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通过切割锌结合调节结构域激活哺乳动物DNA甲基转移酶。

Activation of mammalian DNA methyltransferase by cleavage of a Zn binding regulatory domain.

作者信息

Bestor T H

机构信息

Department of Anatomy and Cellular Biology, Harvard Medical School, Boston, MA 02115.

出版信息

EMBO J. 1992 Jul;11(7):2611-7. doi: 10.1002/j.1460-2075.1992.tb05326.x.

Abstract

Mammalian DNA (cytosine-5) methyltransferase contains a C-terminal domain that is closely related to bacterial cytosine-5 restriction methyltransferase. This methyltransferase domain is linked to a large N-terminal domain. It is shown here that the N-terminal domain contains a Zn binding site and that the N- and C-terminal domains can be separated by cleavage with trypsin or Staphylococcus aureus protease V8; the protease V8 cleavage site was determined by Edman degradation to lie 10 residues C-terminal of the run of alternating lysyl and glycyl residues which joins the two domains and six residues N-terminal of the first sequence motif conserved between the mammalian and bacterial cytosine methyltransferases. While the intact enzyme had little activity on unmethylated DNA substrates, cleavage between the domains caused a large stimulation of the initial velocity of methylation of unmethylated DNA without substantial change in the rate of methylation of hemimethylated DNA. These findings indicate that the N-terminal domain of DNA methyltransferase ensures the clonal propagation of methylation patterns through inhibition of the de novo activity of the C-terminal domain. Mammalian DNA methyltransferase is likely to have arisen via fusion of a prokaryotic-like restriction methyltransferase and an unrelated DNA binding protein. Stimulation of the de novo activity of DNA methyltransferase by proteolytic cleavage in vivo may contribute to the process of ectopic methylation observed in the DNA of aging animals, tumors and in lines of cultured cells.

摘要

哺乳动物DNA(胞嘧啶-5)甲基转移酶含有一个与细菌胞嘧啶-5限制甲基转移酶密切相关的C末端结构域。这个甲基转移酶结构域与一个大的N末端结构域相连。本文表明,N末端结构域含有一个锌结合位点,并且N末端和C末端结构域可以通过胰蛋白酶或金黄色葡萄球菌蛋白酶V8切割而分离;通过埃德曼降解确定蛋白酶V8切割位点位于连接两个结构域的交替赖氨酸和甘氨酸残基序列的C末端10个残基处,以及哺乳动物和细菌胞嘧啶甲基转移酶之间保守的第一个序列基序的N末端6个残基处。虽然完整的酶对未甲基化的DNA底物几乎没有活性,但结构域之间的切割导致未甲基化DNA甲基化初始速度的大幅刺激,而半甲基化DNA的甲基化速率没有实质性变化。这些发现表明,DNA甲基转移酶的N末端结构域通过抑制C末端结构域的从头活性来确保甲基化模式的克隆传播。哺乳动物DNA甲基转移酶可能是通过原核样限制甲基转移酶和一个不相关的DNA结合蛋白融合产生的。体内蛋白水解切割对DNA甲基转移酶从头活性的刺激可能有助于在衰老动物、肿瘤和培养细胞系的DNA中观察到的异位甲基化过程。

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