PCNA Controls Establishment of Sister Chromatid Cohesion during S Phase

Moldovan, George‐Lucian; Pfander, Boris; Jentsch, Stefan

doi:10.1016/j.molcel.2006.07.007

Cited by 269 publications

(338 citation statements)

References 39 publications

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“…Circumstantial evidence has indeed indicated a relationship between DNA replication and the establishment of sister chromatid cohesion. Sister chromatid cohesion requires not only chromosome-bound cohesin complexes but also Eco1 and PCNA, 4,6,28 as well as several accessory factors such as Ctf18. 29,30 These proteins locali�e to replication forks, at least when cells are arrested in early S phase by hydroxy urea (HU) treatment.…”

Section: Ino80 Complex In Sister Chromatid Cohesion Chromosome XV Andmentioning

confidence: 99%

“…Here we have shown that the INO80 chromatin remodeling complex locali�es to replication forks, at least during replication arrest in early S phase cells, and colocali�es with Ctf18 and PCNA, which are involved in cohesion establishment. 6,7 Furthermore, arp8 cells are defective in sister chromatid cohesion and perturbed in the recruitment of Ctf18 and PCNA to replication forks.…”

Section: Ino80 Complex In Sister Chromatid Cohesion Chromosome XV Andmentioning

confidence: 99%

“…Interaction between PCNA and Eco1 is required for the Eco1 function in sister chromatid cohesion and for its timely recruitment to chromatin. [4][5][6] These cohesion proteins have been locali�ed to replication forks.…”

Section: Introductionmentioning

confidence: 99%

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The INO80 Chromatin Remodeling Complex Functions in Sister Chromatid Cohesion

Ogiwara

Enomoto²,

Seki³

2007

Cell Cycle

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Previously published online as a Cell Cycle E-publication: http://www.landesbioscience.com/journals/cc/abstract.php?id=4130 KEy wOrdSIno80, Arp8, Ctf18, RFC, PCNA, cohesin, chromosome segregation/sister chromatid cohesion, chromatin remodeling, replication fork AcKnOwlEdgEMEnTSWe thank P. Hieter, A. Sugino, Y. Kawasaki, and M. Arisawa for strains, antibodies and plasmids used in this study. We thank all members of the Enomoto lab for their support. This work was supported by Grants-in-Aid for Scientific Research on Priority Areas from The Ministry of Education, Science, Sports and Culture of Japan. nOTESupplemental material can be found at: http://www.landesbioscience.com/supplement/ogiwaraCC6-9-sup.pdf AbSTrAcTHere we identify a defect in sister chromatid cohesion in the Saccharomyces serevisiae arp8 mutant, which impairs the chromatin remodeling activity of the INO80 complex, and we report the direct association of Ino80 with centromeres and cohesin-associated regions. In early S phase, Ino80 is recruited to replication forks along with Ctf18 and PCNA, both of which are involved in the establishment of sister chromatid cohesion. The arp8 mutation perturbs the association of Ctf18 and PCNA but not of cohesin with replication forks. We propose that the INO80 complex is required for the proper establishment of sister chromatid cohesion.

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Section: Ino80 Complex In Sister Chromatid Cohesion Chromosome XV Andmentioning

confidence: 99%

Section: Ino80 Complex In Sister Chromatid Cohesion Chromosome XV Andmentioning

confidence: 99%

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The INO80 Chromatin Remodeling Complex Functions in Sister Chromatid Cohesion

Ogiwara

Enomoto²,

Seki³

2007

Cell Cycle

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“…Monoubiquitinated PCNA can be polyubiquitinated by the Rad5-Ubc13-Mms2 complex (Hofmann and Pickart, 1999) to allow error-free mechanisms (Torres-Ramos et al, 2002). Alternatively, K164 of PCNA can be SUMOylated to regulate recombination at the fork (Pfander et al, 2005;Moldovan et al, 2006) via a direct interaction with Srs2 (Pfander et al, 2005), a 3 -5 DNA helicase (Rong and Klein, 1993), thought to exert a negative control on HR (Krejci et al, 2003;Veaute et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Genetic evidence for a role of Saccharomyces cerevisiae Mph1 in recombinational DNA repair under replicative stress

Panico

Ede

Schildmann

et al. 2009

Yeast

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In yeast as in human, DNA helicases play critical roles in assisting replication fork progression. The Saccharomyces cerevisiae MPH1 gene, homologue of human FANCM, has been involved in homologous recombination and DNA repair. We describe a synthetic growth defect of an mph1 deletion if combined with an srs2 deletion that can result -depending on the genetic background -in synthetic lethality. The lethality is suppressed by mutations in homologous recombination (rad51, rad52, rad55, rad57 ) and in the DNA damage checkpoint (rad9, rad24, rad17 ). Importantly, rad54 and mph1, epistatic for damage sensitivity, are subadditive for spontaneous mutator phenotype. Therefore, Mph1 could be placed at the Rad51-mediated strand invasion process, with a function distinct from Rad54. Moreover, siz1 mutation is viable with mph1 and additive for DNA damage sensitivity. mph1 srs2 double mutants, isolated in a background where they are viable, are synergistically sensitive to DNA damage. Moderate overexpression of SGS1 partially suppresses this sensitivity. Finally, we observe an epistatic relationship in terms of sensitivity to camptothecin of mms4 or mus81 to mph1. Overall, our results support a role of Mph1 in assisting replication progression. We propose two models for the resumption of DNA synthesis under replicative stress where Mph1 is placed at the sister chromatid interaction step.

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“…21 In addition, variations in cytosine methylation may be the indirect result of disturbed recruitment of proteins to the replication fork. In yeast, ECO1 can interact with the PCNA subunit 22 , a key regulator of replication fork function, but several other proteins can also interact with PCNA and include ARABI-DOPSIS TRITHORAX-RELATED PROTEIN 5 (ATXR5) and ATXR6. 23 The respective ATXR5/6 loci cause a wide range of defects when mutated, such as re-replication of pericentromeric regions 23 , a phenotype possibly observed in CTF7 mutants.…”

Section: Hypothetical Mechanisms For Ctf7/ Eco1 Functionmentioning

confidence: 99%