Dual recognition-incision enzymes might be involved in mismatch repair and meiosis
Dual recognition-incision enzymes might be involved in mismatch repair and meiosis
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DOI：
10.1016/s0968-0004(00)01623-6
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发表时间：
2000-09-01
影响因子：
13.8
通讯作者：
Henikoff, S
中科院分区：
文献类型：
--
作者：
Malik, HS;Henikoff, S
许多生物体中的错配修复取决于三种蛋白质：错配识别蛋白 MutS、切口核酸内切酶 MutH 和 MutL（充当它们之间的支架）。然而，许多基因组缺乏 MutL 但拥有 MutS。在其中一种情况下，在珊瑚线粒体基因组中，存在编码与 HNH 切口核酸内切酶融合的 MutS 蛋白的基因，可能消除对 MutL 的需求。同样，许多原核生物可以通过编码融合的 MutS-Smr (MutS2) 蛋白来独立于 MutL 进行类似的操作。 Smr 被认为是一种切口核酸内切酶，也可以在许多真核生物中单独发现，它可能在错配修复或减数分裂染色体交换中发挥作用。
Mismatch repair in many organisms depends on three proteins: the mismatch-recognition protein MutS, a nicking endonuclease MutH, and MutL, which acts as a scaffold between these. However, many genomes lack MutL but possess MutS. In one of these cases, in a coral mitochondrial genome, a gene is present that encodes a MutS protein fused to an HNH nicking endonuclease, potentially eliminating the requirement for MutL, Likewise, many prokaryotes could operate similarly, independently of MutL by encoding a fused MutS-Smr (MutS2) protein. Smr, which is proposed to be a nicking endonuclease, can also be found separately in many eukaryotes, where it might play a role in mismatch repair or meiotic chromosome crossing-over.