Goldmark J P, Fazzio T G, Estep P W, Church G M, Tsukiyama T
Division of Basic Sciences, Fred Hutchinson Cancer Research Institute, Fred Hutchinson Cancer Research Center and University of Washington, Seattle 98109, USA.
Cell. 2000 Oct 27;103(3):423-33. doi: 10.1016/s0092-8674(00)00134-3.
The ISWI class of chromatin remodeling factors exhibits potent chromatin remodeling activities in vitro. However, the in vivo functions of this class of factors are unknown at a molecular level. We have found that S. cerevisiae Isw2 complex represses transcription of early meiotic genes during mitotic growth in a parallel pathway to Rpd3-Sin3 histone deacetylase complex. This repressor function of lsw2 complex is largely dependent upon Ume6p, which recruits the complex to target genes. Nuclease digestion analyses revealed that lsw2 complex establishes nuclease-inaccessible chromatin structure near the Ume6p binding site in vivo. Based on these findings, we propose a model for the mechanism of transcriptional repression by two distinct chromatin remodeling complexes.
ISWI类染色质重塑因子在体外表现出强大的染色质重塑活性。然而,这类因子在体内的分子水平功能尚不清楚。我们发现,酿酒酵母Isw2复合物在有丝分裂生长期间通过与Rpd3-Sin3组蛋白去乙酰化酶复合物平行的途径抑制早期减数分裂基因的转录。Isw2复合物的这种抑制功能很大程度上依赖于Ume6p,它将该复合物招募到靶基因上。核酸酶消化分析表明,Isw2复合物在体内Ume6p结合位点附近建立了核酸酶不可接近的染色质结构。基于这些发现,我们提出了一个由两种不同染色质重塑复合物进行转录抑制机制的模型。