Rad51-Independent Interchromosomal Double-Strand Break Repair by Gene Conversion Requires Rad52 but Not Rad55, Rad57, or Dmc1

Pohl, Thomas J.; Nickoloff, Jac A.

doi:10.1128/mcb.00524-07

Cited by 29 publications

(26 citation statements)

References 62 publications

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“…The differences between the ILT and the ALT-like pathways, both amplifying the TG 1-3 repeats (type II), were an absence of a requirement for Rad52, Rad59, and functional RPA for the ILT pathway, in contrast to the type II-ALT pathway, which requires all three proteins. Gene conversion, which normally requires both Rad51 and Rad52, can be possible in the absence of Rad51 for ectopic events but, surprisingly, also for interchromosomal conversion (61,62,67). Allelic conversion is also possible in the absence of Rad52 but not in the absence of both Rad51 and Rad52 (62).…”

Section: Discussionmentioning

confidence: 99%

“…Gene conversion, which normally requires both Rad51 and Rad52, can be possible in the absence of Rad51 for ectopic events but, surprisingly, also for interchromosomal conversion (61,62,67). Allelic conversion is also possible in the absence of Rad52 but not in the absence of both Rad51 and Rad52 (62). It is assumed that each of these proteins can perform part of the other one's functions in its absence.…”

Section: Discussionmentioning

confidence: 99%

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Telomerase- and Rad52-Independent Immortalization of Budding Yeast by an Inherited-Long-Telomere Pathway of Telomeric Repeat Amplification

Grandin

Charbonneau

2009

Molecular and Cellular Biology

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In the absence of telomerase, telomeres erode, provoking accumulation of DNA damage and death by senescence. Rare survivors arise, however, due to Rad52-based amplification of telomeric sequences by homologous recombination. The present study reveals that in budding yeast cells, postsenescence survival relying on amplification of the TG 1-3 telomeric repeats can take place in the absence of Rad52 when overelongated telomeres are present during senescence (hence its designation ILT, for inherited-long-telomere, pathway). By growth competition, the Rad52-independent pathway was almost as efficient as the Rad51-and Rad52-dependent pathway that predominates in telomerase-negative cells. The ILT pathway could also be triggered by increased telomerase accessibility before telomerase removal, combined with loss of telomere protection, indicating that prior accumulation of recombination proteins was not required. The ILT pathway was dependent on Rad50 and Mre11 but not on the Rad51 recombinase and Rad59, thus making it distinct from both the type II (budding yeast ALT [alternative lengthening of telomeres]) and type I pathways amplifying the TG 1-3 repeats and subtelomeric sequences, respectively. The ILT pathway also required the Rad1 endonuclease and Elg1, a replication factor C (RFC)-like complex subunit, but not Rad24 or Ctf18 (two subunits of two other RFC-like complexes), the Dnl4 ligase, Yku70, or Nej1. Possible mechanisms for this Rad52-independent pathway of telomeric repeat amplification are discussed. The effects of inherited long telomeres on Rad52-dependent recombination are also reported.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Telomerase- and Rad52-Independent Immortalization of Budding Yeast by an Inherited-Long-Telomere Pathway of Telomeric Repeat Amplification

Grandin

Charbonneau

2009

Molecular and Cellular Biology

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“…studies on HR revealed several recombination pathways that do not require Rad51; they include SSA and BIR, although a majority of BIR is dependent on Rad51 (43,46,(75)(76)(77). In addition, a subset of sister chromatid recombination (SCR) events, which is facilitated by the RSC chromatin-remodeling complex, also can occur independently of Rad51 (78,79).…”

Section: Suppression Of Dna2-k1080e By Rad52 Depends On Several Factomentioning

confidence: 99%

Rad52/Rad59-dependent Recombination as a Means to Rectify Faulty Okazaki Fragment Processing

Lee

Demin

et al. 2014

Journal of Biological Chemistry

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Background: How faulty Okazaki fragments are repaired remains unclear. Results: The DNA annealing activity of Rad52 and sister chromatid cohesion are important in the repair of faulty Okazaki fragments. Conclusion: Rad52/Rad59-mediated sister chromatid recombination is a major means of repairing faulty Okazaki fragments. Significance: The faithful repair of faulty Okazaki fragments is critical for genome stability.

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“…The human Rad51B-Rad51C-Rad51D-Xrcc2 complex preferentially binds to branched DNA substrates, including a synthetic Holliday junction substrate, over other DNA substrates (Yokoyama et al 2004). XRCC3-and RAD51C-defective cell lines exhibit longerthan-normal gene conversion tract lengths, which could result from defects in the resolution of recombination intermediates or be due to a different mode of recombination by the Rad51-independent pathway (Brenneman et al 2002;Nagaraju et al 2006;Pohl and Nickoloff 2008). Extracts made from XRCC3-or RAD51C-defective Chinese hamster ovary cells show reduced levels of Holliday junction resolvase activity (Liu et al 2004).…”

Section: H Omologous Recombination Is Required Formentioning

confidence: 99%

Suppression of the Double-Strand-Break-Repair Defect of the Saccharomyces cerevisiae rad57 Mutant

Fung¹,

Mozlin²,

Symington

2009

Genetics

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The Rad51 paralogs Rad55 and Rad57 form a heterodimer required to mediate the formation and/or stabilization of the Rad51 filament. To further characterize the function of Rad55-Rad57, we used a combination of rad57 partial suppressors to determine whether the DNA repair and recombination defects of the rad57 mutant could be completely suppressed. The combination of all suppressors, elevated temperature, srs2, rad51-I345T, and mating-type (MAT) heterozygosity resulted in almost complete suppression of the rad57 mutant defect in the recruitment of Rad51 to DNA-damaged sites, as well as survival in response to ionizing radiation and camptothecin. In a physical assay to monitor the kinetics of double-strand-break (DSB)-induced gene conversion, the rad57 mutant defect was effectively suppressed by srs2 and MAT heterozygosity, but these same suppressors failed to suppress the spontaneous recombination defect. Thus the Rad55-Rad57 heterodimer appears to have a unique function in spontaneous recombination that is not essential for DSB repair. Furthermore, we investigated the currently unknown mechanism of rad57 suppression by MAT heterozygosity and found that it is independent of DNL4. H OMOLOGOUS recombination is required forthe faithful repair of DNA double-strand breaks (DSBs) that arise during normal cellular processes or from exposure of cells to DNA-damaging agents. Central to the process of homologous recombination is the Rad51 protein, which facilitates synapsis and strand invasion into homologous duplex DNA (San Filippo et al. 2008). Rad51 belongs to the RecA family of homologous pairing proteins (Aboussekhra et al. 1992;Basile et al. 1992;Shinohara et al. 1992). Yeast and humans have two RecA homologs: Rad51 and the meiosis-specific Dmc1 (Bishop et al. 1992;San Filippo et al. 2008). In addition, the Saccharomyces cerevisiae RAD55 and RAD57 genes encode proteins with sequence similarity to RecA and Rad51 and are considered to be Rad51 paralogs (Kans and Mortimer 1991;Lovett 1994). Mutation of RAD51, RAD55, or RAD57 confers sensitivity of ionizing radiation (IR) and defects in mitotic and meiotic recombination, indicating that their functions are not redundant (Symington 2002). rad51 mutants generally exhibit more severe defects than rad55 or rad57 mutants in DSB-induced recombination assays; however, rad55 and rad57 mutants are more defective than rad51 in some assays that measure spontaneous recombination between repeated sequences (Rattray and Symington 1995;Mozlin et al. 2008).The molecular details of homologous recombination are largely based on genetic, physical, and cytological studies of DSB repair (DSBR) and on biochemical characterization of purified proteins (Paques and Haber 1999;Sugawara et al. 2003;Lisby et al. 2004;San Filippo et al. 2008). The single-stranded DNA (ssDNA)-binding protein, replication protein A (RPA), initially binds ssDNA that forms by nucleolytic processing of DNA ends at DSBs. In vitro, RPA has been shown to be inhibitory to Rad51 binding to ssDNA, but this inhibition c...

show abstract

Rad51-Independent Interchromosomal Double-Strand Break Repair by Gene Conversion Requires Rad52 but Not Rad55, Rad57, or Dmc1

Cited by 29 publications

References 62 publications

Telomerase- and Rad52-Independent Immortalization of Budding Yeast by an Inherited-Long-Telomere Pathway of Telomeric Repeat Amplification

Telomerase- and Rad52-Independent Immortalization of Budding Yeast by an Inherited-Long-Telomere Pathway of Telomeric Repeat Amplification

Rad52/Rad59-dependent Recombination as a Means to Rectify Faulty Okazaki Fragment Processing

Suppression of the Double-Strand-Break-Repair Defect of the Saccharomyces cerevisiae rad57 Mutant

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