Gavin I M, Kladde M P, Simpson R T
Department of Biochemistry and Molecular Biology, The Pennsylvania State University, 308 Althouse Laboratory, University Park, PA 16802, USA.
EMBO J. 2000 Nov 1;19(21):5875-83. doi: 10.1093/emboj/19.21.5875.
In yeast, a number of regulatory proteins expressed only in specific cell types interact with general transcription factors in a combinatorial manner to control expression of cell-type-specific genes. We report a detailed analysis of activation and repression events that occur at the promoter of the a-cell-specific STE6 gene fused to a beta-galactosidase gene in a yeast minichromosome, as well as factors that control the chromatin structure of this promoter both in the minichromosome and in the genomic STE6 locus. Mcm1p results in chromatin remodeling and is responsible for all transcriptional activity from the STE6 promoter in both wild-type a and alpha cells. Matalpha2p cooperates with Tup1p to block both chromatin remodeling and Mcm1p-associated activation. While Matalpha2p represses only Mcm1p, the Tup1p-mediated repression involves both Mcm1p-dependent and -independent mechanisms. Swi/Snf and Gcn5p, required for full induction of the STE6 gene, do not contribute to chromatin remodeling. We suggest that Tup1p can contribute to repression by blocking transcriptional activators, in addition to interacting with transcription machinery and stabilizing chromatin.
在酵母中，一些仅在特定细胞类型中表达的调控蛋白以组合方式与通用转录因子相互作用，以控制细胞类型特异性基因的表达。我们报告了对酵母微型染色体中与β-半乳糖苷酶基因融合的a细胞特异性STE6基因启动子处发生的激活和抑制事件的详细分析，以及在微型染色体和基因组STE6基因座中控制该启动子染色质结构的因素。Mcm1p导致染色质重塑，并负责野生型a细胞和α细胞中STE6启动子的所有转录活性。Matalpha2p与Tup1p协同作用，阻止染色质重塑和与Mcm1p相关的激活。虽然Matalpha2p仅抑制Mcm1p，但Tup1p介导的抑制涉及Mcm1p依赖性和非依赖性机制。STE6基因完全诱导所需的Swi/Snf和Gcn5p对染色质重塑没有贡献。我们认为，Tup1p除了与转录机制相互作用并稳定染色质外，还可以通过阻断转录激活因子来促进抑制作用。
