CELL CYCLE ARREST AND SIGNAL TRANSDUCTION IN YEAST

酵母细胞周期停滞和信号转导

• 批准号: 3306479
• 负责人: ELAINE A. ELION
• 金额: $ 23.25万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 1992
• 资助国家: 美国
• 起止时间: 1992-08-01 至 1997-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3306479
• 关键词: Escherichia coli; G protein; Saccharomyces cerevisiae; biological signal transduction; cell cycle; developmental genetics; enzyme mechanism; enzyme substrate; fungal genetics; gene expression; gene mutation; growth inhibitors; immunoprecipitation; laboratory mouse; laboratory rabbit; molecular cloning; mutant; phosphorylation; polymerase chain reaction; protein kinase; receptor expression; regulatory gene; suppressor mutations

The yeast mating pathway provides an excellent paradigm for negative growth control and differentiation in higher eukaryotes. The goal of the proposed research is to define how an evolutionarily conserved protein kinase, FUS3, exerts critical functions which regulate the cell cycle and signal transduction during mating and vegetative growth. It is proposed that a combination of genetic and biochemical approaches be taken in an effort to determine: A) How FUS3 simultaneously arrests the mitotic cell cycle through inhibition of a G1-cyclins and activates a receptor/G protein- coupled signal transduction pathway; B) The basis of the functional redundancy between FUS3 and KSS1, a homologous putative protein kinase which also promotes signal transduction. To accomplish these goals, the specific aims of the proposal are: 1) To mutagenize FUS3 to identify the protein domains that specify its multiple functions and to make mutants for subsequent aims. 2) To use a FUS3 immune complex kinase assay to test whether physiologically relevant proteins are either phosphorylated by FUS3 in vitro or associated with FUS3 in vivo, and to examine how FUS3 is regulated in vitro and in vivo. 3) To identify proteins which either interact with FUS3 or are its functional homologues by genetic screens.

酵母的交配途径为负增长提供了一个极好的范例