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Cell cycle regulation in response to plasma membrane stress in S. cerevisae

酿酒酵母质膜应激的细胞周期调节

基本信息

批准号：
9209454
负责人：
Amy E Ikui
金额：
$ 36.69万
依托单位：
BROOKLYN COLLEGE
依托单位国家：
美国
项目类别：
财政年份：
2017
资助国家：
美国
起止时间：
2017-04-01 至 2021-03-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9209454
关键词：
Biological Assay CDK2 gene Cell Cycle Cell Cycle Arrest Cell Cycle Checkpoint Cell Cycle Regulation Cell Wall Cell membrane Cell surface Cells Chromosomal Instability Chromosomes Consensus Consensus Sequence Cyclin A Cyclin-Dependent Kinases Cyclins DNA DNA biosynthesis Eukaryota Eukaryotic Cell Failure Fluorescence Microscopy G1 Phase Gene Expression Gene Proteins Genes Glycogen Synthase Kinase 3 Goals Growth Human In Vitro Lead Link Malignant Neoplasms Membrane Mitogen-Activated Protein Kinase Kinases Mitogen-Activated Protein Kinases Molecular Monomeric GTP-Binding Proteins Organism PRKCA gene Pathway interactions Phenotype Phosphorylation Phosphorylation Site Phosphotransferases Plasma Cells Population Growth Protein Dephosphorylation Protein Kinase C Proteins Signal Transduction Site Stress Structure Testing Transcriptional Activation Two-Hybrid System Techniques Yeasts biological adaptation to stress cell growth environmental change kinase inhibitor mutant novel pathogen polarized cell prevent response sensor time use tumorigenesis

项目摘要

Project Summary/Abstract Yeast cells need to rapidly control their cell cycle profile, gene expression or protein stability in response to the activation of stress response pathways. It is common for cells to suffer from various attacks to their plasma membrane and cell wall, such as physical damage, pathogen invasion and various environmental perturbations. Here we propose to study that plasma membrane stress inhibits cell growth and DNA replication through a novel cell cycle checkpoint pathway. Eukaryotic cells duplicate their chromosomes. Errors in the DNA replication control could lead to chromosome instability which is a hallmark of cancer. Our long- term goal is to understand the molecular mechanism of DNA replication control in response to stress. In this proposal, three aims will test my hypothesis if plasma membrane damage inhibits polarized cell growth and DNA replication through a novel cell cycle checkpoint pathway. Aim1 will determine how membrane damage drives Pkc1 relocation to inhibit polarized cell growth. Aim2 will determine how plasma membrane stress signal activates Mpk1 to inhibit DNA replication. Aim3 will determine if a yeast GSK-3 kinase Mck1 targets replication proteins upon plasma membrane stress DNA replication and membrane integrity pathways are well conserved from yeast to humans. The results obtained from this study can be applied to understand the molecular mechanism of DNA replication control in response to stress in higher eukaryotes.

项目总结/文摘