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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Formation of deletions during double-strand break repair in Drosophila DmBlm mutants occurs after strand invasion.
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Formation of deletions during double-strand break repair in Drosophila DmBlm mutants occurs after strand invasion.

机译：果蝇DmBlm突变体在双链断裂修复过程中缺失的形成发生在链入侵之后。

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摘要

Bloom syndrome is a rare disorder associated with cancer predisposition and genomic instability and is caused by loss of the RecQ helicase BLM. The Drosophila ortholog of BLM (DmBlm) is required for accurate repair of DNA double-strand gaps by homologous recombination. Repair products from DmBlm mutants have shorter repair synthesis tract lengths compared to wild type and are frequently associated with deletions flanking the break site. To determine the mechanisms responsible for deletion formation in the absence of DmBlm, we characterized repair after excision of the P{w(a)} element in various genetic backgrounds. Flies lacking DmRad51 do not have an elevated deletion frequency. Moreover, loss of DmRad51 suppresses deletion formation in DmBlm mutants. These data support a model in which DmBlm acts downstream of strand invasion to unwind a D-loop intermediate to free the newly synthesized strand. In the absence of DmBlm, alternative pathways of D-loop disassembly result in short repair synthesis tractsor flanking deletions. This model explains how RecQ helicases can promote homologous recombination while preventing illegitimate recombination.
机译：Bloom综合征是与癌症易感性和基因组不稳定相关的罕见疾病，并且是由RecQ解旋酶BLM的丢失引起的。 BLM的果蝇直系同源物（DmBlm）是通过同源重组准确修复DNA双链缺口所必需的。与野生型相比，来自DmBlm突变体的修复产物的修复合成通道长度短，并且经常与位于断裂位点两侧的缺失相关。为了确定在缺少DmBlm的情况下造成缺失形成的机制，我们在各种遗传背景下，将P {w（a）}元素切除后的修复特征进行了表征。缺少DmRad51的苍蝇的缺失频率不高。此外，DmRad51的丢失抑制了DmBlm突变体中的缺失形成。这些数据支持一个模型，其中DmBlm在链入侵的下游起作用，以展开D环中间体以释放新合成的链。在没有DmBlm的情况下，D环拆卸的替代途径会导致较短的修复合成链或侧翼缺失。该模型说明了RecQ解旋酶如何在防止非法重组的同时促进同源重组。

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