scholarly journals THE GENETIC ANALYSIS OF A CHROMOSOME-SPECIFIC MEIOTIC MUTANT THAT PERMITS A PREMATURE SEPARATION OF SISTER CHROMATIDS IN DROSOPHILA MELANOGASTER

Genetics ◽  
1984 ◽  
Vol 107 (1) ◽  
pp. 65-77
Author(s):  
Richard C Gethmann
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Sister Chromatid ◽  
Significant Proportion ◽  
Sister Chromatid Cohesion ◽  
Crossover Frequency ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Males And Females ◽  
Chromosome Nondisjunction

ABSTRACT mei-G87 is a recessive meiotic mutant that increases second chromosome nondisjunction in both males and females. A significant proportion of the diplo-2 exceptions are equational. In females, diplo-2 reductional exceptions are usually noncrossovers, but, in equational exceptions, crossover frequency and distribution are the same as that found in the haplo-2 controls. The frequencies of nondisjunction are relatively low: 0.6% in females and 1.3% in males. Nondisjunction frequency is affected by environmental conditions (possibly humidity). The defect in mei-G87, as in other "second division" mutants, appears to be a failure to maintain sister-chromatid cohesion. mei-G87 increases nondisjunction of only the second chromosome. This may indicate either a weak mutant with only the second chromosome being sensitive enough to misbehave or it may indicate that chromosome-specific regions responsible for sister-chromatid cohesion exist.

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 The Cohesion Protein MEI-S332 Localizes to Condensed Meiotic and Mitotic Centromeres until Sister Chromatids Separate

1998 ◽  
Vol 140 (5) ◽  
pp. 1003-1012 ◽  
Author(s):  
Daniel P. Moore ◽  
Andrea W. Page ◽  
Tracy Tzu-Ling Tang ◽  
Anne W. Kerrebrock ◽  
Terry L. Orr-Weaver
Keyword(s):  
Drosophila Melanogaster ◽  
Sister Chromatid ◽  
Sister Chromatid Cohesion ◽  
Male Meiosis ◽  
Mitotic Chromosomes ◽  
Female Meiosis ◽  
Male And Female ◽  
Sister Chromatids ◽  
Chromatid Cohesion

The Drosophila MEI-S332 protein has been shown to be required for the maintenance of sister-chromatid cohesion in male and female meiosis. The protein localizes to the centromeres during male meiosis when the sister chromatids are attached, and it is no longer detectable after they separate. Drosophila melanogaster male meiosis is atypical in several respects, making it important to define MEI-S332 behavior during female meiosis, which better typifies meiosis in eukaryotes. We find that MEI-S332 localizes to the centromeres of prometaphase I chromosomes in oocytes, remaining there until it is delocalized at anaphase II. By using oocytes we were able to obtain sufficient material to investigate the fate of MEI-S332 after the metaphase II–anaphase II transition. The levels of MEI-S332 protein are unchanged after the completion of meiosis, even when translation is blocked, suggesting that the protein dissociates from the centromeres but is not degraded at the onset of anaphase II. Unexpectedly, MEI-S332 is present during embryogenesis, localizes onto the centromeres of mitotic chromosomes, and is delocalized from anaphase chromosomes. Thus, MEI-S332 associates with the centromeres of both meiotic and mitotic chromosomes and dissociates from them at anaphase.

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 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.

scholarly journals Pericentromeric Sister Chromatid Cohesion Promotes Kinetochore Biorientation

2009 ◽  
Vol 20 (17) ◽  
pp. 3818-3827 ◽  
Author(s):  
Tessie M. Ng ◽  
William G. Waples ◽  
Brigitte D. Lavoie ◽  
Sue Biggins
Keyword(s):  
Protein Kinase ◽  
Genetic Analysis ◽  
Chromosome Segregation ◽  
Sister Chromatid ◽  
Budding Yeast ◽  
Sister Chromatid Cohesion ◽  
Specific Role ◽  
Aurora B ◽  
Chromatid Cohesion ◽  
Yeast Genes

Accurate chromosome segregation depends on sister kinetochores making bioriented attachments to microtubules from opposite poles. An essential regulator of biorientation is the Ipl1/Aurora B protein kinase that destabilizes improper microtubule–kinetochore attachments. To identify additional biorientation pathways, we performed a systematic genetic analysis between the ipl1-321 allele and all nonessential budding yeast genes. One of the mutants, mcm21Δ, precociously separates pericentromeres and this is associated with a defect in the binding of the Scc2 cohesin-loading factor at the centromere. Strikingly, Mcm21 becomes essential for biorientation when Ipl1 function is reduced, and this appears to be related to its role in pericentromeric cohesion. When pericentromeres are artificially tethered, Mcm21 is no longer needed for biorientation despite decreased Ipl1 activity. Taken together, these data reveal a specific role for pericentromeric linkage in ensuring kinetochore biorientation.

scholarly journals Multivalent interaction of ESCO2 with the replication machinery is required for sister chromatid cohesion in vertebrates

2019 ◽  
Vol 117 (2) ◽  
pp. 1081-1089 ◽  
Author(s):  
Dawn Bender ◽  
Eulália Maria Lima Da Silva ◽  
Jingrong Chen ◽  
Annelise Poss ◽  
Lauren Gawey ◽  
...  
Keyword(s):  
Dna Replication ◽  
Sister Chromatid ◽  
Sister Chromatid Cohesion ◽  
Replication Machinery ◽  
Replicative Helicase ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
N Terminus ◽  
Mcm Complex ◽  
Unique Ability

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 of DNA replication, through interaction with PCNA. We show that ESCO2 contains multiple PCNA-interaction motifs in its N terminus, each of which is essential to its ability to establish cohesion. We propose that multiple PCNA-interaction motifs embedded in a largely flexible and disordered region of the protein underlie the unique ability of ESCO2 to establish cohesion between sister chromatids precisely as they are born during DNA replication.

scholarly journals From a single double helix to paired double helices and back

2004 ◽  
Vol 359 (1441) ◽  
pp. 99-108 ◽  
Author(s):  
Kim Nasmyth ◽  
Alexander Schleiffer
Keyword(s):  
Cell Proliferation ◽  
Sister Chromatid ◽  
Double Helix ◽  
Ring Structure ◽  
Sister Chromatid Cohesion ◽  
Eukaryotic Cells ◽  
Sister Chromatids ◽  
Double Helices ◽  
Chromatid Cohesion ◽  
Error Correction Mechanism

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 stabilizing kinetochore–microtubule attachments. Efficient amphitelic attachment is therefore achieved by an error correction mechanism that selectively eliminates connections that do not give rise to tension. Cohesion between sister chromatids is mediated by a multisubunit complex called cohesin which forms a gigantic ring structure. It has been proposed that sister DNAs are held together owing to their becoming entrapped within a single cohesin ring. Cohesion between sister chromatids is destroyed at the metaphase to anaphase transition by proteolytic cleavage of cohesin's Scc1 subunit by a thiol protease called separase, which severs the ring and thereby releases sister DNAs.

scholarly journals Genetic Interactions Between mei-S332 and ord in the Control of Sister-Chromatid Cohesion

Genetics ◽  
1998 ◽  
Vol 150 (4) ◽  
pp. 1467-1476
Author(s):  
Sharon E Bickel ◽  
Daniel P Moore ◽  
Cary Lai ◽  
Terry L Orr-Weaver
Keyword(s):  
Chromosome Segregation ◽  
Sister Chromatid ◽  
Double Mutant ◽  
Sex Chromosome ◽  
Meiotic Chromosome ◽  
Sister Chromatid Cohesion ◽  
Gene Products ◽  
Wild Type ◽  
Chromatid Cohesion ◽  
Males And Females

Abstract The Drosophila mei-S332 and ord gene products are essential for proper sister-chromatid cohesion during meiosis in both males and females. We have constructed flies that contain null mutations for both genes. Double-mutant flies are viable and fertile. Therefore, the lack of an essential role for either gene in mitotic cohesion cannot be explained by compensatory activity of the two proteins during mitotic divisions. Analysis of sex chromosome segregation in the double mutant indicates that ord is epistatic to mei-S332. We demonstrate that ord is not required for MEI-S332 protein to localize to meiotic centromeres. Although overexpression of either protein in a wild-type background does not interfere with normal meiotic chromosome segregation, extra ORD+ protein in mei-S332 mutant males enhances nondisjunction at meiosis II. Our results suggest that a balance between the activity of mei-S332 and ord is required for proper regulation of meiotic cohesion and demonstrate that additional proteins must be functioning to ensure mitotic sister-chromatid cohesion.

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