Set2催化的组蛋白H3甲基化抑制酿酒酵母中GAL4的基础表达。
Set2-catalyzed methylation of histone H3 represses basal expression of GAL4 in Saccharomyces cerevisiae.
作者信息
Landry Joseph, Sutton Ann, Hesman Tina, Min Jinrong, Xu Rui-Ming, Johnston Mark, Sternglanz Rolf
机构信息
Program in Genetics, Stony Brook University, Stony Brook, New York 11794, USA.
出版信息
Mol Cell Biol. 2003 Sep;23(17):5972-8. doi: 10.1128/MCB.23.17.5972-5978.2003.
Abstract
Recent work has shown that histone methylation is an important regulator of transcription. While much is known about the roles of histone methyltransferases (HMTs) in the establishment of heterochromatin, little is known of their roles in the regulation of actively transcribed genes. We describe an in vivo role of the Saccharomyces cerevisiae HMT, Set2. We identified SET2 as a gene necessary for repression of GAL4 basal expression and show that the evolutionarily conserved SACI, SACII, and SET domains of Set2 are necessary for this repression. We confirm that Set2 catalyzes methylation of lysine 36 on the N-terminal tail of histone H3. Conversion of lysine 36 to an unmethylatable arginine causes a decrease in the repression of GAL4 transcription, as does a Delta set2 mutation. We further show that lysine 36 of histone H3 at GAL4 is methylated and that this methylation is dependent upon the presence of SET2.
摘要
近期研究表明，组蛋白甲基化是转录的重要调节因子。虽然人们对组蛋白甲基转移酶（HMTs）在异染色质形成中的作用了解颇多，但对其在活跃转录基因调控中的作用却知之甚少。我们描述了酿酒酵母HMT，Set2在体内的作用。我们鉴定出SET2是抑制GAL4基础表达所必需的基因，并表明Set2进化上保守的SACI、SACII和SET结构域对于这种抑制作用是必需的。我们证实Set2催化组蛋白H3 N端尾巴上赖氨酸36的甲基化。将赖氨酸36转化为不可甲基化的精氨酸会导致GAL4转录抑制作用降低，Delta set2突变也是如此。我们进一步表明，GAL4处组蛋白H3的赖氨酸36被甲基化，且这种甲基化依赖于SET2的存在。
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