A phenotype for enigmatic DNA polymerase II: A pivotal role for pol II in replication restart in UV-irradiated
            <i>Escherichia</i>
            <i>coli</i>

Rangarajan, Savithri; Woodgate, Roger; Goodman, Myron F.

doi:10.1073/pnas.96.16.9224

Cited by 143 publications

(140 citation statements)

References 42 publications

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“…Although DNA replication is strongly inhibited almost immediately after irradiation with UV light, it resumes about 30 s later in wild-type cells (8,40,41). We proposed that pol II plays a pivotal role in alleviating stalled DNA replication, based on the observation that UV-irradiated cells lacking pol II exhibit about a 50-min delay in the resumption of DNA synthesis (8).…”

Section: Coping With Dna Damage In E Colimentioning

confidence: 99%

“…pol II is induced immediately after DNA damage, Ϸ30 s post-UV irradiation (8), whereas pol V induction occurs roughly 50 min later (42). The earlier appearance of pol II makes teleological sense because it is preferable for E. coli to try to rescue its DNA without introducing mutations.…”

Section: Future Perspectivesmentioning

confidence: 99%

“…A ⌬polB strain shows no measurable UV sensitivity, and SOS-induced mutagenesis occurs at normal levels (6,7). However, a ⌬polB ⌬umuDC double mutant strain is more sensitive to killing by UV light than either of the single mutant strains, implying that the two SOS-induced polymerases might play compensatory roles in vivo (8).…”

mentioning

confidence: 99%

“…TLS generates mutations targeted specifically to DNA template damage sites (9)(10)(11)(12). In contrast, pol II copies chromosomal DNA during error-free replication-restart (8). Although both polymerases are induced by DNA damage, they appear to function on widely disparate time frames-pol II-catalyzed replication-restart occurs 2 min post-UV irradiation whereas pol V-catalyzed TLS begins roughly 50 min later (8).…”

mentioning

confidence: 99%

“…In contrast, pol II copies chromosomal DNA during error-free replication-restart (8). Although both polymerases are induced by DNA damage, they appear to function on widely disparate time frames-pol II-catalyzed replication-restart occurs 2 min post-UV irradiation whereas pol V-catalyzed TLS begins roughly 50 min later (8). In this paper, we discuss current models for the roles of pol V in TLS and pol II in replication-restart.…”

mentioning

confidence: 99%

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Roles of DNA polymerases V and II in SOS-induced error-prone and error-free repair in Escherichia coli

Pham

Rangarajan

Woodgate

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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DNA polymerase V, composed of a heterotrimer of the DNA damage-inducible UmuC and UmuD 2 proteins, working in conjunction with RecA, single-stranded DNA (ssDNA)-binding protein (SSB), ␤ sliding clamp, and ␥ clamp loading complex, are responsible for most SOS lesion-targeted mutations in Escherichia coli, by catalyzing translesion synthesis (TLS). DNA polymerase II, the product of the damage-inducible polB (dinA ) gene plays a pivotal role in replication-restart, a process that bypasses DNA damage in an error-free manner. Replication-restart takes place almost immediately after the DNA is damaged (Ϸ2 min post-UV irradiation), whereas TLS occurs after pol V is induced Ϸ50 min later. We discuss recent data for pol V-catalyzed TLS and pol II-catalyzed replicationrestart. Specific roles during TLS for pol V and each of its accessory factors have been recently determined. Although the precise molecular mechanism of pol II-dependent replication-restart remains to be elucidated, it has recently been shown to operate in conjunction with RecFOR and PriA proteins.T wo seemingly unconnected questions arising during the early and mid 1970s were to decipher the biochemical basis of SOS mutagenesis in Escherichia coli, often referred to as SOS errorprone repair (1), and to determine a cellular role for E. coli DNA polymerase II. A tentative link between the two was established when it was determined that pol II was induced as part of the LexA-regulon (2). pol II was subsequently shown to be encoded by the DNA damage-inducible polB (dinA) gene (3-5). A ⌬polB strain shows no measurable UV sensitivity, and SOS-induced mutagenesis occurs at normal levels (6, 7). However, a ⌬polB ⌬umuDC double mutant strain is more sensitive to killing by UV light than either of the single mutant strains, implying that the two SOS-induced polymerases might play compensatory roles in vivo (8).The ability of pols II and V to complement each other does not mean that these activities are functionally redundant, and indeed they are not. pol V is able to copy UV-damaged DNA in a process referred to as error-prone translesion synthesis (TLS). TLS generates mutations targeted specifically to DNA template damage sites (9-12). In contrast, pol II copies chromosomal DNA during error-free replication-restart (8). Although both polymerases are induced by DNA damage, they appear to function on widely disparate time frames-pol II-catalyzed replication-restart occurs 2 min post-UV irradiation whereas pol V-catalyzed TLS begins roughly 50 min later (8). In this paper, we discuss current models for the roles of pol V in TLS and pol II in replication-restart.Coping with DNA Damage in E. coli There are over 40 genes induced on DNA damage in E. coli that have been identified recently by using microarray chip technology (13), of which at least 31 are known to be negatively regulated at the transcriptional level by the LexA protein (14). Many of these genes encode proteins required to repair DNA damage (15). The overriding importance of DNA repair is apparent from the ob...

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