scholarly journals RFCCtf18 and the Swi1-Swi3 Complex Function in Separate and Redundant Pathways Required for the Stabilization of Replication Forks to Facilitate Sister Chromatid Cohesion in Schizosaccharomyces pombe

2008 ◽  
Vol 19 (2) ◽  
pp. 595-607 ◽  
Author(s):  
Alison B. Ansbach ◽  
Chiaki Noguchi ◽  
Ian W. Klansek ◽  
Mike Heidlebaugh ◽  
Toru M. Nakamura ◽  
...  
Keyword(s):  
Stress Response ◽  
Fission Yeast ◽  
Sister Chromatid ◽  
Replication Fork ◽  
Complex Function ◽  
Dna Helicase ◽  
Sister Chromatid Cohesion ◽  
S Phase ◽  
Chromatid Cohesion ◽  
Factor C

Sister chromatid cohesion is established during S phase near the replication fork. However, how DNA replication is coordinated with chromosomal cohesion pathway is largely unknown. Here, we report studies of fission yeast Ctf18, a subunit of the RFCCtf18 replication factor C complex, and Chl1, a putative DNA helicase. We show that RFCCtf18 is essential in the absence of the Swi1–Swi3 replication fork protection complex required for the S phase stress response. Loss of Ctf18 leads to an increased sensitivity to S phase stressing agents, a decreased level of Cds1 kinase activity, and accumulation of DNA damage during S phase. Ctf18 associates with chromatin during S phase, and it is required for the proper resumption of replication after fork arrest. We also show that chl1Δ is synthetically lethal with ctf18Δ and that a dosage increase of chl1+ rescues sensitivities of swi1Δ to S phase stressing agents, indicating that Chl1 is involved in the S phase stress response. Finally, we demonstrate that inactivation of Ctf18, Chl1, or Swi1-Swi3 leads to defective centromere cohesion, suggesting the role of these proteins in chromosome segregation. We propose that RFCCtf18 and the Swi1–Swi3 complex function in separate and redundant pathways essential for replication fork stabilization to facilitate sister chromatid cohesion in fission yeast.

scholarly journals Interaction of the Warsaw breakage syndrome DNA helicase DDX11 with the replication fork-protection factor Timeless promotes sister chromatid cohesion

PLoS Genetics ◽  
2018 ◽  
Vol 14 (10) ◽  
pp. e1007622 ◽  
Author(s):  
Giuseppe Cortone ◽  
Ge Zheng ◽  
Pasquale Pensieri ◽  
Viviana Chiappetta ◽  
Rosarita Tatè ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Replication Fork ◽  
Dna Helicase ◽  
Sister Chromatid Cohesion ◽  
Protection Factor ◽  
Chromatid Cohesion

scholarly journals Fission Yeast Eso1p Is Required for Establishing Sister Chromatid Cohesion during S Phase

2000 ◽  
Vol 20 (10) ◽  
pp. 3459-3469 ◽  
Author(s):  
Koichi Tanaka ◽  
Toshihiro Yonekawa ◽  
Yosuke Kawasaki ◽  
Mihoko Kai ◽  
Kanji Furuya ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Sister Chromatid ◽  
Sister Chromatid Cohesion ◽  
S Phase ◽  
Chromatid Cohesion

scholarly journals MCM2–7-dependent cohesin loading during S phase promotes sister-chromatid cohesion

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Ge Zheng ◽  
Mohammed Kanchwala ◽  
Chao Xing ◽  
Hongtao Yu
Keyword(s):  
Sister Chromatid ◽  
Replication Fork ◽  
Sister Chromatid Cohesion ◽  
S Phase ◽  
Nucleosome Assembly ◽  
Okazaki Fragment ◽  
Replicative Helicase ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Okazaki Fragment Processing

DNA replication transforms cohesin rings dynamically associated with chromatin into the cohesive form to establish sister-chromatid cohesion. Here, we show that, in human cells, cohesin loading onto chromosomes during early S phase requires the replicative helicase MCM2–7 and the kinase DDK. Cohesin and its loader SCC2/4 (NIPBL/MAU2 in humans) associate with DDK and phosphorylated MCM2–7. This binding does not require MCM2–7 activation by CDC45 and GINS, but its persistence on activated MCM2–7 requires fork-stabilizing replisome components. Inactivation of these replisome components impairs cohesin loading and causes interphase cohesion defects. Interfering with Okazaki fragment processing or nucleosome assembly does not impact cohesion. Therefore, MCM2–7-coupled cohesin loading promotes cohesion establishment, which occurs without Okazaki fragment maturation. We propose that the cohesin–loader complex bound to MCM2–7 is mobilized upon helicase activation, transiently held by the replisome, and deposited behind the replication fork to encircle sister chromatids and establish cohesion.

scholarly journals Checkpoint-Dependent and -Independent Roles of Swi3 in Replication Fork Recovery and Sister Chromatid Cohesion in Fission Yeast

PLoS ONE ◽  
2010 ◽  
Vol 5 (10) ◽  
pp. e13379 ◽  
Author(s):  
Jordan B. Rapp ◽  
Chiaki Noguchi ◽  
Mukund M. Das ◽  
Lisa K. Wong ◽  
Alison B. Ansbach ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Sister Chromatid ◽  
Replication Fork ◽  
Sister Chromatid Cohesion ◽  
Chromatid Cohesion

Fission yeast Pds5 is required for accurate chromosome segregation and for survival after DNA damage or metaphase arrest

2002 ◽  
Vol 115 (3) ◽  
pp. 587-598 ◽  
Author(s):  
Shao-Win Wang ◽  
Rebecca L. Read ◽  
Chris J. Norbury
Keyword(s):  
Dna Damage ◽  
Fission Yeast ◽  
Sister Chromatid ◽  
Budding Yeast ◽  
Eukaryotic Cell ◽  
Sister Chromatid Cohesion ◽  
Chromosome Loss ◽  
Dependent Manner ◽  
Yeast Saccharomyces Cerevisiae ◽  
Chromatid Cohesion

Sister chromatid cohesion, which is established during the S phase of the eukaryotic cell cycle and persists until the onset of anaphase, is essential for the maintenance of genomic integrity. Cohesion requires the multi-protein complex cohesin, as well as a number of accessory proteins including Pds5/BIMD/Spo76. In the budding yeast Saccharomyces cerevisiae Pds5 is an essential protein that localises to chromosomes in a cohesin-dependent manner. Here we describe the characterisation in the fission yeast Schizosaccharomyces pombe of pds5+, a novel,non-essential orthologue of S. cerevisiae PDS5. The S. pombePds5 protein was localised to punctate nuclear foci in a manner that was dependent on the Rad21 cohesin component. This, together with additional genetic evidence, points towards an involvement of S. pombe Pds5 in sister chromatid cohesion. S. pombe pds5 mutants were hypersensitive to DNA damage and to mitotic metaphase delay, but this sensitivity was apparently not due to precocious loss of sister chromatid cohesion. These cells also suffered increased spontaneous chromosome loss and meiotic defects and their viability was dependent on the spindle checkpoint protein Bub1. Thus, while S. pombe Pds5 has an important cohesin-related role, this differs significantly from that of the equivalent budding yeast protein.

scholarly journals PCNA Controls Establishment of Sister Chromatid Cohesion during S Phase

2006 ◽  
Vol 23 (5) ◽  
pp. 723-732 ◽  
Author(s):  
George-Lucian Moldovan ◽  
Boris Pfander ◽  
Stefan Jentsch
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Cohesion ◽  
S Phase ◽  
Chromatid Cohesion

scholarly journals Hst3 Is Regulated by Mec1-dependent Proteolysis and Controls the S Phase Checkpoint and Sister Chromatid Cohesion by Deacetylating Histone H3 at Lysine 56

2007 ◽  
Vol 282 (52) ◽  
pp. 37805-37814 ◽  
Author(s):  
Safia Thaminy ◽  
Benjamin Newcomb ◽  
Jessica Kim ◽  
Tonibelle Gatbonton ◽  
Eric Foss ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Histone H3 ◽  
Sister Chromatid Cohesion ◽  
S Phase ◽  
Chromatid Cohesion ◽  
S Phase Checkpoint

scholarly journals Rec8p, a Meiotic Recombination and Sister Chromatid Cohesion Phosphoprotein of the Rad21p Family Conserved from Fission Yeast to Humans

1999 ◽  
Vol 19 (5) ◽  
pp. 3515-3528 ◽  
Author(s):  
Sandro Parisi ◽  
Michael J. McKay ◽  
Monika Molnar ◽  
M. Anne Thompson ◽  
Peter J. van der Spek ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Sister Chromatid ◽  
Germ Line ◽  
Sequence Similarity ◽  
Sister Chromatid Cohesion ◽  
Specific Expression ◽  
Chromatid Cohesion ◽  
Prophase Nucleus ◽  
Chromosome Iii ◽  
Meiosis I

ABSTRACT Our work and that of others defined mitosis-specific (Rad21 subfamily) and meiosis-specific (Rec8 subfamily) proteins involved in sister chromatid cohesion in several eukaryotes, including humans. Mutation of the fission yeast Schizosaccharomyces pombe rec8 gene was previously shown to confer a number of meiotic phenotypes, including strong reduction of recombination frequencies in the central region of chromosome III, absence of linear element polymerization, reduced pairing of homologous chromosomes, reduced sister chromatid cohesion, aberrant chromosome segregation, defects in spore formation, and reduced spore viability. Here we extend the description of recombination reduction to the central regions of chromosomes I and II. We show at the protein level that expression ofrec8 is meiosis specific and that Rec8p localizes to approximately 100 foci per prophase nucleus. Rec8p was present in an unphosphorylated form early in meiotic prophase but was phosphorylated prior to meiosis I, as demonstrated by analysis of the mei4mutant blocked before meiosis I. Evidence for the persistence of Rec8p beyond meiosis I was obtained by analysis of the mutantmes1 blocked before meiosis II. A human gene, which we designate hrec8, showed significant primary sequence similarity to rec8 and was mapped to chromosome 14. High mRNA expression of mouse and human rec8 genes was found only in germ line cells, specifically in testes and, interestingly, in spermatids. hrec8 was also expressed at a low level in the thymus. Sequence similarity and testis-specific expression indicate evolutionarily conserved functions of Rec8p in meiosis. Possible roles of Rec8p in the integration of different meiotic events are discussed.

scholarly journals Establishment of Sister Chromatid Cohesion at the S. cerevisiae Replication Fork

2006 ◽  
Vol 23 (6) ◽  
pp. 787-799 ◽  
Author(s):  
Armelle Lengronne ◽  
John McIntyre ◽  
Yuki Katou ◽  
Yutaka Kanoh ◽  
Karl-Peter Hopfner ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Replication Fork ◽  
Sister Chromatid Cohesion ◽  
Chromatid Cohesion
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