Regulation and function of yeast transcr#itional activator ADR1

酵母转录的调控和功能

• 批准号: 8916584
• 负责人: Clyde Denis
• 金额: $ 36.74万
• 依托单位: University of New Hampshire Agricultural Experiment Station
• 依托单位国家: 美国
• 项目类别: Continuing Grant
• 财政年份: 1990
• 资助国家: 美国
• 起止时间: 1990-02-01 至 1994-01-31
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=8916584&HistoricalAwards=false
• 关键词: Regulation; function; yeast; transcr#itional; activator

The goal of this research is to elucidate the mechanisms of eucaryotic gene regulation. The system chosen for study is the yeast transcriptional activator ADR1 in its control of glucose repressible alcohol dehydrogenase (ADH2). Particular emphasis will be placed on defining the mechanisms by which ADR1 is regulated, the functional regions of ADR1, the factors which mediate or influence ADR1 function, and the means by which these factors and ADR control ADH2 transcription. A combination of biochemical, recombinant DNA, and genetic analyses will be used. The in vivo phosphorylation site of ADR1 will be identified and the role of cAMP-dependent (cAPK) and -independent protein kinases in ADR1 regulation will be ascertained. The mechanisms by which ADR1 will be identified. The ADR1 protein will be isolated and its regions important to transcriptional activation, regulation of glycerol growth, oligomerization, glucose control, and induction of petites will be identified. The proteins which bind to or mediate ADR1 action will be studied biochemically and genetically. The SAF1-3 genes required for ADR1 activation of ADH2 transcription will be cloned and sequenced. The role of the CCR1 and SCH9 protein kinases which act independently of ADR1 controlling ADH2 will also be determined.

本研究的目的是阐明真核生物基因调控的机制。本研究选用酵母转录激活剂ADR1调控葡萄糖抑制醇脱氢酶（ADH2）。重点将放在定义ADR1被调节的机制，ADR1的功能区域，介导或影响ADR1功能的因素，以及这些因素和ADR控制ADH2转录的方法。将使用生物化学、重组DNA和遗传分析相结合的方法。将确定ADR1的体内磷酸化位点，并确定camp依赖性（cAPK）和非依赖性蛋白激酶在ADR1调控中的作用。识别ADR1的机制。将分离ADR1蛋白，并鉴定其对转录激活、甘油生长调节、寡聚化、葡萄糖控制和小细胞诱导重要的区域。结合或介导ADR1作用的蛋白质将进行生物化学和遗传学研究。克隆ADR1激活ADH2转录所需的SAF1-3基因并测序。CCR1和SCH9蛋白激酶独立于ADR1控制ADH2的作用也将被确定。