Compagnone-Post P A, Osley M A
Program in Molecular Biology, Sloan Kettering Cancer Center, New York, New York 10021, USA.
Genetics. 1996 Aug;143(4):1543-54. doi: 10.1093/genetics/143.4.1543.
The SPT4, SPT5, and SPT6 gene products define a class of transcriptional repressors in Saccharomyces cerevisiae that are thought to function through their effects on chromatin assembly or stability. Mutations in these genes confer a similar range of phenotypes to mutations in HIR genes, which encode transcriptional repressors that regulate expression of many of the core histone genes. Here we show that mutations in the three SPT genes also affect transcription of the histone genes that reside at the HTA1-HTB1 locus. HTA1-lacZ transcription was reduced in each spt mutant background, an effect that required a negative site in the HTA1 promoter. The transcriptional effect could be reversed by the overproduction of histones H2A and H2B in an spt4 mutant and histones H3 and H4 in all three spt mutants. Suppression of the spt4 transcriptional defect was dependent on the overproduction of both histones H2A and H2B, and required the presence of N-terminal amino acids in both histones. The results are consistent with the idea that the effects of the spt mutations on nucleosome assembly and/or stability activate repressors of HTA1 transcription.
SPT4、SPT5和SPT6基因产物在酿酒酵母中定义了一类转录抑制因子,人们认为它们通过对染色质组装或稳定性的影响发挥作用。这些基因的突变赋予了与HIR基因(编码调节许多核心组蛋白基因表达的转录抑制因子)突变相似的一系列表型。在这里,我们表明三个SPT基因的突变也会影响位于HTA1-HTB1位点的组蛋白基因的转录。在每个spt突变体背景中,HTA1-lacZ转录均降低,这种效应需要HTA1启动子中的一个负调控位点。在spt4突变体中,组蛋白H2A和H2B的过量表达以及在所有三个spt突变体中组蛋白H3和H4的过量表达均可逆转转录效应。spt4转录缺陷的抑制取决于组蛋白H2A和H2B的过量表达,并且需要两种组蛋白中都存在N端氨基酸。这些结果与以下观点一致:spt突变对核小体组装和/或稳定性的影响激活了HTA1转录的抑制因子。