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所有三种SOS诱导型DNA聚合酶(Pol II、Pol IV和Pol V)都参与诱导诱变。

All three SOS-inducible DNA polymerases (Pol II, Pol IV and Pol V) are involved in induced mutagenesis.

作者信息

Napolitano R, Janel-Bintz R, Wagner J, Fuchs R P

机构信息

UPR 9003, CNRS Cancérogenèse et Mutagenèse Moléculaire et Structurale, ESBS and IRCAD, Strasbourg, France.

出版信息

EMBO J. 2000 Nov 15;19(22):6259-65. doi: 10.1093/emboj/19.22.6259.

Abstract

Most organisms contain several members of a recently discovered class of DNA polymerases (umuC/dinB superfamily) potentially involved in replication of damaged DNA. In Escherichia coli, only Pol V (umuDC) was known to be essential for base substitution mutagenesis induced by UV light or abasic sites. Here we show that, depending upon the nature of the DNA damage and its sequence context, the two additional SOS-inducible DNA polymerases, Pol II (polB) and Pol IV (dinB), are also involved in error-free and mutagenic translesion synthesis (TLS). For example, bypass of N:-2-acetylaminofluorene (AAF) guanine adducts located within the NAR:I mutation hot spot requires Pol II for -2 frameshifts but Pol V for error-free TLS. On the other hand, error-free and -1 frameshift TLS at a benzo(a)pyrene adduct requires both Pol IV and Pol V. Therefore, in response to the vast diversity of existing DNA damage, the cell uses a pool of 'translesional' DNA polymerases in order to bypass the various DNA lesions.

摘要

大多数生物体都含有最近发现的一类DNA聚合酶(umuC/dinB超家族)的多个成员,这些聚合酶可能参与受损DNA的复制。在大肠杆菌中,只有Pol V(umuDC)被认为对紫外线或无碱基位点诱导的碱基置换诱变至关重要。在此我们表明,根据DNA损伤的性质及其序列背景,另外两种SOS诱导型DNA聚合酶,即Pol II(polB)和Pol IV(dinB),也参与无差错和诱变的跨损伤合成(TLS)。例如,位于NAR:I突变热点内的N:-2-乙酰氨基芴(AAF)鸟嘌呤加合物的绕过,-2移码需要Pol II,但无差错的TLS需要Pol V。另一方面,苯并(a)芘加合物处的无差错和-1移码TLS需要Pol IV和Pol V两者。因此,为应对现有DNA损伤的巨大多样性,细胞使用一组“跨损伤”DNA聚合酶来绕过各种DNA损伤。

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本文引用的文献

1
The beta clamp targets DNA polymerase IV to DNA and strongly increases its processivity.
EMBO Rep. 2000 Dec;1(6):484-8. doi: 10.1093/embo-reports/kvd109.
4
Mutation enhancement by DINB1, a mammalian homologue of the Escherichia coli mutagenesis protein dinB.
Genes Cells. 1999 Nov;4(11):607-18. doi: 10.1046/j.1365-2443.1999.00289.x.
5
SOS mutagenesis results from up-regulation of translesion synthesis.
J Mol Biol. 1999 Nov 26;294(2):299-306. doi: 10.1006/jmbi.1999.3272.
6
Replication of damaged DNA: molecular defect in xeroderma pigmentosum variant cells.
Mutat Res. 1999 Oct 22;435(2):111-9. doi: 10.1016/s0921-8777(99)00047-6.
8
Human and mouse homologs of Escherichia coli DinB (DNA polymerase IV), members of the UmuC/DinB superfamily.
Proc Natl Acad Sci U S A. 1999 Oct 12;96(21):11922-7. doi: 10.1073/pnas.96.21.11922.
9
The dinB gene encodes a novel E. coli DNA polymerase, DNA pol IV, involved in mutagenesis.
Mol Cell. 1999 Aug;4(2):281-6. doi: 10.1016/s1097-2765(00)80376-7.
10
Novel human and mouse homologs of Saccharomyces cerevisiae DNA polymerase eta.
Genomics. 1999 Aug 15;60(1):20-30. doi: 10.1006/geno.1999.5906.

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