UNDERSTANDING THE FIDELITY OF MAP KINASE SIGNALING

了解 MAP 激酶信号转导的保真度

• 批准号: 7957735
• 负责人: Hiten D Madhani
• 金额: $ 0.33万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-09-01 至 2010-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7957735
• 关键词: Binding; Biological Process; Biology; Computer Retrieval of Information on Scientific Projects Database; Differentiation and Growth; Ensure; Eukaryotic Cell; Funding; Fungal Genome; Gene Targeting; Genes; Glycerol; Grant; Institution; MEKs; Mitogen-Activated Protein Kinases; Osmolar Concentration; Partner in relationship; Pathway interactions; Play; Recruitment Activity; Regulation; Research; Research Personnel; Resources; Role; Signal Transduction; Source; Specificity; Stimulus; Stress; Testing; Transducers; United States National Institutes of Health; Yeasts; novel; prevent; promoter; response; transcription factor

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Mitogen-activated protein kinase (MAPK) signaling cascades play a fundamental role in eukaryotic cells, acting as signal transducers involved in many biological processes including growth, differentiation and response to stress. In yeast, the mating, filamentation, and high osmolarity glycerol (HOG) pathways elicit specific responses to distinct stimuli, yet share multiple components. We observed that both the MEK and the MAPKs of the mating and filamentation pathways are phosphorylated on their activating residues during signaling through the HOG pathway. Therefore, mechanisms must exist downstream of the MAPKs to ensure that mating and filamentation genes are not transcribed in response to osmotic stress. In addition, we found that this is a novel mechanism, distinct from the mechanisms used to prevent cross-talk between the filamentation and mating pathways. We tested whether specificity is achieved before or after the mating and filamentation specific transcription factors, Ste12 and Tec1, are recruited to their gene targets, and found that in the absence of Hog1 there is a large increase in the levels of Tec1 binding to filamentation specific promoters. This indicates that Hog1 plays an essential role in inhibiting erroneous signaling by preventing Tec1 from binding to its target promoters. These results point to new modes of regulation used by eukaryotic cells to perform the indispensable function of maintaining signaling specificity.

这个子项目是众多研究子项目之一