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The Werner and Bloom syndrome proteins catalyze regression of a model replication fork

机译：Werner和Bloom综合征蛋白催化模型复制叉的回归

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摘要

The premature aging and cancer-prone diseases Werner and Bloom syndromes are caused by loss of function of WRN and BLM proteins, respectively. At the cellular level, WRN or BLM deficiency causes replication abnormalities, DNA damage hypersensitivity, and genome instability, suggesting that these proteins might participate in resolution of replication blockage. Although WRN and BLM are helicases belonging to the RecQ family, both have been recently shown to also facilitate pairing of complementary DNA strands. In this study, we demonstrate that both WRN and BLM (but not other selected helicases) can coordinate their unwinding and pairing activities to regress a model replication fork substrate. Notably, fork regression is widely believed to be the initial step in responding to replication blockage. Our findings suggest that WRN and/or BLM might regress replication forks in vivo as part of a genome maintenance pathway, consistent with the phenotypes of WRN- and BLM-deficient cells.
机译：早衰和易患癌症的Werner和Bloom综合征分别由WRN和BLM蛋白的功能丧失引起。在细胞水平上，WRN或BLM缺乏会引起复制异常，DNA损伤超敏反应和基因组不稳定，这表明这些蛋白质可能参与了复制阻滞的解决。尽管WRN和BLM是属于RecQ家族的解旋酶，但最近都显示它们也都有助于互补DNA链的配对。在这项研究中，我们证明WRN和BLM（但不是其他选定的解旋酶）都可以协调其展开和配对活动，从而使模型复制叉底物回归。值得注意的是，广泛认为fork回归是响应复制阻塞的第一步。我们的发现表明，WRN和/或BLM可能会将体内的复制叉作为基因组维持途径的一部分消退，这与WRN和BLM缺陷细胞的表型一致。

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