal diets. Development and maturation of tomato fruit is a well-programmed process, and yet, only a limited number of factors involved in its regulation have been characterized. Micro-RNAs (miRNAs) are small, endogenous RNAs that regulate gene expression in animals and plants. Plant miRNAs have a vital role in the generation of plant forms through post-transcriptional regulation of the accumulation of developmental regulators, especially transcription factors. Recently, we and others have demonstrated that miRNAs and other type of small RNAs are expressed in tomato fruit, and target putative transcription factors during its development and maturation. The original objectives of the approved proposal were: 1. To identify fruit miRNA transcription factor target genes through a bioinformatic approach. 2. To identify fruit miRNA transcription factor target genes up-regulated in tomato Dicer-like 1 silenced fruit. 3. To establish the biological functions of selected transcription factors and examine their utility for improving fleshy fruit quality trait. This project was approved by BARD as a feasibility study to allow initial experiments to peruse objective 2 as described above in order to provide initial evidence that miRNAs do play a role in fruit development. The approach planned to achieve objective 2, namely to identify miRNA transcription factor targets was to clone and silence the expression of a tomato DCL1 homolog in different stages of fruit development and examine alterations to gene expression in such a fruit in order to identify pathways and target genes that are regulated by miRNA via DCL1. In parallel, we characterized two transcription factors that are regulated by miRNAs in the fruit. We report here on the cloning of tomato DCL1 homolog, characterization of its expression in fruit flesh and peel of wild type and ripening mutants and generation of transgenic plants that silence SlDCL1 specifically in the fruit. Our results suggest that the tomato homolog of DCL1, which is the major plant enzyme involved in miRNA biogenesis, is present in fruit flesh and peel and differentially expressed during various stages of fruit development. In addition, its expression is altered in ripening mutants. We also report on the cloning and expression analysis of Sl_SBP and Sl_ARF transcription factors, which serve as targets of miR157 and miR160, respectively. Our data suggest that Sl_SBP levels are highest during fruit ripening supporting a role for this gene in that process. On the other hand Sl_ARF is strongly expressed in green fruit up to breaker indicating a role for that gene at preripening stage which is consistent with preliminary in_situ analyses that suggest expression in ovules of immature green fruit. The results of this feasibility study together with our previous results that miRNAs are expressed in the fruit indeed provide initial evidence that these regulators and their targets play roles in fruit development and ripening. These genes are expected to provide novel means for genetic improvement of tomato fleshy fruit.

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Ohad, Nir, and Robert Fischer. Regulation of Fertilization-Independent Endosperm Development by Polycomb Proteins. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695869.bard.

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Arabidopsis mutants that we have isolated, encode for fertilization-independent endosperm (fie), fertilization-independent seed2 (fis2) and medea (mea) genes, act in the female gametophyte and allow endosperm to develop without fertilization when mutated. We cloned the FIE and MEA genes and showed that they encode WD and SET domain polycomb (Pc G) proteins, respectively. Homologous proteins of FIE and MEA in other organisms are known to regulate gene transcription by modulating chromatin structure. Based on our results, we proposed a model whereby both FIE and MEA interact to suppress transcription of regulatory genes. These genes are transcribed only at proper developmental stages, as in the central cell of the female gametophyte after fertilization, thus activating endosperm development. To test our model, the following questions were addressed: What is the Composition and Function of the Polycomb Complex? Molecular, biochemical, genetic and genomic approaches were offered to identify members of the complex, analyze their interactions, and understand their function. What is the Temporal and Spatial Pattern of Polycomb Proteins Accumulation? The use of transgenic plants expressing tagged FIE and MEA polypeptides as well as specific antibodies were proposed to localize the endogenous polycomb complex. How is Polycomb Protein Activity Controlled? To understand the molecular mechanism controlling the accumulation of FIE protein, transgenic plants as well as molecular approaches were proposed to determine whether FIE is regulated at the translational or posttranslational levels. The objectives of our research program have been accomplished and the results obtained exceeded our expectation. Our results reveal that fie and mea mutations cause parent-of-origin effects on seed development by distinct mechanisms (Publication 1). Moreover our data show that FIE has additional functions besides controlling the development of the female gametophyte. Using transgenic lines in which FIE was not expressed or the protein level was reduced during different developmental stages enabled us for the first time to explore FIE function during sporophyte development (Publication 2 and 3). Our results are consistent with the hypothesis that FIE, a single copy gene in the Arabidopsis genome, represses multiple developmental pathways (i.e., endosperm, embryogenesis, shot formation and flowering). Furthermore, we identified FIE target genes, including key transcription factors known to promote flowering (AG and LFY) as well as shoot and leaf formation (KNAT1) (Publication 2 and 3), thus demonstrating that in plants, as in mammals and insects, PcG proteins control expression of homeobox genes. Using the Yeast two hybrid system and pull-down assays we demonstrated that FIE protein interact with MEA via the N-terminal region (Publication 1). Moreover, CURLY LEAF protein, an additional member of the SET domain family interacts with FIE as well. The overlapping expression patterns of FIE, with ether MEA or CLF and their common mutant phenotypes, demonstrate the versatility of FIE function. FIE association with different SET domain polycomb proteins, results in differential regulation of gene expression throughout the plant life cycle (Publication 3). In vitro interaction assays we have recently performed demonstrated that FIE interacts with the cell cycle regulatory component Retinobalsoma protein (pRb) (Publication 4). These results illuminate the potential mechanism by which FIE may restrain embryo sac central cell division, at least partly, through interaction with, and suppression of pRb-regulated genes. The results of this program generated new information about the initiation of reproductive development and expanded our understanding of how PcG proteins regulate developmental programs along the plant life cycle. The tools and information obtained in this program will lead to novel strategies which will allow to mange crop plants and to increase crop production.

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Grumet, Rebecca, Rafael Perl-Treves, and Jack Staub. Ethylene Mediated Regulation of Cucumis Reproduction - from Sex Expression to Fruit Set. United States Department of Agriculture, February 2010. http://dx.doi.org/10.32747/2010.7696533.bard.

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Reproductive development is a critical determinant of agricultural yield. For species with unisexual flowers, floral secualdifferentation adds additional complexity, that can influenec productivity. The hormone ethylene has long, been known to play a primary role in sex determination in the Cucumis species cucumber (C. sativus) and melon (C. melo). Our objectives were to: (1) Determine critical sites of ethylene production and perception for sex determination; (2) Identify additional ethylene related genes associated with sex expression; and (3) Examine the role of environment ami prior fruit set on sex expression, pistillate flower maturation, and fruit set. We made progress in each of these areas. (1) Transgenic melon produced with the Arabidopsis dominant negative ethylene perception mutant gene, etrl-1, under the control of floral primordia targeted promoters [AP3 (petal and stamen) and CRC (carpel and nectary)], showed that ethylene perception by the stamen primordia, rather than carpel primordia, is critical for carpel development at the time of sex determination. Transgenic melons also were produced with the ethylene production enzyme gene. ACS, encoding l-aminocyclopropane-lcarboylate synthase, fused to the AP3 or CRC promoters. Consistent with the etr1-1 results, CRC::ACS did not increase femaleness; however, AP3::ACS reduced or eliminated male flower production. The effects of AP3:ACS were stronger than those of 35S::ACS plants, demonstratin g the importance of targeted expression, while avoiding disadvantages of constitutive ethylene production. (2) Linkage analysis coupled with SNP discovery was per formed on ethylene and floral development genes in cucumber populations segregating for the three major sex genes. A break-through towards cloning the cucumber M gene occurred when the melon andromonoecious gene (a), an ACS gene, was cloned in 2008. Both cucumber M and melon a suppress stamen development in pistillate flowers. We hypothesized that cucumber M could be orthologous to melon a, and found that mutations in CsACS2 co-segregated perfectly with the M gene. We also sought to identify miRNA molecules associated with sex determination. miRNA159, whose target in Arabidopsis is GAMYB[a transcription factor gene mediating response to10 gibberellin (GA)], was more highly expressed in young female buds than male. Since GA promotes maleness in cucumber, a micro RNA that counteracts GAMYB could promote femaleness. miRNA157, which in other plants targets transcription factors involved in flower development , was expressed in young male buds and mature flower anthers. (3) Gene expression profiling showed that ethylene-, senescence-, stress- and ubiquitin-related genes were up-regulated in senescing and inhibited fruits, while those undergoing successful fruit set up-regulated photosynthesis, respiration and metabolic genes. Melon plants can change sex expression in response to environmental conditions, leading to changes in yield potential. Unique melon lines with varying sex expression were developed and evaluated in the field in Hancock, Wisconsin . Environmental changes during the growing season influenced sex expression in highly inbred melon lines. Collectively these results are of significance for understanding regulation of sex expression. The fact that both cucumber sex loci identified so far (F and M) encode isoforms of the same ethylene synthesis enzyme, underscores the importance of ethylene as the main sex determining hormone in cucumber. The targeting studies give insight into developmental switch points and suggest a means to develop lines with earlier carpel-bearing flower production and fruit set. These results are of significance for understanding regulation of sex expression to facilitate shorter growing seasons and earlier time to market. Field results provide information for development of management strategies for commercial production of melon cultivars with different sex expression characteristics during fruit production.

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Shaw, John, Arieh Rosner, Thomas Pirone, Benjamin Raccah, and Yehezkiel Antignus. The Role of Specific Viral Genes and Gene Products in Potyviral Pathogenicity, Host Range and Aphid Transmission. United States Department of Agriculture, August 1992. http://dx.doi.org/10.32747/1992.7561070.bard.

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In this research we have studied the molecular biology of carotenoid biosynthesis in tomato. The investigations focused on the genes Pds and Psy, encoding desaturase and phytoene synthase, respectively, which are key enzymes in the biosynthetic pathway of lycopene and b-carotene. In addition, we have investigated the genes for lycopene cyclase. We have cloned from tomato and characterized the cDNA of CrtL-e, which encodes the lycopene e-cyclase, and analyzed its expression during fruit development. The results establish a paradigm for the regulation of carotenoid pigment biosynthesis during the ripening process of fruits. It is concluded that transcriptional regulation of genes that encode carotenoid-biosynthesis enzymes is the major mechanism that governs specific pigment accumulation. During the ripening of tomato fruits transcription of the genes encoding the enzymes phytoene synthase and phytoene desaturase is up-regulated, while the transcription of the genes for both lycopene cyclases decreases and thus the conversion of lycopene to subsequent carotenoids is inhibited. These findings support the working hypothesis of the molecular approach to manipulating carotenogenesis by altering gene expression in transgenic plants, and offer obvious strategies to future application in agriculture. The molecular and physiological knowledge on carotenogenesis gained in this project, suggest a concept for manipulating gene expression that will alter carotenoid composition in fruits and flowers.

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Pichersky, Eran, Alexander Vainstein, and Natalia Dudareva. Scent biosynthesis in petunia flowers under normal and adverse environmental conditions. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7699859.bard.

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The ability of flowering plants to prosper throughout evolution, and for many crop plants to set fruit, is strongly dependent on their ability to attract pollinators. To that end many plants synthesize a spectrum of volatile compounds in their flowers. Scent is a highly dynamic trait that is strongly influenced by the environment. However, with high temperature conditions becoming more common, the molecular interplay between this type of stress and scent biosynthesis need to be investigated. Using petunia as a model system, our project had three objectives: (1) Determine the expression patterns of genes encoding biosynthetic scent genes (BSGs) and of several genes previously identified as encoding transcription factors involved in scent regulation under normal and elevated temperature conditions. (2) Examine the function of petunia transcription factors and a heterologous transcription factor, PAPl, in regulating genes of the phenylpropanoid/benzenoid scent pathway. (3) Study the mechanism of transcriptional regulation by several petunia transcription factors and PAPl of scent genes under normal and elevated temperature conditions by examining the interactions between these transcription factors and the promoters of target genes. Our work accomplished the first two goals but was unable to complete the third goal because of lack of time and resources. Our general finding was that when plants grew at higher temperatures (28C day/22C night, vs. 22C/16C), their scent emission decreased in general, with the exception of a few volatiles such as vanillin. To understand why, we looked at gene transcription levels, and saw that generally there was a good correlation between levels of transcriptions of gene specifying enzymes for specific scent compounds and levels of emission of the corresponding scent compounds. Enzyme activity levels, however, showed little difference between plants growing at different temperature regimes. Plants expressing the heterologous gene PAPl showed general increase in scent emission in control temperature conditions but emission decreased at the higher temperature conditions, as seen for control plants. Finally, expression of several transcription factor genes decreased at high temperature, but expression of new transcription factor, EOB-V, increased, implicating it in the decrease of transcription of BSGs. The major conclusion of this work is that high temperature conditions negatively affect scent emission from plants, but that some genetic engineering approaches could ameliorate this problem.

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Barg, Rivka, Erich Grotewold, and Yechiam Salts. Regulation of Tomato Fruit Development by Interacting MYB Proteins. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7592647.bard.

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Background to the topic: Early tomato fruit development is executed via extensive cell divisions followed by cell expansion concomitantly with endoreduplication. The signals involved in activating the different modes of growth during fruit development are still inadequately understood. Addressing this developmental process, we identified SlFSM1 as a gene expressed specifically during the cell-division dependent stages of fruit development. SlFSM1 is the founder of a class of small plant specific proteins containing a divergent SANT/MYB domain (Barg et al 2005). Before initiating this project, we found that low ectopic over-expression (OEX) of SlFSM1 leads to a significant decrease in the final size of the cells in mature leaves and fruits, and the outer pericarp is substantially narrower, suggesting a role in determining cell size and shape. We also found the interacting partners of the Arabidopsis homologs of FSM1 (two, belonging to the same family), and cloned their tomato single homolog, which we named SlFSB1 (Fruit SANT/MYB–Binding1). SlFSB1 is a novel plant specific single MYB-like protein, which function was unknown. The present project aimed at elucidating the function and mode of action of these two single MYB proteins in regulating tomato fruit development. The specific objectives were: 1. Functional analysis of SlFSM1 and its interacting protein SlFSB1 in relation to fruit development. 2. Identification of the SlFSM1 and/or SlFSB1 cellular targets. The plan of work included: 1) Detailed phenotypic, histological and cellular analyses of plants ectopically expressing FSM1, and plants either ectopically over-expressing or silenced for FSB1. 2) Extensive SELEX analysis, which did not reveal any specific DNA target of SlFSM1 binding, hence the originally offered ChIP analysis was omitted. 3) Genome-wide transcriptional impact of gain- and loss- of SlFSM1 and SlFSB1 function by Affymetrix microarray analyses. This part is still in progress and therefore results are not reported, 4) Search for additional candidate partners of SlFSB1 revealed SlMYBI to be an alternative partner of FSB1, and 5) Study of the physical basis of the interaction between SlFSM1 and SlFSB1 and between FSB1 and MYBI. Major conclusions, solutions, achievements: We established that FSM1 negatively affects cell expansion, particularly of those cells with the highest potential to expand, such as the ones residing inner to the vascular bundles in the fruit pericarp. On the other hand, FSB1 which is expressed throughout fruit development acts as a positive regulator of cell expansion. It was also established that besides interacting with FSM1, FSB1 interacts also with the transcription factor MYBI, and that the formation of the FSB1-MYBI complex is competed by FSM1, which recognizes in FSB1 the same region as MYBI does. Based on these findings a model was developed explaining the role of this novel network of the three different MYB containing proteins FSM1/FSB1/MYBI in the control of tomato cell expansion, particularly during fruit development. In short, during early stages of fruit development (Phase II), the formation of the FSM1-FSB1 complex serves to restrict the expansion of the cells with the greatest expansion potential, those non-dividing cells residing in the inner mesocarp layers of the pericarp. Alternatively, during growth phase III, after transcription of FSM1 sharply declines, FSB1, possibly through complexing with the transcription factor MYBI serves as a positive regulator of the differential cell expansion which drives fruit enlargement during this phase. Additionally, a novel mechanism was revealed by which competing MYB-MYB interactions could participate in the control of gene expression. Implications, both scientific and agricultural: The demonstrated role of the FSM1/FSB1/MYBI complex in controlling differential cell growth in the developing tomato fruit highlights potential exploitations of these genes for improving fruit quality characteristics. Modulation of expression of these genes or their paralogs in other organs could serve to modify leaf and canopy architecture in various crops.

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