TRANSCRIPTIONAL REGULATION OF MEIOTIC GENES IN YEAST

酵母减数分裂基因的转录调控

• 批准号: 6096916
• 负责人: ANDREW VERSHON
• 金额: $ 18.06万
• 依托单位: RUTGERS, THE STATE UNIV OF N.J.
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-04-01 至 2004-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6096916
• 关键词: DNA binding protein; Saccharomyces cerevisiae; chromatin; fungal genetics; fungal proteins; gene induction /repression; genetic promoter element; genetic transcription; meiosis; mitogen activated protein kinase; spores; yeast two hybrid system

DESCRIPTION (adapted from the applicant's abstract): This proposal describes experiments to investigate the regulation of meiosis-specific target genes in yeast. This research has initially focused on the transcriptional regulation of HOP1, a gene expressed early in the meiotic pathway. The URS1H site in the HOP1 promoter is bound by the Ume6 protein and functions as a repressor during mitosis and an activator during the early stages of meiosis. However, Ume6 also binds to URS1 sites in non-meiotic promoters to regulate transcription. This raises the question of how the cell distinguishes between Ume6 bound to meiotic and non-meiotic promoters to differentially regulate genes. One of the objectives is to identify the proteins that bind to URS1 and determine how they contribute to the specificity of meiotic induction. To investigate the mechanisms that control transcription of genes expressed later in the meiotic pathway, the regulation of SMK1, a mid-sporulation specific MAP kinase required for spore development, has been examined. A regulatory site in the SMK1 promoter called MSE has been identified, which function to repress transcription during vegetative growth and the early stages of meiosis and activate transcription during middle stages of meiosis. This site sets the timing of SMK1 expression. The Ndt80 protein binds to this site to activate transcription during meiosis. Preliminary studies have shown the Sum1 and Hst1 proteins are required for MSE-mediated repression and that Sum1 protein binds to the site. Interestingly, these proteins have previously been identified based upon their sequence or functional similarity to proteins involved in transcriptional silencing of the mating type, telomeres, and rDNA loci. However, unlike silencing proteins, Sum1 and Hst1 are gene-specific regulation and therefore may function by a novel mechanism. Experiments are proposed to investigate the interactions and mechanisms of DNA binding of Sum1 and Hst1, potentially novel DNA binding proteins. The mechanism by which Sum1 and Hst1 repress transcription will be investigated. Additionally, the regulation of Sum1 and Hst1 activity by the meiotic regulatory pathway will be examined.

描述（改编自申请人的摘要）：该提案描述 研究减数分裂特异性靶基因的实验 酵母。这项研究最初集中于 Hop1，一个基因在减数分裂途径早期表达。 Hop1中的URS1H网站 启动子受UME6蛋白的约束，并在 有丝分裂和减数分裂早期阶段的激活剂。 但是，ume6 还与非求解启动子中的URS1位点结合以调节转录。 这就提出了一个问题，即细胞如何区分UME6与 减数分裂和非脱生物启动子对差异调节基因。 中的一个 目标是识别与URS1结合的蛋白质并确定它们的方式 有助于减数分裂诱导的特异性。 研究控制表达基因转录的机制 后来在减数分裂途径中，SMK1的调节，一种中期。 已经检查了孢子发育所需的特定地图激酶。 一个 已经确定了称为MSE的SMK1启动子中的监管部位，已确定 在营养生长和早期阶段抑制转录的功能 减数分裂和激活减数分裂的转录。 这 站点设置SMK1表达式的时间。 NDT80蛋白与该部位结合 在减数分裂过程中激活转录。 初步研究表明 SUM1和HST1蛋白是MSE介导的抑制所必需的，该SUM1需要 蛋白质与该部位结合。 有趣的是，这些蛋白质以前是 根据其序列或功能相似性与蛋白质相似 参与交配类型，端粒和rDNA的转录沉默 基因座。 但是，与沉默蛋白不同，sum1和hst1是基因特异性的 调节，因此可能通过一种新型机制起作用。 实验是 提议研究SUM1的DNA结合的相互作用和机制 和Hst1，可能是新型的DNA结合蛋白。 sum1的机制 将研究HST1抑制转录。 另外， 减数分裂调节途径对SUM1和HST1活性的调节将是 检查。