The Chromatin Assembly Factor 1 Promotes Rad51-Dependent Template Switches at Replication Forks by Counteracting D-Loop Disassembly by the RecQ-Type Helicase Rqh1

Pietrobon, Violena; Fréon, Karine; Hardy, Julien; Costes, Audrey; Iraqui, Ismaïl; Ochsenbein, Françoise; Lambert, Sarah

doi:10.1371/journal.pbio.1001968

Cited by 33 publications

(56 citation statements)

References 68 publications

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“…Hoek et al postulated that KU70/80 recruits CAF-1 to DNA damage repair sites independently of PCNA because there is a need for new nucleosome assembly without a need for large-scale DNA synthesis [37]. Furthermore, Werner syndrome protein (WRN), a RecQ family DNA helicase, has recently been shown to recruit CHAF1a to sites of DNA damage through direct interactions mediated by its helicase and RQC domains: this complex is promotes DNA repair through homologous recombination [39, 40]. …”

Section: The Chaf1a Subunitmentioning

confidence: 99%

The role of the chromatin assembly complex (CAF-1) and its p60 subunit (CHAF1b) in homeostasis and disease

Volk

Crispino

2015

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

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Nucleosome assembly following DNA synthesis is critical for maintaining genomic stability. The proteins directly responsible for shuttling newly synthesized histones H3 and H4 from the cytoplasm to the assembly fork during DNA replication comprise the Chromatin Assembly Factor 1 complex (CAF-1). Whereas the diverse functions of the large (CAF-1-p150, CHAF1a) and small (RbAp48, p48) subunits of the CAF-1 complex have been well-characterized in many tissues and extend beyond histone chaperone activity, the contributions of the medium subunit (CAF-1-p60, CHAF1b) are much less well understood. Although it is known that CHAF1b has multiple functional domains (7x WD repeat domain, B-like domain, and a PEST domain), how these components come together to elicit the functions of this protein are still unclear. Here, we review the biology of the CAF-1 complex, with an emphasis on CHAF1b, including its structure, regulation, and function. In addition, we discuss the possible contributions of CHAF1b and the CAF-1 complex to human diseases. Of note, CHAF1b is located within the Down syndrome critical region (DSCR) of chromosome 21. Therefore, we also address the putative contributions of its trisomy to the various manifestations of DS.

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Section: The Chaf1a Subunitmentioning

confidence: 99%

The role of the chromatin assembly complex (CAF-1) and its p60 subunit (CHAF1b) in homeostasis and disease

Volk

Crispino

2015

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

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“…Rationale for the experiments performed in this study. CAF-1 was shown to stabilize Dloops in S. pombe that occur as the result of template switching at replication forks (Pietrobon et al 2014). This observation encouraged us to test if the histone chaperones CAF-1 and Rtt106 play roles in stabilizing recombination intermediates during HR, and in turn suppressing rejection.…”

Section: Resultsmentioning

confidence: 97%

“…in S. pombe and BLM and WRN in humans) physically interact with the large subunit of CAF-1 (Pietrobon et al 2014;Jiao et al 2004;Jiao et al 2007). Additionally, Pietrobon et al (2014) showed that CAF-1 suppresses D-loop disassembly by Rqh1 during template switching. Based on these observations, it is possible that CAF-1 physically interacts with Sgs1 in budding yeast and counteracts its unwinding activity during heteroduplex rejection.…”

Section: Various Studies Have Shown In Fission Yeast and Humans That mentioning

confidence: 99%

“…These chaperones include CAF-1, Asf1 and Rtt106, which are all involved in DNA replication-dependent nucleosome assembly (Tyler et al 1999;Tagami et al 2004;Huang et al 2005). For example, nucleosome assembly mediated by CAF-1 during DNA repair is coupled with DNA synthesis and requires an interaction with PCNA (Gaillard et al 1996;Tyler et al 1999;Linger and Tyler 2005;Polo, Roche and Almouzni 2006;Pietrobon et al 2014), and CAF-1 and Asf1 play roles in restoring chromatin after DNA repair in budding yeast at repair sites by turning off the DNA damage checkpoint (Chen et al 2008;Kim and Haber 2009;Diao et al 2017).…”

Section: Introductionmentioning

confidence: 99%

“…Additionally, human MSH2-MSH6 inhibits CAF-1 and ASF1A-dependent packaging of a DNA mismatch into a nucleosome, and deposition of the (H3-H4)2 tetramers on DNA protects the discontinuous daughter strand from unnecessary degradation during MMR (Blanko, Kadyrova and Kadyrov 2016). Moreover, Pietrobon et al (2014) showed in fission yeast that CAF-1 stabilizes D-loops in an HR pathway, by counteracting their disassembly mediated by the RecQ family helicase Rqh1 when cells replicate a damaged template.…”

Section: Introductionmentioning

confidence: 99%

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Chromatin modifiers alter recombination between divergent DNA sequences

Chakraborty

Mackenroth

Alani

2019

Preprint

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Recombination between divergent DNA sequences is actively prevented by heteroduplex rejection mechanisms. In baker's yeast such anti-recombination mechanisms can be initiated by the recognition of DNA mismatches in heteroduplex DNA by MSH proteins, followed by recruitment of the Sgs1-Top3-Rmi1 helicase-topoisomerase complex to unwind the recombination intermediate. We previously showed that the repair/rejection decision during single-strand annealing recombination is temporally regulated by MSH protein levels and by factors that excise non-homologous single-stranded tails. These observations, coupled with recent studies indicating that mismatch repair factors interact with components of the histone chaperone machinery, encouraged us to explore roles for epigenetic factors and chromatin conformation in regulating the decision to reject vs. repair recombination between divergent DNA substrates. This work involved the use of an inverted repeat recombination assay thought to measure sister chromatid repair during DNA replication. Our observations are consistent with the histone chaperones CAF-1 and Rtt106 and the histone deacetylase Sir2 acting to suppress heteroduplex rejection and the Rpd3, Hst3 and Hst4 deacetylases acting to promote heteroduplex rejection. These observations and double mutant analysis have led to a model in which nucleosomes located at DNA lesions stabilize recombination intermediates and compete with mismatch repair factors that mediate heteroduplex rejection.

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The Chromatin Assembly Factor 1 Promotes Rad51-Dependent Template Switches at Replication Forks by Counteracting D-Loop Disassembly by the RecQ-Type Helicase Rqh1

Abstract: A molecular switch for times of replication stress - Chromatin Assembly Factor 1 helps to protect DNA during recombination-mediated template-switching, favoring the rescue of stalled replication forks by both beneficial and detrimental homologous recombination events.

Cited by 33 publications

References 68 publications

The role of the chromatin assembly complex (CAF-1) and its p60 subunit (CHAF1b) in homeostasis and disease

The role of the chromatin assembly complex (CAF-1) and its p60 subunit (CHAF1b) in homeostasis and disease

Chromatin modifiers alter recombination between divergent DNA sequences

Parental histone distribution and location of the replication obstacle at nascent strands control homologous recombination

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