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首页> 外文期刊>Nature >RecA acts in trans to allow replication of damaged DNA by DNA polymerase V
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RecA acts in trans to allow replication of damaged DNA by DNA polymerase V

机译：RecA反式作用，允许DNA聚合酶V复制受损的DNA

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The DNA polymerase V (pol V) and RecA proteins are essential components of a mutagenic translesion synthesis pathway in Escherichia coli designed to cope with DNA damage. Previously, it has been assumed that RecA binds to the DNA template strand being copied. Here we show, however, that pol-V-catalysed translesion synthesis, in the presence or absence of the beta-processivity-clamp, occurs only when RecA nucleoprotein filaments assemble or RecA protomers bind on separate single-stranded ( ss) DNA molecules in trans. A 3'-proximal RecA filament end on trans DNA is essential for stimulation; however, synthesis is strengthened by further pol V - RecA interactions occurring elsewhere along a trans nucleoprotein filament. We suggest that trans-stimulation of pol V by RecA bound to ssDNA reflects a distinctive regulatory mechanism of mutation that resolves the paradox of RecA filaments assembled in cis on a damaged template strand obstructing translesion DNA synthesis despite the absolute requirement of RecA for SOS mutagenesis.
机译：DNA聚合酶V（pol V）和RecA蛋白是大肠杆菌中诱变的跨病变合成途径的重要组成部分，旨在解决DNA损伤。以前，已经假定RecA与要复制的DNA模板链结合。但是，我们在这里显示，仅在RecA核蛋白丝组装或RecA前列腺素结合在单独的单链（ss）DNA分子中时，在存在或不存在β合成钳的情况下，pol-V催化的跨病变合成才会发生。反式反式DNA的3'-近端RecA细丝末端对于刺激至关重要；然而，通过沿着反核蛋白丝发生在其他地方的进一步的pol V-RecA相互作用增强了合成。我们建议，RecA结合ssDNA对pol V的反刺激反映出独特的突变调节机制，该解决方案解决了RecA丝的悖论，即在受损的模板链上顺式组装的顺式组装，阻碍了损伤DNA的合成，尽管RecA对SOS诱变具有绝对的要求。

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