Postreplication Repair and PCNA Modification in<i>Schizosaccharomyces pombe</i>

Frampton, Jonathan; Irmisch, Anja; Green, Catherine; Neiss, Andrea; Trickey, Michelle; Ulrich, Helle D.; Furuya, Kanji; Watts, Felicity Z.; Carr, Antony; Lehmann, Alan R.

doi:10.1091/mbc.e05-11-1008

Cited by 119 publications

(202 citation statements)

References 40 publications

(54 reference statements)

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“…We note that the pcn1-K164R mutation confers greater MMS sensitivity than does the 3TLSD strain and that pcn1-K164R cells are sensitive to UV-C irradiation in G 2 , whereas 3TLSD cells are not (Frampton et al 2006). We also note that the requirement for Rhp18 extends to the repair of lesions in cells irradiated in G 2 (Verkade et al 2001).…”

Section: Brc1 Suppresses Smc6-74 Via a Novel Prr Pathwaymentioning

confidence: 65%

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Brc1-Mediated Rescue of Smc5/6 Deficiency: Requirement for Multiple Nucleases and a Novel Rad18 Function

et al. 2007

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Smc5/6 is a structural maintenance of chromosomes complex, related to the cohesin and condensin complexes. Recent studies implicate Smc5/6 as being essential for homologous recombination. Each gene is essential, but hypomorphic alleles are defective in the repair of a diverse array of lesions. A particular allele of smc6 (smc6-74) is suppressed by overexpression of Brc1, a six-BRCT domain protein that is required for DNA repair during S-phase. This suppression requires the postreplication repair (PRR) protein Rhp18 and the structure-specific endonucleases Slx1/4 and Mus81/Eme1. However, we show here that the contribution of Rhp18 is via a novel pathway that is independent of PCNA ubiquitination and PRR. Moreover, we identify Exo1 as an additional nuclease required for Brc1-mediated suppression of smc6-74, independent of mismatch repair. Further, the Apn2 endonuclease is required for the viability of smc6 mutants without extrinsic DNA damage, although this is not due to a defect in base excision repair. Several nucleotide excision repair genes are similarly shown to ensure viability of smc6 mutants. The requirement for excision factors for the viability of smc6 mutants is consistent with an inability to respond to spontaneous lesions by Smc5/6-dependent recombination.

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Section: Brc1 Suppresses Smc6-74 Via a Novel Prr Pathwaymentioning

confidence: 65%

“…Analysis of PCNA ubiquitination: Ubiqutination of PCNA was detected by Western blotting using polyclonal anti-PCNA antisera as described (Frampton et al 2006). Note that this antiserum detects a nonspecific band that comigrates with diubiquitinated PCNA.…”

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confidence: 99%

Brc1-Mediated Rescue of Smc5/6 Deficiency: Requirement for Multiple Nucleases and a Novel Rad18 Function

et al. 2007

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“…18 However, in contrast to budding yeast, damage-induced ubiquitylation can occur outside of S phase even in untransfected cells. 19 In S. pombe, PCNA mono-ubiquitylation occurs constitutively in S phase, 20 resembling conditions of RAD18 overexpression in S. cerevisiae. Thus, variations in the requirements for PCNA ubiquitylation among different organisms may reflect differences in the expression levels of RAD18.…”

Section: Rad18 Is a Limiting Factor For Pcna Ubiquitylation At Stallementioning

confidence: 98%

Cooperation of replication Protein A with the ubiquitin ligase Rad18 in DNA damage bypass

Huttner¹,

Ulrich²

2008

Cell Cycle

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Replicative DNA damage bypass promotes cell viability in the presence of genotoxic agents but at the same time may lead to mutations, thereby contributing to genomic instability. In eukaryotes, DNA damage bypass is mediated by damage-induced ubiquitylation of the sliding clamp protein, proliferating cell nuclear antigen (PCNA). We have recently shown that replication protein A (RPA), a single-stranded (ss)DNA-binding protein essential for DNA replication, repair and recombination, is required for PCNA ubiquitylation in budding yeast. Both in yeast and in mammalian cells, RPA physically interacts with Rad18, the ubiquitin ligase responsible for PCNA mono-ubiquitylation. The association of Rad18 with chromatin correlates with that of RPA, and purified RPA can recruit the ligase to ssDNA in vitro. Here we have examined in more detail the interactions between Rad18, RPA and DNA and discuss their contribution to the activation of DNA damage bypass.

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“…59 In eukaryotes it has recently been discovered that posttranslational modification of the PCNA processivity clamp by ubiquitination is required for TLS in vivo. [60][61][62][63] Furthermore, interaction with PCNA is a requirement for focus formation of pol k in response to DNA damage. 64 The alternative processivity clamp Rad9-Rad1-Hus1 (9-1-1) has been also shown to be important for DinB function in Schizosaccharomyces pombe.…”

confidence: 99%

“…Moreover, whether selection of the proper polymerase occurs merely by stochastic competition or by more a more orchestrated mechanism is a topic of intense debate. 62,66,68,69 Another key question is whether TLS occurs solely at static stalled replication forks or perhaps additionally at gaps left after replication reinitiation. Recent results in S. cerevisiae have suggested that replication blocking lesions can induce both leading and lagging strand gaps, 70 evoking early models of replication in E. coli.…”

Section: Conclusion and Future Questionsmentioning

confidence: 99%

Proficient and Accurate Bypass of Persistent DNA Lesions by DinB DNA Polymerases

Jarosz¹,

Godoy²,

Walker³

2007

Cell Cycle

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Despite nearly universal conservation through evolution, the precise function of the DinB/pol k branch of the Y-family of DNA polymerases has remained unclear. Recent results suggest that DinB orthologs from all domains of life proficiently bypass replication blocking lesions that may be recalcitrant to DNA repair mechanisms. Like other translesion DNA polymerases, the error frequency of DinB and its orthologs is higher than the DNA polymerases that replicate the majority of the genome. However, recent results suggest that some Y-family polymerases, including DinB and pol k, bypass certain types of DNA damage with greater proficiency than an undamaged template. Moreover, they do so relatively accurately. The ability to employ this mechanism to manage DNA damage may be especially important for types of DNA modification that elude repair mechanisms. For these lesions, translesion synthesis may represent a more important line of defense than for other types of DNA damage that are more easily dealt with by other more accurate mechanisms.

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Postreplication Repair and PCNA Modification inSchizosaccharomyces pombe

Cited by 119 publications

References 40 publications

Brc1-Mediated Rescue of Smc5/6 Deficiency: Requirement for Multiple Nucleases and a Novel Rad18 Function

Brc1-Mediated Rescue of Smc5/6 Deficiency: Requirement for Multiple Nucleases and a Novel Rad18 Function

Cooperation of replication Protein A with the ubiquitin ligase Rad18 in DNA damage bypass

Proficient and Accurate Bypass of Persistent DNA Lesions by DinB DNA Polymerases

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