Cohesin organizes chromatin loops at DNA replication factories

Guillou, Emmanuelle; Ibarra, Arkaitz; Coulon, Vincent; Casado‐Vela, Juan; Rico, Daniel; Casal, J. Ignacio; Schwob, Étienne; Losada, Ana; Méndez, Juan Pablo

doi:10.1101/gad.608210

Cited by 208 publications

(231 citation statements)

References 56 publications

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“…Our experiments with heterokaryon-mediated reprogramming support studies that have shown a role for cohesin in DNA replication (Terret et al 2009;Guillou et al 2010), and this emerging role is important for the activation of pluripotency gene expression by somatic cells in ES cell heterokaryons, where the depletion of cohesin results in slow S-phase progression and impaired pluripotency gene expression. This role is mechanistically distinct from chromosome segregation in mitosis (Nasmyth and Haering 2009;Terret et al 2009;Guillou et al 2010).…”

Section: Emerging Cohesin Functions In Dna Replicationsupporting

confidence: 61%

“…Cohesin and replication are intimately linked, since cohesion between sister chromatids is established during replication in S phase (Gerlich et al 2006;Nasmyth and Haering 2009;Terret et al 2009;Gause et al 2010). Cohesin associates with origins of DNA replication in Xenopus (Gillespie and Hirano 2004;Takahashi et al 2004), Drosophila (MacAlpine et al 2010, and mammalian genomes (Guillou et al 2010), where cohesin affects the spacing of replication origins in cohesin-depleted cells (Guillou et al 2010), the progression of replication forks (Terret et al 2009), and the restart of stalled forks (Tittel-Elmer et al 2012). As a result, altering the dosage or function of cohesin can affect DNA replication (Terret et al 2009;Guillou et al 2010;Tedeschi et al 2013).…”

Section: Cohesin Myc Dna Replication and Reprogrammingmentioning

confidence: 99%

“…As heterokaryon-mediated reprogramming is thought to involve the ES cell-mediated initiation of somatic DNA replication (Tsubouchi et al 2013) and cohesin has been linked to efficient DNA replication (Terret et al 2009;Guillou et al 2010;Tittel-Elmer et al 2012;Tedeschi et al 2013), we considered whether cohesindependent alterations in DNA replication might underlie impaired reprogramming of cohesin-deficient somatic nuclei. We examined the initiation of DNA replication in wild-type and cohesin-deficient pre-B-cell nuclei in heterokaryons with ES cells (Fig.…”

Section: Inefficient Dna Replication In Cohesin-deficient Somatic Nucleimentioning

confidence: 99%

“…Cohesin associates with origins of DNA replication in Xenopus (Gillespie and Hirano 2004;Takahashi et al 2004), Drosophila (MacAlpine et al 2010, and mammalian genomes (Guillou et al 2010), where cohesin affects the spacing of replication origins in cohesin-depleted cells (Guillou et al 2010), the progression of replication forks (Terret et al 2009), and the restart of stalled forks (Tittel-Elmer et al 2012). As a result, altering the dosage or function of cohesin can affect DNA replication (Terret et al 2009;Guillou et al 2010;Tedeschi et al 2013). Similar to the cohesindeficient thymocytes and pre-B cells described here, fibroblasts that have irreversible cohesin binding as a result of Wapl mutations show defects in progression to S phase (Tedeschi et al 2013).…”

Section: Cohesin Myc Dna Replication and Reprogrammingmentioning

confidence: 99%

“…In addition, cohesin has a role in DNA replication (Terret et al 2009;Guillou et al 2010;Tittel-Elmer et al 2012;Tedeschi et al 2013) and contributes to the regulation of gene expression (Dorsett and Merkenschlager 2013) at least in part by forming long-range chromatin interactions (Hadjur et al 2009;Mishiro et al 2009;Nativio et al 2009;Hou et al 2010;Kagey et al 2010;Seitan et al 2011;Apostolou et al 2013;Merkenschlager and Odom 2013;Wei et al 2013;Zhang et al 2013) that contribute to the establishment and maintenance of cell type-specific gene expression patterns (Bickmore and van Steensel 2013;Merkenschlager and Odom 2013).…”

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Initiation and maintenance of pluripotency gene expression in the absence of cohesin

et al. 2015

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Cohesin is implicated in establishing and maintaining pluripotency. Whether this is because of essential cohesin functions in the cell cycle or in gene regulation is unknown. Here we tested cohesin's contribution to reprogramming in systems that reactivate the expression of pluripotency genes in the absence of proliferation (embryonic stem [ES] cell heterokaryons) or DNA replication (nuclear transfer). Contrary to expectations, cohesin depletion enhanced the ability of ES cells to initiate somatic cell reprogramming in heterokaryons. This was explained by increased c-Myc (Myc) expression in cohesin-depleted ES cells, which promoted DNA replicationdependent reprogramming of somatic fusion partners. In contrast, cohesin-depleted somatic cells were poorly reprogrammed in heterokaryons, due in part to defective DNA replication. Pluripotency gene induction was rescued by Myc, which restored DNA replication, and by nuclear transfer, where reprogramming does not require DNA replication. These results redefine cohesin's role in pluripotency and reveal a novel function for Myc in promoting the replication-dependent reprogramming of somatic nuclei.

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Section: Emerging Cohesin Functions In Dna Replicationsupporting

confidence: 61%

Section: Cohesin Myc Dna Replication and Reprogrammingmentioning

confidence: 99%

Section: Inefficient Dna Replication In Cohesin-deficient Somatic Nucleimentioning

confidence: 99%

Section: Cohesin Myc Dna Replication and Reprogrammingmentioning

confidence: 99%

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Initiation and maintenance of pluripotency gene expression in the absence of cohesin

et al. 2015

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DNA Replication Origins

Rodríguez‐Martínez

Méchali

2014

Encyclopedia of Life Sciences

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The onset of genomic DNA synthesis requires precise interactions of specialized initiator proteins with DNA at sites where the replication machinery can be loaded. These sites, defined as replication origins, are found at a few unique locations in all of the prokaryotic chromosomes examined so far. However, replication origins are dispersed among tens of thousands of loci in metazoan chromosomes, thereby raising questions regarding the role of specific nucleotide sequences and chromatin environment in origin selection and the mechanisms used by initiators to recognize replication origins. Close examination of bacterial and archaeal replication origins reveals an array of DNA sequence motifs that position individual initiator protein molecules and promote initiator oligomerization on origin DNA. Conversely, the need for specific recognition sequences in eukaryotic replication origins is relaxed. In fact, the primary rule for origin selection appears to be flexibility, a feature that is modulated either by structural elements or by epigenetic mechanisms at least partly linked to the organization of the genome for gene expression.

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Sister Chromatid Cohesion, Chromosome Instability (CIN) and Diseases

Zhang

Yuen

2020

Encyclopedia of Life Sciences

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To pass on the complete set of genetic information from mother to daughter cells in mitosis, or from parental germ cells to gametes in meiosis, chromosomal deoxyribonucleic acid (DNA) must be accurately replicated and sister chromatids must be held together before they separate in anaphase. Sister chromatid cohesion is a dynamic process that is regulated by the cohesin complex, cell cycle regulation of cohesin ring loading, cohesion establishment, maintenance and dissolution. Cohesion‐related proteins also play additional roles in DNA replication, DNA repair, and gene regulation. Defects in sister chromatid cohesion or cohesion dissolution will lead to aneuploidy and chromosome instability (CIN). Mutations or misregulation of cohesin subunits, or cohesion‐related genes have been implicated in cancers, cohesinopathies, neurological diseases and aneuploid oocytes observed in maternal ageing. Understanding of the pathology of these diseases enables recent development of cohesion genes as biomarkers in prognosis and therapies that target cohesion defects or CIN. Key Concepts Sister chromatid cohesion is an important cell cycle‐regulated process that maintains chromosome stability. Sister chromatid cohesion is established in S phase coupled with DNA replication, maintained in G2/M phase until anaphase onset. Many cohesion‐related proteins also play roles in DNA replication, DNA repair and gene regulation. Mutations or misregulation of cohesin subunits, or cohesion‐related genes have been implicated in cancers, cohesinopathies, neurological diseases and aneuploid oocytes observed in maternal ageing. Cohesion genes can be used as biomarkers in cancer prognosis, and cancer therapies can target tumours with cohesion defects or CIN.

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Cohesin organizes chromatin loops at DNA replication factories

Cited by 208 publications

References 56 publications

Initiation and maintenance of pluripotency gene expression in the absence of cohesin

Initiation and maintenance of pluripotency gene expression in the absence of cohesin

DNA Replication Origins

Sister Chromatid Cohesion, Chromosome Instability (CIN) and Diseases

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