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1

Sapkota, Hem, Emilia Wasiak, John R. Daum, and Gary J. Gorbsky. "Multiple determinants and consequences of cohesion fatigue in mammalian cells." Molecular Biology of the Cell 29, no. 15 (2018): 1811–24. http://dx.doi.org/10.1091/mbc.e18-05-0315.

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Cells delayed in metaphase with intact mitotic spindles undergo cohesion fatigue, where sister chromatids separate asynchronously, while cells remain in mitosis. Cohesion fatigue requires release of sister chromatid cohesion. However, the pathways that breach sister chromatid cohesion during cohesion fatigue remain unknown. Using moderate-salt buffers to remove loosely bound chromatin cohesin, we show that “cohesive” cohesin is not released during chromatid separation during cohesion fatigue. Using a regulated protein heterodimerization system to lock different cohesin ring interfaces at speci
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Mishra, Prashant K., Sultan Ciftci-Yilmaz, David Reynolds, et al. "Polo kinase Cdc5 associates with centromeres to facilitate the removal of centromeric cohesin during mitosis." Molecular Biology of the Cell 27, no. 14 (2016): 2286–300. http://dx.doi.org/10.1091/mbc.e16-01-0004.

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Sister chromatid cohesion is essential for tension-sensing mechanisms that monitor bipolar attachment of replicated chromatids in metaphase. Cohesion is mediated by the association of cohesins along the length of sister chromatid arms. In contrast, centromeric cohesin generates intrastrand cohesion and sister centromeres, while highly cohesin enriched, are separated by >800 nm at metaphase in yeast. Removal of cohesin is necessary for sister chromatid separation during anaphase, and this is regulated by evolutionarily conserved polo-like kinase (Cdc5 in yeast, Plk1 in humans). Here we addre
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3

Oliveira, Raquel A., and Kim Nasmyth. "Getting through anaphase: splitting the sisters and beyond." Biochemical Society Transactions 38, no. 6 (2010): 1639–44. http://dx.doi.org/10.1042/bst0381639.

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Sister-chromatid cohesion, thought to be primarily mediated by the cohesin complex, is essential for chromosome segregation. The forces holding the two sisters resist the tendency of microtubules to prematurely pull sister DNAs apart and thereby prevent random segregation of the genome during mitosis, and consequent aneuploidy. By counteracting the spindle pulling forces, cohesion between the two sisters generates the tension necessary to stabilize microtubule–kinetochore attachments. Upon entry into anaphase, however, the linkages that hold the two sister DNAs must be rapidly destroyed to all
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4

Stanyte, Rugile, Johannes Nuebler, Claudia Blaukopf, et al. "Dynamics of sister chromatid resolution during cell cycle progression." Journal of Cell Biology 217, no. 6 (2018): 1985–2004. http://dx.doi.org/10.1083/jcb.201801157.

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Faithful genome transmission in dividing cells requires that the two copies of each chromosome’s DNA package into separate but physically linked sister chromatids. The linkage between sister chromatids is mediated by cohesin, yet where sister chromatids are linked and how they resolve during cell cycle progression has remained unclear. In this study, we investigated sister chromatid organization in live human cells using dCas9-mEGFP labeling of endogenous genomic loci. We detected substantial sister locus separation during G2 phase irrespective of the proximity to cohesin enrichment sites. Alm
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Chen, Yu-Fan, Chia-Ching Chou, and Marc R. Gartenberg. "Determinants of Sir2-Mediated, Silent Chromatin Cohesion." Molecular and Cellular Biology 36, no. 15 (2016): 2039–50. http://dx.doi.org/10.1128/mcb.00057-16.

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Cohesin associates with distinct sites on chromosomes to mediate sister chromatid cohesion. Single cohesin complexes are thought to bind by encircling both sister chromatids in a topological embrace. Transcriptionally repressed chromosomal domains in the yeastSaccharomyces cerevisiaerepresent specialized sites of cohesion where cohesin binds silent chromatin in a Sir2-dependent fashion. In this study, we investigated the molecular basis for Sir2-mediated cohesion. We identified a cluster of charged surface residues of Sir2, collectively termed the EKDK motif, that are required for cohesin func
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6

van Schie, Janne J. M., and Job de Lange. "The Interplay of Cohesin and the Replisome at Processive and Stressed DNA Replication Forks." Cells 10, no. 12 (2021): 3455. http://dx.doi.org/10.3390/cells10123455.

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The cohesin complex facilitates faithful chromosome segregation by pairing the sister chromatids after DNA replication until mitosis. In addition, cohesin contributes to proficient and error-free DNA replication. Replisome progression and establishment of sister chromatid cohesion are intimately intertwined processes. Here, we review how the key factors in DNA replication and cohesion establishment cooperate in unperturbed conditions and during DNA replication stress. We discuss the detailed molecular mechanisms of cohesin recruitment and the entrapment of replicated sister chromatids at the r
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7

Yan, Rihui, Sharon E. Thomas, Jui-He Tsai, Yukihiro Yamada, and Bruce D. McKee. "SOLO: a meiotic protein required for centromere cohesion, coorientation, and SMC1 localization in Drosophila melanogaster." Journal of Cell Biology 188, no. 3 (2010): 335–49. http://dx.doi.org/10.1083/jcb.200904040.

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Sister chromatid cohesion is essential to maintain stable connections between homologues and sister chromatids during meiosis and to establish correct centromere orientation patterns on the meiosis I and II spindles. However, the meiotic cohesion apparatus in Drosophila melanogaster remains largely uncharacterized. We describe a novel protein, sisters on the loose (SOLO), which is essential for meiotic cohesion in Drosophila. In solo mutants, sister centromeres separate before prometaphase I, disrupting meiosis I centromere orientation and causing nondisjunction of both homologous and sister c
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8

Lee, Janice Y., Aki Hayashi-Hagihara, and Terry L. Orr-Weaver. "Roles and regulation of the Drosophila centromere cohesion protein MEI-S332 family." Philosophical Transactions of the Royal Society B: Biological Sciences 360, no. 1455 (2005): 543–52. http://dx.doi.org/10.1098/rstb.2005.1619.

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In meiosis, a physical attachment, or cohesion, between the centromeres of the sister chromatids is retained until their separation at anaphase II. This cohesion is essential for ensuring accurate segregation of the sister chromatids in meiosis II and avoiding aneuploidy, a condition that can lead to prenatal lethality or birth defects. The Drosophila MEI-S332 protein localizes to centromeres when sister chromatids are attached in mitosis and meiosis, and it is required to maintain cohesion at the centromeres after cohesion along the sister chromatid arms is lost at the metaphase I/anaphase I
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9

Jin, Hui, Vincent Guacci, and Hong-Guo Yu. "Pds5 is required for homologue pairing and inhibits synapsis of sister chromatids during yeast meiosis." Journal of Cell Biology 186, no. 5 (2009): 713–25. http://dx.doi.org/10.1083/jcb.200810107.

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During meiosis, homologues become juxtaposed and synapsed along their entire length. Mutations in the cohesin complex disrupt not only sister chromatid cohesion but also homologue pairing and synaptonemal complex formation. In this study, we report that Pds5, a cohesin-associated protein known to regulate sister chromatid cohesion, is required for homologue pairing and synapsis in budding yeast. Pds5 colocalizes with cohesin along the length of meiotic chromosomes. In the absence of Pds5, the meiotic cohesin subunit Rec8 remains bound to chromosomes with only minor defects in sister chromatid
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10

Boavida, Ana, Diana Santos, Mohammad Mahtab, and Francesca M. Pisani. "Functional Coupling between DNA Replication and Sister Chromatid Cohesion Establishment." International Journal of Molecular Sciences 22, no. 6 (2021): 2810. http://dx.doi.org/10.3390/ijms22062810.

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Several lines of evidence suggest the existence in the eukaryotic cells of a tight, yet largely unexplored, connection between DNA replication and sister chromatid cohesion. Tethering of newly duplicated chromatids is mediated by cohesin, an evolutionarily conserved hetero-tetrameric protein complex that has a ring-like structure and is believed to encircle DNA. Cohesin is loaded onto chromatin in telophase/G1 and converted into a cohesive state during the subsequent S phase, a process known as cohesion establishment. Many studies have revealed that down-regulation of a number of DNA replicati
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11

Revenkova, E., and R. Jessberger. "Keeping sister chromatids together: cohesins in meiosis." Reproduction 130, no. 6 (2005): 783–90. http://dx.doi.org/10.1530/rep.1.00864.

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Meiosis poses unique challenges to chromosome dynamics. Before entry into meiosis, each chromosome is duplicated and gives rise to two sister chromatids linked to each other by cohesion. Production of haploid gametes requires segregation of homologous chromosomes in the first meiotic division and of sister chromatids in the second. To ensure precise distribution of chromosomes to the daughter cells, sister chromatid cohesion (SCC) has to be dissolved in two steps. Maintenance and regulation of SCC is performed by the cohesin protein complex. This short review will primarily focus on the core c
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12

Finardi, Alice, Lucia F. Massari, and Rosella Visintin. "Anaphase Bridges: Not All Natural Fibers Are Healthy." Genes 11, no. 8 (2020): 902. http://dx.doi.org/10.3390/genes11080902.

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At each round of cell division, the DNA must be correctly duplicated and distributed between the two daughter cells to maintain genome identity. In order to achieve proper chromosome replication and segregation, sister chromatids must be recognized as such and kept together until their separation. This process of cohesion is mainly achieved through proteinaceous linkages of cohesin complexes, which are loaded on the sister chromatids as they are generated during S phase. Cohesion between sister chromatids must be fully removed at anaphase to allow chromosome segregation. Other (non-proteinaceo
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13

Shi, Di, Shuaijun Zhao, Mei-Qing Zuo, et al. "The acetyltransferase Eco1 elicits cohesin dimerization during S phase." Journal of Biological Chemistry 295, no. 22 (2020): 7554–65. http://dx.doi.org/10.1074/jbc.ra120.013102.

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Cohesin is a DNA-associated protein complex that forms a tripartite ring controlling sister chromatid cohesion, chromosome segregation and organization, DNA replication, and gene expression. Sister chromatid cohesion is established by the protein acetyltransferase Eco1, which acetylates two conserved lysine residues on the cohesin subunit Smc3 and thereby ensures correct chromatid separation in yeast (Saccharomyces cerevisiae) and other eukaryotes. However, the consequence of Eco1-catalyzed cohesin acetylation is unknown, and the exact nature of the cohesive state of chromatids remains controv
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14

Uchiyama, Susumu, and Kiichi Fukui. "Condensin in Chromatid Cohesion and Segregation." Cytogenetic and Genome Research 147, no. 4 (2015): 212–16. http://dx.doi.org/10.1159/000444868.

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After replication of genomic DNA during the S phase, 2 chromatids hold together longitudinally. When cells enter mitosis, the paired sister chromatids start to condense and then segregate into individual chromatids except for the centromeric region. Upon attachment of microtubules to the kinetochore, subsequent pulling of the 2 sister chromatids by the spindles towards opposite poles results in 2 completely separated chromatids. Besides more than 100 kinds of kinetochore proteins, several key proteins such as cohesin, separase, shugoshin, and condensin contribute to chromatid cohesion and segr
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15

Nasmyth, Kim, and Alexander Schleiffer. "From a single double helix to paired double helices and back." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1441 (2004): 99–108. http://dx.doi.org/10.1098/rstb.2003.1417.

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The propagation of our genomes during cell proliferation depends on the movement of sister DNA molecules produced by DNA replication to opposite sides of the cell before it divides. This feat is achieved by microtubules in eukaryotic cells but it has long remained a mystery how cells ensure that sister DNAs attach to microtubules with opposite orientations, known as amphitelic attachment. It is currently thought that sister chromatid cohesion has a crucial role. By resisting the forces exerted by microtubules, sister chromatid cohesion gives rise to tension that is thought essential for stabil
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16

Henrikus, Sarah S., and Alessandro Costa. "Towards a Structural Mechanism for Sister Chromatid Cohesion Establishment at the Eukaryotic Replication Fork." Biology 10, no. 6 (2021): 466. http://dx.doi.org/10.3390/biology10060466.

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Cohesion between replicated chromosomes is essential for chromatin dynamics and equal segregation of duplicated genetic material. In the G1 phase, the ring-shaped cohesin complex is loaded onto duplex DNA, enriching at replication start sites, or “origins”. During the same phase of the cell cycle, and also at the origin sites, two MCM helicases are loaded as symmetric double hexamers around duplex DNA. During the S phase, and through the action of replication factors, cohesin switches from encircling one parental duplex DNA to topologically enclosing the two duplicated DNA filaments, which are
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17

Nakamura, Akito, Hiroyuki Arai, and Naoya Fujita. "Centrosomal Aki1 and cohesin function in separase-regulated centriole disengagement." Journal of Cell Biology 187, no. 5 (2009): 607–14. http://dx.doi.org/10.1083/jcb.200906019.

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Sister chromatid separation at anaphase is triggered by cleavage of the cohesin subunit Scc1, which is mediated by separase. Centriole disengagement also requires separase. This dual role of separase permits concurrent control of these events for accurate metaphase to anaphase transition. Although the molecular mechanism underlying sister chromatid cohesion has been clarified, that of centriole cohesion is poorly understood. In this study, we show that Akt kinase–interacting protein 1 (Aki1) localizes to centrosomes and regulates centriole cohesion. Aki1 depletion causes formation of multipola
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18

McNally, Karen P., Elizabeth A. Beath, Brennan M. Danlasky, et al. "Cohesin is required for meiotic spindle assembly independent of its role in cohesion in C. elegans." PLOS Genetics 18, no. 10 (2022): e1010136. http://dx.doi.org/10.1371/journal.pgen.1010136.

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Accurate chromosome segregation requires a cohesin-mediated physical attachment between chromosomes that are to be segregated apart, and a bipolar spindle with microtubule plus ends emanating from exactly two poles toward the paired chromosomes. We asked whether the striking bipolar structure of C. elegans meiotic chromosomes is required for bipolarity of acentriolar female meiotic spindles by time-lapse imaging of mutants that lack cohesion between chromosomes. Both a spo-11 rec-8 coh-4 coh-3 quadruple mutant and a spo-11 rec-8 double mutant entered M phase with separated sister chromatids la
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19

Chiroli, Elena, Valentina Rossio, Giovanna Lucchini, and Simonetta Piatti. "The budding yeast PP2ACdc55 protein phosphatase prevents the onset of anaphase in response to morphogenetic defects." Journal of Cell Biology 177, no. 4 (2007): 599–611. http://dx.doi.org/10.1083/jcb.200609088.

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Faithful chromosome transmission requires establishment of sister chromatid cohesion during S phase, followed by its removal at anaphase onset. Sister chromatids are tethered together by cohesin, which is displaced from chromosomes through cleavage of its Mcd1 subunit by the separase protease. Separase is in turn inhibited, up to this moment, by securin. Budding yeast cells respond to morphogenetic defects by a transient arrest in G2 with high securin levels and unseparated chromatids. We show that neither securin elimination nor forced cohesin cleavage is sufficient for anaphase in these cond
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20

Warren, Cheryl D., D. Mark Eckley, Marina S. Lee, et al. "S-Phase Checkpoint Genes Safeguard High-Fidelity Sister Chromatid Cohesion." Molecular Biology of the Cell 15, no. 4 (2004): 1724–35. http://dx.doi.org/10.1091/mbc.e03-09-0637.

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Cohesion establishment and maintenance are carried out by proteins that modify the activity of Cohesin, an essential complex that holds sister chromatids together. Constituents of the replication fork, such as the DNA polymerase α-binding protein Ctf4, contribute to cohesion in ways that are poorly understood. To identify additional cohesion components, we analyzed a ctf4Δ synthetic lethal screen performed on microarrays. We focused on a subset of ctf4Δ-interacting genes with genetic instability of their own. Our analyses revealed that 17 previously studied genes are also necessary for the mai
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Alomer, Reem M., Eulália M. L. da Silva, Jingrong Chen, et al. "Esco1 and Esco2 regulate distinct cohesin functions during cell cycle progression." Proceedings of the National Academy of Sciences 114, no. 37 (2017): 9906–11. http://dx.doi.org/10.1073/pnas.1708291114.

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Sister chromatids are tethered together by the cohesin complex from the time they are made until their separation at anaphase. The ability of cohesin to tether sister chromatids together depends on acetylation of its Smc3 subunit by members of the Eco1 family of cohesin acetyltransferases. Vertebrates express two orthologs of Eco1, called Esco1 and Esco2, both of which are capable of modifying Smc3, but their relative contributions to sister chromatid cohesion are unknown. We therefore set out to determine the precise contributions of Esco1 and Esco2 to cohesion in vertebrate cells. Here we sh
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Bender, Dawn, Eulália Maria Lima Da Silva, Jingrong Chen, et al. "Multivalent interaction of ESCO2 with the replication machinery is required for sister chromatid cohesion in vertebrates." Proceedings of the National Academy of Sciences 117, no. 2 (2019): 1081–89. http://dx.doi.org/10.1073/pnas.1911936117.

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The tethering together of sister chromatids by the cohesin complex ensures their accurate alignment and segregation during cell division. In vertebrates, sister chromatid cohesion requires the activity of the ESCO2 acetyltransferase, which modifies the Smc3 subunit of cohesin. It was shown recently that ESCO2 promotes cohesion through interaction with the MCM replicative helicase. However, ESCO2 does not significantly colocalize with the MCM complex, suggesting there are additional interactions important for ESCO2 function. Here we show that ESCO2 is recruited to replication factories, sites o
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Suja, J. A., C. Antonio, A. Debec, and J. S. Rufas. "Phosphorylated proteins are involved in sister-chromatid arm cohesion during meiosis I." Journal of Cell Science 112, no. 17 (1999): 2957–69. http://dx.doi.org/10.1242/jcs.112.17.2957.

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Sister-chromatid arm cohesion is lost during the metaphase I/anaphase I transition to allow homologue separation. To obtain needed information on this process we have analysed in grasshopper bivalents the sequential release of arm cohesion in relation to the behaviour of chromatid axes. Results show that sister axes are associated during early metaphase I but separate during late metaphase I leading to a concomitant change of chromosome structure that implies the loss of sister-kinetochore cohesion. Afterwards, homologues initiate their separation asynchronously depending on their size, and nu
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Morrison, C., P. Vagnarelli, E. Sonoda, S. Takeda, and W. C. Earnshaw. "Sister chromatid cohesion and genome stability in vertebrate cells." Biochemical Society Transactions 31, no. 1 (2003): 263–65. http://dx.doi.org/10.1042/bst0310263.

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For successful eukaryotic mitosis, sister chromatid pairs remain linked after replication until their kinetochores have been attached to opposite spindle poles by microtubules. This linkage is broken at the metaphase–anaphase transition and the sisters separate. In budding yeast, this sister chromatid cohesion requires a multi-protein complex called cohesin. A key component of cohesin is Scc1/Mcd1 (Rad21 in fission yeast). Disruption of the chicken orthologue of Scc1 by gene targeting in DT40 cells causes premature sister chromatid separation. Cohesion between sister chromatids is likely to pr
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McNicoll, François, Anne Kühnel, Uddipta Biswas, et al. "Meiotic sex chromosome cohesion and autosomal synapsis are supported by Esco2." Life Science Alliance 3, no. 3 (2020): e201900564. http://dx.doi.org/10.26508/lsa.201900564.

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In mitotic cells, establishment of sister chromatid cohesion requires acetylation of the cohesin subunit SMC3 (acSMC3) by ESCO1 and/or ESCO2. Meiotic cohesin plays additional but poorly understood roles in the formation of chromosome axial elements (AEs) and synaptonemal complexes. Here, we show that levels of ESCO2, acSMC3, and the pro-cohesion factor sororin increase on meiotic chromosomes as homologs synapse. These proteins are less abundant on the largely unsynapsed sex chromosomes, whose sister chromatid cohesion appears weaker throughout the meiotic prophase. Using three distinct conditi
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Eng, Thomas, Vincent Guacci, and Douglas Koshland. "Interallelic complementation provides functional evidence for cohesin–cohesin interactions on DNA." Molecular Biology of the Cell 26, no. 23 (2015): 4224–35. http://dx.doi.org/10.1091/mbc.e15-06-0331.

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The cohesin complex (Mcd1p, Smc1p, Smc3p, and Scc3p) has multiple roles in chromosome architecture, such as promoting sister chromatid cohesion, chromosome condensation, DNA repair, and transcriptional regulation. The prevailing embrace model for sister chromatid cohesion posits that a single cohesin complex entraps both sister chromatids. We report interallelic complementation between pairs of nonfunctional mcd1 alleles (mcd1-1 and mcd1-Q266) or smc3 alleles (smc3-42 and smc3-K113R). Cells bearing individual mcd1 or smc3 mutant alleles are inviable and defective for both sister chromatid cohe
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Guacci, Vincent, and Douglas Koshland. "Cohesin-independent segregation of sister chromatids in budding yeast." Molecular Biology of the Cell 23, no. 4 (2012): 729–39. http://dx.doi.org/10.1091/mbc.e11-08-0696.

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Cohesin generates cohesion between sister chromatids, which enables chromosomes to form bipolar attachments to the mitotic spindle and segregate. Cohesin also functions in chromosome condensation, transcriptional regulation, and DNA damage repair. Here we analyze the role of acetylation in modulating cohesin functions and how it affects budding yeast viability. Previous studies show that cohesion establishment requires Eco1p-mediated acetylation of the cohesin subunit Smc3p at residue K113. Smc3p acetylation was proposed to promote establishment by merely relieving Wpl1p inhibition because del
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Canudas, Silvia, and Susan Smith. "Differential regulation of telomere and centromere cohesion by the Scc3 homologues SA1 and SA2, respectively, in human cells." Journal of Cell Biology 187, no. 2 (2009): 165–73. http://dx.doi.org/10.1083/jcb.200903096.

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Replicated sister chromatids are held together until mitosis by cohesin, a conserved multisubunit complex comprised of Smc1, Smc3, Scc1, and Scc3, which in vertebrate cells exists as two closely related homologues (SA1 and SA2). Here, we show that cohesinSA1 and cohesinSA2 are differentially required for telomere and centromere cohesion, respectively. Cells deficient in SA1 are unable to establish or maintain cohesion between sister telomeres after DNA replication in S phase. The same phenotype is observed upon depletion of the telomeric protein TIN2. In contrast, in SA2-depleted cells telomer
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Balicky, Eric M., Matthew W. Endres, Cary Lai, and Sharon E. Bickel. "Meiotic Cohesion Requires Accumulation of ORD on Chromosomes before Condensation." Molecular Biology of the Cell 13, no. 11 (2002): 3890–900. http://dx.doi.org/10.1091/mbc.e02-06-0332.

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Cohesion between sister chromatids is a prerequisite for accurate chromosome segregation during mitosis and meiosis. To allow chromosome condensation during prophase, the connections that hold sister chromatids together must be maintained but still permit extensive chromatin compaction. In Drosophila, null mutations in the orientation disruptor (ord) gene lead to meiotic nondisjunction in males and females because cohesion is absent by the time that sister kinetochores make stable microtubule attachments. We provide evidence that ORD is concentrated within the extrachromosomal domains of the n
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Nasmyth, Kim. "How might cohesin hold sister chromatids together?" Philosophical Transactions of the Royal Society B: Biological Sciences 360, no. 1455 (2005): 483–96. http://dx.doi.org/10.1098/rstb.2004.1604.

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The sister chromatid cohesion essential for the bi-orientation of chromosomes on mitotic spindles depends on a multi-subunit complex called cohesin. This paper reviews the evidence that cohesin is directly responsible for holding sister DNAs together and considers how it might perform this function in the light of recent data on its structure.
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Kateneva, Anna V., Anton A. Konovchenko, Vincent Guacci, and Michael E. Dresser. "Recombination protein Tid1p controls resolution of cohesin-dependent linkages in meiosis in Saccharomyces cerevisiae." Journal of Cell Biology 171, no. 2 (2005): 241–53. http://dx.doi.org/10.1083/jcb.200505020.

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Sister chromatid cohesion and interhomologue recombination are coordinated to promote the segregation of homologous chromosomes instead of sister chromatids at the first meiotic division. During meiotic prophase in Saccharomyces cerevisiae, the meiosis-specific cohesin Rec8p localizes along chromosome axes and mediates most of the cohesion. The mitotic cohesin Mcd1p/Scc1p localizes to discrete spots along chromosome arms, and its function is not clear. In cells lacking Tid1p, which is a member of the SWI2/SNF2 family of helicase-like proteins that are involved in chromatin remodeling, Mcd1p an
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32

Galander, Stefan, Rachael E. Barton, David A. Kelly, and Adèle L. Marston. "Spo13 prevents premature cohesin cleavage during meiosis." Wellcome Open Research 4 (September 2, 2019): 29. http://dx.doi.org/10.12688/wellcomeopenres.15066.2.

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Background: Meiosis produces gametes through two successive nuclear divisions, meiosis I and meiosis II. In contrast to mitosis and meiosis II, where sister chromatids are segregated, during meiosis I, homologous chromosomes are segregated. This requires the monopolar attachment of sister kinetochores and the loss of cohesion from chromosome arms, but not centromeres, during meiosis I. The establishment of both sister kinetochore mono-orientation and cohesion protection rely on the budding yeast meiosis I-specific Spo13 protein, the functional homolog of fission yeast Moa1 and mouse MEIKIN. Me
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Lin, Weiqiang, Hui Jin, Xiuwen Liu, Kristin Hampton, and Hong-Guo Yu. "Scc2 regulates gene expression by recruiting cohesin to the chromosome as a transcriptional activator during yeast meiosis." Molecular Biology of the Cell 22, no. 12 (2011): 1985–96. http://dx.doi.org/10.1091/mbc.e10-06-0545.

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To tether sister chromatids, a protein-loading complex, including Scc2, recruits cohesin to the chromosome at discrete loci. Cohesin facilitates the formation of a higher-order chromosome structure that could also influence gene expression. How cohesin directly regulates transcription remains to be further elucidated. We report that in budding yeast Scc2 is required for sister-chromatid cohesion during meiosis for two reasons. First, Scc2 is required for activating the expression of REC8, which encodes a meiosis-specific cohesin subunit; second, Scc2 is necessary for recruiting meiotic cohesin
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34

Galander, Stefan, Rachael E. Barton, David A. Kelly, and Adèle L. Marston. "Spo13 prevents premature cohesin cleavage during meiosis." Wellcome Open Research 4 (February 13, 2019): 29. http://dx.doi.org/10.12688/wellcomeopenres.15066.1.

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Background: Meiosis produces gametes through two successive nuclear divisions, meiosis I and meiosis II. In contrast to mitosis and meiosis II, where sister chromatids are segregated, during meiosis I, homologous chromosomes are segregated. This requires the monopolar attachment of sister kinetochores and the loss of cohesion from chromosome arms, but not centromeres, during meiosis I. The establishment of both sister kinetochore mono-orientation and cohesin protection rely on the budding yeast meiosis I-specific Spo13 protein, the functional homolog of fission yeast Moa1 and mouse MEIKIN. Met
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Konecna, Marketa, Soodabeh Abbasi Sani, and Martin Anger. "Separase and Roads to Disengage Sister Chromatids during Anaphase." International Journal of Molecular Sciences 24, no. 5 (2023): 4604. http://dx.doi.org/10.3390/ijms24054604.

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Receiving complete and undamaged genetic information is vital for the survival of daughter cells after chromosome segregation. The most critical steps in this process are accurate DNA replication during S phase and a faithful chromosome segregation during anaphase. Any errors in DNA replication or chromosome segregation have dire consequences, since cells arising after division might have either changed or incomplete genetic information. Accurate chromosome segregation during anaphase requires a protein complex called cohesin, which holds together sister chromatids. This complex unifies sister
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36

Miyazaki, W. Y., and T. L. Orr-Weaver. "Sister-chromatid misbehavior in Drosophila ord mutants." Genetics 132, no. 4 (1992): 1047–61. http://dx.doi.org/10.1093/genetics/132.4.1047.

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Abstract In Drosophila males and females mutant for the ord gene, sister chromatids prematurely disjoin in meiosis. We have isolated five new alleles of ord and analyzed them both as homozygotes and in trans to deficiencies for the locus, and we show that ord function is necessary early in meiosis of both sexes. Strong ord alleles result in chromosome nondisjunction in meiosis I that appears to be the consequence of precocious separation of the sister chromatids followed by their random segregation. Cytological analysis in males confirmed that precocious disjunction of the sister chromatids oc
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37

Meadows, John C., and Jonathan B. A. Millar. "Sharpening the anaphase switch." Biochemical Society Transactions 43, no. 1 (2015): 19–22. http://dx.doi.org/10.1042/bst20140250.

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The segregation of sister chromatids during mitosis is one of the most easily visualized, yet most remarkable, events during the life cycle of a cell. The accuracy of this process is essential to maintain ploidy during cell duplication. Over the past 20 years, substantial progress has been made in identifying components of both the kinetochore and the mitotic spindle that generate the force to move mitotic chromosomes. Additionally, we now have a reasonable, albeit incomplete, understanding of the molecular and biochemical events that are involved in establishing and dissolving sister-chromati
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38

Zhang, Nenggang, Sergey G. Kuznetsov, Shyam K. Sharan, Kaiyi Li, Pulivarthi H. Rao, and Debananda Pati. "A handcuff model for the cohesin complex." Journal of Cell Biology 183, no. 6 (2008): 1019–31. http://dx.doi.org/10.1083/jcb.200801157.

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The cohesin complex is responsible for the accurate separation of sister chromatids into two daughter cells. Several models for the cohesin complex have been proposed, but the one-ring embrace model currently predominates the field. However, the static configuration of the embrace model is not flexible enough for cohesins to perform their functions during DNA replication, transcription, and DNA repair. We used coimmunoprecipitation, a protein fragment complement assay, and a yeast two-hybrid assay to analyze the protein–protein interactions among cohesin subunits. The results show that three o
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39

Eijpe, Maureen, Hildo Offenberg, Rolf Jessberger, Ekaterina Revenkova та Christa Heyting. "Meiotic cohesin REC8 marks the axial elements of rat synaptonemal complexes before cohesins SMC1β and SMC3". Journal of Cell Biology 160, № 5 (2003): 657–70. http://dx.doi.org/10.1083/jcb.200212080.

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In meiotic prophase, the sister chromatids of each chromosome develop a common axial element (AE) that is integrated into the synaptonemal complex (SC). We analyzed the incorporation of sister chromatid cohesion proteins (cohesins) and other AE components into AEs. Meiotic cohesin REC8 appeared shortly before premeiotic S phase in the nucleus and formed AE-like structures (REC8-AEs) from premeiotic S phase on. Subsequently, meiotic cohesin SMC1β, cohesin SMC3, and AE proteins SCP2 and SCP3 formed dots along REC8-AEs, which extended and fused until they lined REC8-AEs along their length. In met
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Landeira, David, Jean-Mathieu Bart, Daria Van Tyne, and Miguel Navarro. "Cohesin regulates VSG monoallelic expression in trypanosomes." Journal of Cell Biology 186, no. 2 (2009): 243–54. http://dx.doi.org/10.1083/jcb.200902119.

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Antigenic variation allows Trypanosoma brucei to evade the host immune response by switching the expression of 1 out of ∼15 telomeric variant surface glycoprotein (VSG) expression sites (ESs). VSG ES transcription is mediated by RNA polymerase I in a discrete nuclear site named the ES body (ESB). However, nothing is known about how the monoallelic VSG ES transcriptional state is maintained over generations. In this study, we show that during S and G2 phases and early mitosis, the active VSG ES locus remains associated with the single ESB and exhibits a delay in the separation of sister chromat
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41

Severin, Fedor, Anthony A. Hyman, and Simonetta Piatti. "Correct spindle elongation at the metaphase/anaphase transition is an APC-dependent event in budding yeast." Journal of Cell Biology 155, no. 5 (2001): 711–18. http://dx.doi.org/10.1083/jcb.200104096.

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At the metaphase to anaphase transition, chromosome segregation is initiated by the splitting of sister chromatids. Subsequently, spindles elongate, separating the sister chromosomes into two sets. Here, we investigate the cell cycle requirements for spindle elongation in budding yeast using mutants affecting sister chromatid cohesion or DNA replication. We show that separation of sister chromatids is not sufficient for proper spindle integrity during elongation. Rather, successful spindle elongation and stability require both sister chromatid separation and anaphase-promoting complex activati
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42

Rieder, C. L., and R. Cole. "Chromatid cohesion during mitosis: lessons from meiosis." Journal of Cell Science 112, no. 16 (1999): 2607–13. http://dx.doi.org/10.1242/jcs.112.16.2607.

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The equal distribution of chromosomes during mitosis and meiosis is dependent on the maintenance of sister chromatid cohesion. In this commentary we review the evidence that, during meiosis, the mechanism underlying the cohesion of chromatids along their arms is different from that responsible for cohesion in the centromere region. We then argue that the chromatids on a mitotic chromosome are also tethered along their arms and in the centromere by different mechanisms, and that the functional action of these two mechanisms can be temporally separated under various conditions. Finally, we demon
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43

Gartenberg, Marc. "Heterochromatin and the cohesion of sister chromatids." Chromosome Research 17, no. 2 (2009): 229–38. http://dx.doi.org/10.1007/s10577-008-9012-z.

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44

Kerrebrock, A. W., W. Y. Miyazaki, D. Birnby, and T. L. Orr-Weaver. "The Drosophila mei-S332 gene promotes sister-chromatid cohesion in meiosis following kinetochore differentiation." Genetics 130, no. 4 (1992): 827–41. http://dx.doi.org/10.1093/genetics/130.4.827.

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Abstract The Drosophila mei-S332 gene acts to maintain sister-chromatid cohesion before anaphase II of meiosis in both males and females. By isolating and analyzing seven new alleles and a deficiency uncovering the mei-S332 gene we have demonstrated that the onset of the requirement for mei-S332 is not until late anaphase I. All of our alleles result primarily in equational (meiosis II) nondisjunction with low amounts of reductional (meiosis I) nondisjunction. Cytological analysis revealed that sister chromatids frequently separate in late anaphase I in these mutants. Since the sister chromati
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Rogers, Eric, John D. Bishop, James A. Waddle, Jill M. Schumacher, and Rueyling Lin. "The aurora kinase AIR-2 functions in the release of chromosome cohesion in Caenorhabditis elegans meiosis." Journal of Cell Biology 157, no. 2 (2002): 219–29. http://dx.doi.org/10.1083/jcb.200110045.

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Accurate chromosome segregation during cell division requires not only the establishment, but also the precise, regulated release of chromosome cohesion. Chromosome dynamics during meiosis are more complicated, because homologues separate at anaphase I whereas sister chromatids remain attached until anaphase II. How the selective release of chromosome cohesion is regulated during meiosis remains unclear. We show that the aurora-B kinase AIR-2 regulates the selective release of chromosome cohesion during Caenorhabditis elegans meiosis. AIR-2 localizes to subchromosomal regions corresponding to
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46

Pinto, Belinda S., and Terry L. Orr-Weaver. "Drosophila protein phosphatases 2A B′ Wdb and Wrd regulate meiotic centromere localization and function of the MEI-S332 Shugoshin." Proceedings of the National Academy of Sciences 114, no. 49 (2017): 12988–93. http://dx.doi.org/10.1073/pnas.1718450114.

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Proper segregation of chromosomes in meiosis is essential to prevent miscarriages and birth defects. This requires that sister chromatids maintain cohesion at the centromere as cohesion is released on the chromatid arms when the homologs segregate at anaphase I. The Shugoshin proteins preserve centromere cohesion by protecting the cohesin complex from cleavage, and this has been shown in yeasts to be mediated by recruitment of the protein phosphatase 2A B′ (PP2A B′). In metazoans, delineation of the role of PP2A B′ in meiosis has been hindered by its myriad of other essential roles. The Drosop
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Hsiao, Susan J., and Susan Smith. "Sister telomeres rendered dysfunctional by persistent cohesion are fused by NHEJ." Journal of Cell Biology 184, no. 4 (2009): 515–26. http://dx.doi.org/10.1083/jcb.200810132.

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Telomeres protect chromosome ends from being viewed as double-strand breaks and from eliciting a DNA damage response. Deprotection of chromosome ends occurs when telomeres become critically short because of replicative attrition or inhibition of TRF2. In this study, we report a novel form of deprotection that occurs exclusively after DNA replication in S/G2 phase of the cell cycle. In cells deficient in the telomeric poly(adenosine diphosphate ribose) polymerase tankyrase 1, sister telomere resolution is blocked. Unexpectedly, cohered sister telomeres become deprotected and are inappropriately
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48

Sumara, Izabela, Elisabeth Vorlaufer, Christian Gieffers, Beate H. Peters, and Jan-Michael Peters. "Characterization of Vertebrate Cohesin Complexes and Their Regulation in Prophase." Journal of Cell Biology 151, no. 4 (2000): 749–62. http://dx.doi.org/10.1083/jcb.151.4.749.

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In eukaryotes, sister chromatids remain connected from the time of their synthesis until they are separated in anaphase. This cohesion depends on a complex of proteins called cohesins. In budding yeast, the anaphase-promoting complex (APC) pathway initiates anaphase by removing cohesins from chromosomes. In vertebrates, cohesins dissociate from chromosomes already in prophase. To study their mitotic regulation we have purified two 14S cohesin complexes from human cells. Both complexes contain SMC1, SMC3, SCC1, and either one of the yeast Scc3p orthologs SA1 and SA2. SA1 is also a subunit of 14
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Rankin, Susannah, and Dean S. Dawson. "Recent advances in cohesin biology." F1000Research 5 (August 3, 2016): 1909. http://dx.doi.org/10.12688/f1000research.8881.1.

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Sister chromatids are tethered together from the time they are formed in S-phase until they separate at anaphase. A protein complex called cohesin is responsible for holding the sister chromatids together and serves important roles in chromosome condensation, gene regulation, and the repair of DNA damage. Cohesin contains an open central pore and becomes topologically engaged with its DNA substrates. Entrapped DNA can be released either by the opening of a gate in the cohesin ring or by proteolytic cleavage of a component of the ring. This review summarizes recent research that provides import
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Donnellan, Leigh, Clifford Young, Bradley S. Simpson, et al. "Methylglyoxal Impairs Sister Chromatid Separation in Lymphocytes." International Journal of Molecular Sciences 23, no. 8 (2022): 4139. http://dx.doi.org/10.3390/ijms23084139.

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The accurate segregation of sister chromatids is complex, and errors that arise throughout this process can drive chromosomal instability and tumorigenesis. We recently showed that methylglyoxal (MGO), a glycolytic by-product, can cause chromosome missegregation events in lymphocytes. However, the underlying mechanisms of this were not explored. Therefore, in this study, we utilised shotgun proteomics to identify MGO-modified proteins, and label-free quantitation to measure changes in protein abundance following exposure to MGO. We identified numerous mitotic proteins that were modified by MGO
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