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首页> 外文期刊>Molecular biology of the cell >Plc1p Is Required for SAGA Recruitment and Derepression of Sko1p-regulated Genes
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Plc1p Is Required for SAGA Recruitment and Derepression of Sko1p-regulated Genes

机译：SALC招募和解压Sko1p调控基因需要Plc1p。

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In Saccharomyces cerevisiae , many osmotically inducible genes are regulated by the Sko1p-Ssn6p-Tup1p complex. On osmotic shock, the MAP kinase Hog1p associates with this complex, phosphorylates Sko1p, and converts it into an activator that subsequently recruits Swi/Snf and SAGA complexes. We have found that phospholipase C (Plc1p encoded by PLC1 ) is required for derepression of Sko1p-Ssn6p-Tup1p–controlled osmoinducible genes upon osmotic shock. Although plc1 Δ mutation affects the assembly of the preinitiation complex after osmotic shock, it does not affect the recruitment of Hog1p and Swi/Snf complex at these promoters. However, Plc1p facilitates osmotic shock–induced recruitment of the SAGA complex. Like plc1 Δ cells, SAGA mutants are osmosensitive and display compromised expression of osmotically inducible genes. The reduced binding of SAGA to Sko1p-Ssn6p-Tup1p–repressed promoters in plc1 Δ cells does not correlate with reduced histone acetylation. However, SAGA functions at these promoters to facilitate recruitment of the TATA-binding protein. The results thus provide evidence that Plc1p and inositol polyphosphates affect derepression of Sko1p-Ssn6p-Tup1p–controlled genes by a mechanism that involves recruitment of the SAGA complex and TATA-binding protein.
机译：在酿酒酵母中，许多渗透诱导基因受Sko1p-Ssn6p-Tup1p复合物调控。在渗透性休克中，MAP激酶Hog1p与该复合物缔合，磷酸化Sko1p，并将其转化为激活物，随后激活Swi / Snf和SAGA复合物。我们发现，在渗透压休克后，Sko1p-Ssn6p-Tup1p控制的渗透诱导基因的去阻遏作用需要磷脂酶C（由PLC1编码的Plc1p）。尽管plc1Δ突变会影响渗透性休克后预启动复合物的装配，但不会影响这些启动子上Hog1p和Swi / Snf复合物的募集。但是，Plc1p促进了渗透性休克诱导的SAGA复合物的募集。像plc1Δ细胞一样，SAGA突变体是渗透敏感性的，并且显示渗透诱导基因的表达受损。 SAGA与plc1Δ细胞中受Sko1p-Ssn6p-Tup1p阻抑的启动子的结合减少与组蛋白乙酰化减少无关。但是，SAGA在这些启动子处起作用，以促进TATA结合蛋白的募集。因此，结果提供了证据，表明Plc1p和肌醇多磷酸酯通过涉及募集SAGA复合物和TATA结合蛋白的机制影响Sko1p-Ssn6p-Tup1p调控的基因的抑制。

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