scholarly journals Keeping sister chromatids together: cohesins in meiosis

Reproduction ◽  
2005 ◽  
Vol 130 (6) ◽  
pp. 783-790 ◽  
Author(s):  
E Revenkova ◽  
R Jessberger
Keyword(s):  
Sister Chromatid ◽  
Short Review ◽  
Interacting Proteins ◽  
Homologous Chromosomes ◽  
Chromosome Dynamics ◽  
Daughter Cells ◽  
The Core ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Precise Distribution

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 cohesin proteins before venturing into adjacent territories with an emphasis on interacting proteins and complexes. It will also concentrate on mammalian meiosis and only occasionally discuss cohesion in other organisms.

Centromere Mapping Functions for Aneuploid Meiotic Products: Analysis of rec8, rec10 and rec11 Mutants of the Fission Yeast Schizosaccharomyces pombe

Genetics ◽  
1999 ◽  
Vol 153 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Michelle D Krawchuk ◽  
Wayne P Wahls
Keyword(s):  
Fission Yeast ◽  
Chromosome Segregation ◽  
Sister Chromatid ◽  
Meiotic Division ◽  
Homologous Chromosomes ◽  
Mapping Functions ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Products Analysis ◽  
Meiosis I

AbstractRecent evidence suggests that the position of reciprocal recombination events (crossovers) is important for the segregation of homologous chromosomes during meiosis I and sister chromatids during meiosis II. We developed genetic mapping functions that permit the simultaneous analysis of centromere-proximal crossover recombination and the type of segregation error leading to aneuploidy. The mapping functions were tested in a study of the rec8, rec10, and rec11 mutants of fission yeast. In each mutant we monitored each of the three chromosome pairs. Between 38 and 100% of the chromosome segregation errors in the rec8 mutants were due to meiosis I nondisjunction of homologous chromosomes. The remaining segregation errors were likely the result of precocious separation of sister chromatids, a previously described defect in the rec8 mutants. Between 47 and 100% of segregation errors in the rec10 and rec11 mutants were due to nondisjunction of sister chromatids during meiosis II. In addition, centromere-proximal recombination was reduced as much as 14-fold or more on chromosomes that had experienced nondisjunction. These results demonstrate the utility of the new mapping functions and support models in which sister chromatid cohesion and crossover position are important determinants for proper chromosome segregation in each meiotic division.

scholarly journals SWITCH 1/DYAD is a novel WINGS APART-LIKE antagonist that maintains sister chromatid cohesion in meiosis

2019 ◽  
Author(s):  
Chao Yang ◽  
Yuki Hamamura ◽  
Kostika Sofroni ◽  
Franziska Böwer ◽  
Sara Christina Stolze ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Cohesion ◽  
Daughter Cells ◽  
Anaphase Onset ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Proteolytic Action ◽  
Mitosis And Meiosis ◽  
Sequence Similarities ◽  
Early Mitosis

Mitosis and meiosis both rely on cohesin, which embraces the sister chromatids and plays a crucial role for the faithful distribution of chromosomes to daughter cells. Prior to the cleavage by Separase at anaphase onset, cohesin is largely removed from chromosomes by the non-proteolytic action of WINGS APART-LIKE (WAPL), a mechanism referred to as the prophase pathway. To prevent the premature loss of sister chromatid cohesion, WAPL is inhibited in early mitosis by Sororin. However, Sororin homologs have only been found to function as WAPL inhibitors during mitosis in vertebrates and Drosophila. Here we show that SWITCH 1/DYAD defines a novel WAPL antagonist that acts in meiosis of Arabidopsis. Crucially, SWI1 becomes dispensable for sister chromatid cohesion in the absence of WAPL. Despite the lack of any sequence similarities, we found that SWI1 is regulated and functions in a similar manner as Sororin hence likely representing a case of convergent molecular evolution across the eukaryotic kingdom.

scholarly journals SOLO: a meiotic protein required for centromere cohesion, coorientation, and SMC1 localization in Drosophila melanogaster

2010 ◽  
Vol 188 (3) ◽  
pp. 335-349 ◽  
Author(s):  
Rihui Yan ◽  
Sharon E. Thomas ◽  
Jui-He Tsai ◽  
Yukihiro Yamada ◽  
Bruce D. McKee
Keyword(s):  
Drosophila Melanogaster ◽  
Sister Chromatid ◽  
Sister Chromatid Cohesion ◽  
Early Prophase ◽  
Wild Type ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Mutant Phenotypes ◽  
Meiosis I ◽  
Novel Protein

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 chromatids. Centromeric foci of the cohesin protein SMC1 are absent in solo mutants at all meiotic stages. SOLO and SMC1 colocalize to meiotic centromeres from early prophase I until anaphase II in wild-type males, but both proteins disappear prematurely at anaphase I in mutants for mei-S332, which encodes the Drosophila homologue of the cohesin protector protein shugoshin. The solo mutant phenotypes and the localization patterns of SOLO and SMC1 indicate that they function together to maintain sister chromatid cohesion in Drosophila meiosis.

scholarly journals Meiotic cohesin REC8 marks the axial elements of rat synaptonemal complexes before cohesins SMC1β and SMC3

2003 ◽  
Vol 160 (5) ◽  
pp. 657-670 ◽  
Author(s):  
Maureen Eijpe ◽  
Hildo Offenberg ◽  
Rolf Jessberger ◽  
Ekaterina Revenkova ◽  
Christa Heyting
Keyword(s):  
Synaptonemal Complex ◽  
Sister Chromatid ◽  
Meiotic Prophase ◽  
S Phase ◽  
Synaptonemal Complexes ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Axial Element ◽  
Striking Contrast ◽  
Metaphase I

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 metaphase I, SMC1β, SMC3, SCP2, and SCP3 disappeared from the chromosome arms and accumulated around the centromeres, where they stayed until anaphase II. In striking contrast, REC8 persisted along the chromosome arms until anaphase I and near the centromeres until anaphase II. We propose that REC8 provides a basis for AE formation and that the first steps in AE assembly do not require SMC1β, SMC3, SCP2, and SCP3. Furthermore, SMC1β, SMC3, SCP2, and SCP3 cannot provide arm cohesion during metaphase I. We propose that REC8 then provides cohesion. RAD51 and/or DMC1 coimmunoprecipitates with REC8, suggesting that REC8 may also provide a basis for assembly of recombination complexes.

scholarly journals Chromosome interaction over a distance in meiosis

2015 ◽  
Vol 2 (2) ◽  
pp. 150029 ◽  
Author(s):  
Mary Brady ◽  
Leocadia V. Paliulis
Keyword(s):  
Cell Division ◽  
Sex Chromosomes ◽  
Sister Chromatid ◽  
Daughter Cell ◽  
Sister Chromatid Cohesion ◽  
Sister Chromatids ◽  
Physical Connection ◽  
Chromatid Cohesion ◽  
Different Types ◽  
Random Segregation

The challenge of cell division is to distribute partner chromosomes (pairs of homologues, pairs of sex chromosomes or pairs of sister chromatids) correctly, one into each daughter cell. In the ‘standard’ meiosis, this problem is solved by linking partners together via a chiasma and/or sister chromatid cohesion, and then separating the linked partners from one another in anaphase; thus, the partners are kept track of, and correctly distributed. Many organisms, however, properly separate chromosomes in the absence of any obvious physical connection, and movements of unconnected partner chromosomes are coordinated at a distance. Meiotic distance interactions happen in many different ways and in different types of organisms. In this review, we discuss several different known types of distance segregation and propose possible explanations for non-random segregation of distance-segregating chromosomes.

scholarly journals A conserved activity for cohesin in bridging DNA molecules

2019 ◽  
Author(s):  
Pilar Gutierrez-Escribano ◽  
Matthew D. Newton ◽  
Aida Llauró ◽  
Jonas Huber ◽  
Loredana Tanasie ◽  
...  
Keyword(s):  
Single Molecule ◽  
Sister Chromatid ◽  
Regulation Of Gene Expression ◽  
Sister Chromatid Cohesion ◽  
Dna Molecules ◽  
Chromosome Architecture ◽  
Physiological Conditions ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Core Activity

AbstractEssential processes such as accurate chromosome segregation, regulation of gene expression and DNA repair rely on protein-mediated DNA tethering. Sister chromatid cohesion requires the SMC complex cohesin to act as a protein linker that holds replicated chromatids together (1, 2). The molecular mechanism by which cohesins hold sister chromatids has remained controversial. Here, we used a single molecule approach to visualise the activity of cohesin complexes as they hold DNA molecules. We describe a DNA bridging activity that requires ATP and is conserved from yeast to human cohesin. We show that cohesin can form two distinct classes of bridges at physiological conditions, a “permanent bridge” able to resists high force (over 80pN) and a “reversible bridge” that breaks at lower forces (5-40pN). Both classes of bridges require Scc2/Scc4 in addition to ATP. We demonstrate that bridge formation requires physical proximity of the DNA segments to be tethered and show that “permanent” cohesin bridges can move between two DNA molecules but cannot be removed from DNA when they occur in cis. This suggests that separate physical compartments in cohesin molecules are involved in the bridge. Finally, we show that cohesin tetramers, unlike condensin, cannot compact linear DNA molecules against low force, demonstrating that the core activity of cohesin tetramers is bridging DNA rather than compacting it. Our findings carry important implications for the understanding of the basic mechanisms behind cohesin-dependent establishment of sister chromatid cohesion and chromosome architecture.

scholarly journals Cohesin and microtubule dependent mechanisms regulate sister centromere fusion during meiosis I

2019 ◽  
Author(s):  
Lin-Ing Wang ◽  
Arunika Das ◽  
Kim S. McKim
Keyword(s):  
Protein Phosphatase ◽  
Protein Phosphatase 1 ◽  
Kinetochore Protein ◽  
Homologous Chromosomes ◽  
The Core ◽  
Sister Chromatids ◽  
Different Populations ◽  
Sister Centromere ◽  
Meiosis I

AbstractSister centromere fusion is a process unique to meiosis that promotes co-orientation of the sister kinetochores, ensuring they attach to microtubules from the same pole. We have found that the kinetochore protein SPC105R/KNL1 and Protein Phosphatase 1 (PP1-87B) are required for this process. The analysis of these two proteins, however, has shown that two independent mechanisms maintain sister centromere fusion during meiosis I in Drosophila oocytes. Double depletion experiments demonstrated that the precocious separation of centromeres in Spc105R RNAi oocytes is Separase-dependent, suggesting cohesin proteins must be maintained at the core centromeres. In contrast, precocious sister centromere separation in Pp1-87B RNAi oocytes does not depend on Separase or Wapl. Further analysis with microtubule destabilizing drugs showed that PP1-87B maintains sister centromeres fusion by regulating microtubule dynamics. Additional double depletion experiments demonstrated that PP1-87B has this function by antagonizing Polo kinase and BubR1, two proteins known to promote kinetochore-microtubule (KT-MT) attachments. These results suggest that PP1-87B maintains sister centromere fusion by inhibiting stable KT-MT attachments. Surprisingly, we found that loss of C(3)G, the transverse element of the synaptonemal complex (SC), suppresses centromere separation in Pp1-87B RNAi oocytes. This is evidence for a functional role of centromeric SC in the meiotic divisions. We propose two mechanisms maintain co-orientation in Drosophila oocytes: one involves SPC105R to protect cohesins at sister centromeres and another involves PP1-87B to regulate spindle forces at end-on attachments.Author SummaryMeiosis involves two cell divisions. In the first division, pairs of homologous chromosomes segregate, in the second division, the sister chromatids segregate. These patterns of division are mediated by regulating microtubule attachments to the kinetochores and stepwise release of cohesion between the sister chromatids. During meiosis I, cohesion fusing sister centromeres must be intact so they attach to microtubules from the same pole. At the same time, arm cohesion must be released for anaphase I. Upon entry into meiosis II, the sister centromeres must separate to allow attachment to opposite poles, while cohesion surrounding the centromeres must remain intact until anaphase II. How these different populations of cohesion are regulated is not understood. We identified two genes required for maintaining sister centromere cohesion, and surprisingly found they define two distinct mechanisms. The first is a kinetochore protein that maintains sister centromere fusion by recruiting proteins that protect cohesion. The second is a phosphatase that antagonizes proteins that stabilize microtubule attachments. We propose that entry into meiosis II coincides with stabilization of microtubule attachments, resulting in the separation of sister centromeres without disrupting cohesion in other regions, facilitating attachment of sister chromatids to opposite poles.

scholarly journals Quantitative Cytogenetics Reveals Molecular Stoichiometry and Longitudinal Organization of Meiotic Chromosome Axes and Loops

2019 ◽  
Author(s):  
Alexander Woglar ◽  
Kei Yamaya ◽  
Baptiste Roelens ◽  
Alistair Boettiger ◽  
Simone Köhler ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
De Novo ◽  
Meiotic Chromosome ◽  
S Phase ◽  
C Elegans ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Molecular Bases ◽  
Chromosome Axis ◽  
Specialized Organization

ABSTRACTDuring meiosis, chromosomes adopt a specialized organization involving assembly of a cohesin-based axis along their lengths, with DNA loops emanating from this axis. We applied novel, quantitative and widely applicable cytogenetic strategies to elucidate the molecular bases of this organization using C. elegans. Analyses of WT chromosomes and de novo circular mini-chromosomes revealed that meiosis-specific HORMA-domain proteins assemble into cohorts in defined numbers and co-organize the axis together with two functionally-distinct cohesin complexes (REC-8 and COH-3/4) in defined stoichiometry. We further found that REC-8 cohesins, which load during S phase and mediate sister chromatid cohesion, usually occur as individual complexes, supporting a model wherein sister cohesion is mediated locally by a single cohesin ring. REC-8 complexes are interspersed in an alternating pattern with cohorts of axis-organizing COH-3/4 complexes (averaging three per cohort), which are insufficient to confer cohesion but can bind to individual chromatids, suggesting a mechanism to enable formation of asymmetric sister chromatid loops. Indeed, immuno-FISH assays demonstrate frequent asymmetry in genomic content between the loops formed on sister chromatids. We discuss how features of chromosome axis/loop architecture inferred from our data can help to explain enigmatic, yet essential, aspects of the meiotic program.

scholarly journals Biochemically distinct cohesin complexes mediate positioned loops between CTCF sites and dynamic loops within chromatin domains

2021 ◽  
Author(s):  
Yu Liu ◽  
Job Dekker
Keyword(s):  
Sister Chromatid ◽  
Structural Changes ◽  
Experimental Approach ◽  
Cohesin Complex ◽  
Genomic Context ◽  
Experimental Conditions ◽  
Chromatin Domains ◽  
Isolated Nuclei ◽  
Sister Chromatids ◽  
Chromatid Cohesion

The ring-like cohesin complex mediates sister chromatid cohesion by encircling pairs of sister chromatids. Cohesin also extrudes loops along chromatids. Whether the two activities involve similar mechanisms of DNA engagement is not known. We implemented an experimental approach based on isolated nuclei carrying engineered cleavable RAD21 proteins to precisely control cohesin ring integrity so that its role in chromatin looping could be studied under defined experimental conditions. This approach allowed us to identify cohesin complexes with distinct biochemical, and possibly structural properties, that mediate different sets of chromatin loops. When RAD21 is cleaved and the cohesin ring is opened, cohesin complexes at CTCF sites are released from DNA and loops at these elements are lost. In contrast, cohesin-dependent loops within chromatin domains and that are not anchored at CTCF sites are more resistant to RAD21 cleavage. The results show that the cohesin complex mediates loops in different ways depending on genomic context and suggests that it undergoes structural changes as it dynamically extrudes and encounters CTCF sites.

scholarly journals Multiple determinants and consequences of cohesion fatigue in mammalian cells

2018 ◽  
Vol 29 (15) ◽  
pp. 1811-1824 ◽  
Author(s):  
Hem Sapkota ◽  
Emilia Wasiak ◽  
John R. Daum ◽  
Gary J. Gorbsky
Keyword(s):  
Sister Chromatid ◽  
Mammalian Cells ◽  
Dynamic Balance ◽  
Chromosome Instability ◽  
Sister Chromatid Cohesion ◽  
Complete Separation ◽  
Common Source ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Pulling Forces

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 specific times in mitosis, we show that the Wapl-mediated pathway of cohesin release is not required for cohesion fatigue. By manipulating microtubule stability and cohesin complex integrity in cell lines with varying sensitivity to cohesion fatigue, we show that rates of cohesion fatigue reflect a dynamic balance between spindle pulling forces and resistance to separation by interchromatid cohesion. Finally, while massive separation of chromatids in cohesion fatigue likely produces inviable cell progeny, we find that short metaphase delays, leading to partial chromatid separation, predispose cells to chromosome missegregation. Thus, complete separation of one or a few chromosomes and/or partial separation of sister chromatids may be an unrecognized but common source of chromosome instability that perpetuates the evolution of malignant cells in cancer.

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