A study of biochemical and functional interactions of Htl1p, a putative component of the Saccharomyces cerevisiae, Rsc chromatin-remodeling complex

Florio, Carolina; Moscariello, Mario; Ederle, Sara; Fasano, Rossella; Lanzuolo, Chiara; Pulitzer, John F.

doi:10.1016/j.gene.2007.02.002

Cited by 6 publications

(9 citation statements)

References 38 publications

(56 reference statements)

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“…1A). Indeed, the results are consistent with the finding reported by various groups that deletion of RSC genes leads to temperature-sensitive growth and hypersensitivity to genotoxic agents (5,7,15,27,31,34,45,61,68). The apparent temperature sensitivity of these mutants must be the consequence of the corresponding RSC gene deletions because thermosensitivity can be rescued by ectopic expression of each RSC gene (data not shown).…”

Section: Resultssupporting

confidence: 92%

RSC Facilitates Rad59-Dependent Homologous Recombination between Sister Chromatids by Promoting Cohesin Loading at DNA Double-Strand Breaks

Oum

Seong

Kwon

et al. 2011

Molecular and Cellular Biology

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Homologous recombination repairs DNA double-strand breaks by searching for, invading, and copying information from a homologous template, typically the homologous chromosome or sister chromatid. Tight wrapping of DNA around histone octamers, however, impedes access of repair proteins to DNA damage. To facilitate DNA repair, modifications of histones and energy-dependent remodeling of chromatin are required, but the precise mechanisms by which chromatin modification and remodeling enzymes contribute to homologous DNA repair are unknown. Here we have systematically assessed the role of budding yeast RSC (remodel structure of chromatin), an abundant, ATP-dependent chromatin-remodeling complex, in the cellular response to spontaneous and induced DNA damage. RSC physically interacts with the recombination protein Rad59 and functions in homologous recombination. Multiple recombination assays revealed that RSC is uniquely required for recombination between sister chromatids by virtue of its ability to recruit cohesin at DNA breaks and thereby promoting sister chromatid cohesion. This study provides molecular insights into how chromatin remodeling contributes to DNA repair and maintenance of chromatin fidelity in the face of DNA damage.

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Section: Resultssupporting

confidence: 92%

RSC Facilitates Rad59-Dependent Homologous Recombination between Sister Chromatids by Promoting Cohesin Loading at DNA Double-Strand Breaks

Oum

Seong

Kwon

et al. 2011

Molecular and Cellular Biology

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“…Deletion of RSC subunits results in diminished precise and imprecise NHEJ frequency at the site of an HO induced chromosomal DSB (Shim et al 2005). Plasmid repair assays also revealed NHEJ defects upon deletion of RSC subunits (Florio et al 2007; Moscariello et al 2010; Shim et al 2005), although one group detected increased plasmid repair in rsc1Δ and rsc2Δ strains (Chai et al 2005). The RSC subunit Sth1 is detected at an HO endonuclease-induced DSB by ChIP as early as 10 minutes after break induction (Shim et al 2007; Shim et al 2005).…”

Section: Nhej and Chromatinmentioning

confidence: 99%

Consider the workhorse: Nonhomologous end-joining in budding yeast

Emerson

Bertuch

2016

Biochem. Cell Biol.

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DNA double strand breaks (DSBs) are dangerous sources of genome instability and must be repaired by the cell. Nonhomologous end joining (NHEJ) is an evolutionarily conserved pathway to repair DSBs by direct ligation of the ends, with no requirement for a homologous template. While NHEJ is the primary DSB repair pathway in mammalian cells, conservation of the core NHEJ factors throughout eukaryotes make the pathway attractive for study in model organisms. The budding yeast, Saccharomyces cerevisiae, has been used extensively to develop a functional picture of NHEJ. In this review, we will discuss the current understanding of NHEJ in S. cerevisiae. Topics include canonical end-joining, alternative end-joining, and pathway regulation. Particular attention will be paid to the NHEJ mechanism involving core factors, including Yku70/80, Dnl4, Lif1, and Nej1, as well as the various factors implicated in the processing of the broken ends. The relevance of chromatin dynamics to NHEJ will also be discussed. This review illustrates the use of S. cerevisiae as a powerful system to understand the principles of NHEJ, as well as in pioneering the direction of the field.

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“…The RAD5 allele did not affect the outcome of the plasmid repair experiments. Derivatives of Sc288C (Mortimer and Johnston, 1986) included haploid strain BY4741 ( MAT a his3Δ1 leu2Δ0 met15Δ0 ura3Δ0 ), diploid strain BY4743 ( MAT a /α his3Δ1/his3Δ1 leu2Δ0/leu2Δ0 LYS2/lys2Δ0 met15Δ0/MET15 ura3Δ0/ura3Δ0 ) (Brachmann et al , 1998), diploid strain FY1679 ( MAT a /α ura3–52/ura3–52 trp1 Δ 63/TRP1 leu2 Δ 1/LEU2 his3 Δ 200/HIS3 GAL2/GAL2 ) (Winston et al , 1995) and the haploid derivative FY ( MAT a ura3–52 leu2Δ1 trp1D63 his3Δ200 GAL2 ) W303 rad5 derivatives include YLL941 ku70::HIS3 and YLL rad52::HIS3 (kindly provided by M. P. Longhese), YJP3 W303‐1b htl1::URA3pRS306 (Florio et al , 2007), W303–1a/b ( MAT a/ α ade2–1 trp1–1 leu2–3,112 his3–11,15 ura3 can1–100, ssd1‐d ) and YJP1 W303–1a htl1::HIS3pRS303 (Lanzuolo et al , 2001).…”

Section: Methodsmentioning

confidence: 99%

“…We and others have shown that a 78 amino acid peptide encoded by the HTL1 gene binds to the RSC complex by association with Rsc8, a RSC core subunit (Romeo et al , 2002; Lu et al , 2003; Florio et al , 2007). The phenotypic effects of HTL1 deletion recapitulate phenotypic effects of mutational alteration or depletion of diverse RSC subunits.…”

Section: Introductionmentioning

confidence: 98%

“…The phenotypic effects of HTL1 deletion recapitulate phenotypic effects of mutational alteration or depletion of diverse RSC subunits. The hypersensitivity of htl1 mutants to hydroxyurea (HU) and to methyl methane sulphonate (Florio et al , 2007), both of which can lead to the formation of DSBs, focused our attention on DNA repair and prompted us to determine whether Htl1 shares with RSC a role in DSB repair.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Accurate repair of non‐cohesive, double strand breaks in Saccharomyces cerevisiae: enhancement by homology‐assisted end‐joining

Moscariello

Florio

Pulitzer

2010

Yeast

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Although the joining of blunt ends in yeast by non-homologous end joining (NHEJ) is reported to be inefficient in comparison to cohesive-end joining (Boulton and Jackson, 1996), we find that efficiency varies greatly, depending on strain, growth phase and sequence. In particular, the levels of efficiency of recircularization of a plasmid linearized by non-cohesive cleavage is augmented to that of cohesive end joining if the cleavage cut site is flanked by sequences present in the genome. We call this enhancement 'homology-assisted end joining' (HAEJ), which depends on components of the NHEJ repair pathway and, in some cases, on components of the homologous recombination (HR) pathway and on Htl1 a component of the remodels structure of chromatin (RSC) complex. The homologous genome sequences are not used as templates for repair DNA synthesis, but may facilitate end-to-end collision and ligation by providing a track for guided diffusion.

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A study of biochemical and functional interactions of Htl1p, a putative component of the Saccharomyces cerevisiae, Rsc chromatin-remodeling complex

Cited by 6 publications

References 38 publications

RSC Facilitates Rad59-Dependent Homologous Recombination between Sister Chromatids by Promoting Cohesin Loading at DNA Double-Strand Breaks

RSC Facilitates Rad59-Dependent Homologous Recombination between Sister Chromatids by Promoting Cohesin Loading at DNA Double-Strand Breaks

Consider the workhorse: Nonhomologous end-joining in budding yeast

Accurate repair of non‐cohesive, double strand breaks in Saccharomyces cerevisiae: enhancement by homology‐assisted end‐joining

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