CCR4-NOT CO-ACTIVATOR'S POST-TRANSCRIPTION FUNCTIONS

CCR4-NOT 共激活剂的转录后功能

• 批准号: 8360018
• 负责人: MARK Jude SWANSON
• 金额: $ 6.31万
• 依托单位: UNIVERSITY OF NEBRASKA MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-05-01 至 2012-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8360018
• 关键词: Amino Acids; Cells; Complex; Environment; Eukaryota; Funding; Gene Activation; Gene Expression; Gene Expression Regulation; Genes; Genetic Transcription; Goals; Grant; Messenger RNA; National Center for Research Resources; Nebraska; Pattern; Play; Principal Investigator; Proteins; Research; Research Infrastructure; Resources; Role; Saccharomyces cerevisiae; Signal Transduction; Source; Starvation; Transcription Coactivator; Transcription Initiation; Translations; United States National Institutes of Health; Yeasts; aminoacid biosynthesis; cost; functional genomics

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. All cells respond environmental fluctuations by altering patterns of gene expression. Gene regulation in eukaryotes begins at initiation of transcription and continues through export and translation of messenger RNAs. In the yeast Saccharomyces cerevisiae, starvation for amino acids generates a signal leading to an increase in Gcn4p, a transcriptional activator protein. Gcn4p regulates over 500 genes, including those involved in amino acid biosynthesis. Thus, yeast cells that cannot obtain amino acids from their environment produce their own. Mechanisms of gene activation by Gcn4p have been well studied, but it is not clear how these genes are repressed after starvation conditions are relieved. Gcn4p requires the CCR4-NOT co-activator complex for full target gene expression. However, CCR4-NOT also possesses activities for the destruction of mRNAs. Our recent results indicate that CCR4-NOT plays in regulating genes under Gcn4p control after transcription. The goal of this research is to determine the exact post-transcriptional role(s) of CCR4-NOT in Gcn4p target gene expression.

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的主要研究者可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 代表子项目使用的中心基础设施的估计数量， NCRR 赠款不直接向子项目或子项目工作人员提供资金。 所有细胞都通过改变基因表达模式来应对环境波动。真核生物中的基因调控始于转录起始，并持续通过信使 RNA 的输出和翻译。在酿酒酵母中，氨基酸饥饿会产生信号，导致转录激活蛋白 Gcn4p 增加。 Gcn4p 调节 500 多个基因，包括那些参与氨基酸生物合成的基因。因此，无法从环境中获取氨基酸的酵母细胞会产生自己的氨基酸。 Gcn4p 激活基因的机制已得到充分研究，但尚不清楚饥饿条件缓解后这些基因如何受到抑制。 Gcn4p 需要 CCR4-NOT 共激活剂复合物才能实现靶基因的完整表达。然而，CCR4-NOT 也具有破坏 mRNA 的活性。我们最近的结果表明，CCR4-NOT 在转录后在 Gcn4p 控制下调节基因。本研究的目的是确定 CCR4-NOT 在 Gcn4p 靶基因表达中的确切转录后作用。