scholarly journals Loss of Sister Kinetochore Co-orientation and Peri-centromeric Cohesin Protection after Meiosis I Depends on Cleavage of Centromeric REC8

2020 ◽  
Author(s):  
Sugako Ogushi ◽  
Ahmed Rattani ◽  
Jonathan Godwin ◽  
Jean Metson ◽  
Lothar Schermelleh ◽  
...  
Keyword(s):  
Catalytic Activity ◽  
Sister Chromatid ◽  
Spindle Pole ◽  
Sister Chromatids ◽  
Sister Kinetochore ◽  
Meiosis I

SummaryProtection of peri-centromeric REC8 cohesin from separase and sister kinetochore attachment to microtubules emanating from the same spindle pole (co-orientation) ensure that sister chromatids remain associated after meiosis I. Both features are lost during meiosis II, when sister kinetochores bi-orient and lose peri-centromeric REC8 protection, resulting in sister chromatid disjunction and the production of haploid gametes. By transferring spindle-chromosome complexes (SCCs) between meiosis I and II cells, we have discovered that both sister kinetochore co-orientation and peri-centromeric cohesin protection depend on the SCC and not the cytoplasm. Moreover, the catalytic activity of separase at meiosis I is necessary not only for converting kinetochores from a co-to a bi-oriented state but also for deprotection of peri-centromeric cohesin and that cleavage of REC8 may be the key event. Crucially, we show that selective cleavage of REC8 in the vicinity of kinetochores is sufficient to destroy co-orientation in univalent chromosomes, albeit not in bivalents where resolution of chiasmata through cleavage of Rec8 along chromosome arms may also be required.

Phosphorylated proteins are involved in sister-chromatid arm cohesion during meiosis I

1999 ◽  
Vol 112 (17) ◽  
pp. 2957-2969 ◽  
Author(s):  
J.A. Suja ◽  
C. Antonio ◽  
A. Debec ◽  
J.S. Rufas
Keyword(s):  
Sister Chromatid ◽  
Chromosome Structure ◽  
Metaphase Plate ◽  
Mitotic Chromosomes ◽  
Phosphorylated Proteins ◽  
Sister Chromatids ◽  
Sequential Release ◽  
Sister Kinetochore ◽  
Meiosis I ◽  
Metaphase I

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 number and position of chiasmata. In all bivalents thin chromatin strands at the telomeres appeared as the last point of contact between sister chromatids. Additionally, we have analysed the participation of phosphoproteins recognised by the MPM-2 monoclonal antibody against mitotic phosphoproteins in arm cohesion in bivalents and two different kinds of univalents. Results show the absence of MPM-2 phosphoproteins at the interchromatid domain in mitotic chromosomes and meiotic univalents, but their presence in metaphase I bivalents. These phosphoproteins are lost at the onset of anaphase I. Taken together, these data have prompted us to propose a ‘working’ model for the release of arm cohesion during meiosis I. The model suggests that MPM-2 phosphoproteins may act as cohesive proteins associating sister axes. Their modification, once all bivalents are correctly aligned at the metaphase plate, would trigger a change of chromosome structure and the sequential release of sister-kinetochore, arm, and telomere cohesions.

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 CORRIGENDUM

Genetics ◽  
1987 ◽  
Vol 115 (3) ◽  
pp. 579-579
Keyword(s):  
Sister Chromatid ◽  
Recombination Event ◽  
Linear Plasmid ◽  
Wild Type ◽  
Spore Viability ◽  
Yeast Plasmid ◽  
Type Locus ◽  
Sister Chromatids ◽  
Chromosome Ii ◽  
Meiosis I

ABSTRACT In the paper by Jules O'Rear and Jasper Rine (Genetics  113: 517-529; July, 1986) entitled "Precocious meiotic centromere separation of a novel yeast chromosome," the authors described a gene conversion event between a linear yeast plasmid carrying a LYS2 gene and a mutant lys2 gene at the wild-type locus on chromosome II. When these yeasts were mated to wild-type yeast and the resulting diploids sporulated, linked markers on the linear plasmid showed unusual segregation and poor spore viability was observed. On the basis of these observations, we proposed that the recombination event between the linear plasmid and chromosome II had split chromosome II into two fragments, one of which carried the normal centromere of chromosome II (fragment IIa) and the other, a telocentric fragment (fragment IIb), carried the centromere present on the linear plasmid. Separation of the chromosomes from these cells on OFAGE gels verified that chromosome II had been split into two fragments. Furthermore, we proposed that the sister chromatids of the telocentric fragment (fragment IIb) separated precociously in meiosis I when complete chromosome II and fragment IIa were present. In discussions with colleagues, an alternative explanation arose in which a recombination event between a sister chromatid of fragment IIa and a sister chromatid of chromosome II would result in each chromosome II chromatid being joined to a fragment IIa chromatid at CEN2. The two daughter cells of meiosis I would therefore each receive one chromatid of fragment IIa and one chromatid of chromosome II. Segregation of the two sister chromatids of fragment IIb to one pole in meiosis I without precocious centromere separation would result in the observed tetrad classes. To distinguish between these two mechanisms, a centromere-linked marker was introduced into the cross between the strain containing the two fragments of chromosome II and a wild-type strain. Tetrad analysis of the resulting diploid is consistent with the recombination model for the poor spore viability and inconsistent with precocious centromere separation. We thank Drs. Eric Lambie, Michael Lichten and Tom Petes for helpful discussions.

scholarly journals Shugoshin Promotes Sister Kinetochore Biorientation in Saccharomyces cerevisiae

2008 ◽  
Vol 19 (3) ◽  
pp. 1199-1209 ◽  
Author(s):  
Brendan M. Kiburz ◽  
Angelika Amon ◽  
Adele L. Marston
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Chromosome Segregation ◽  
Minor Role ◽  
Meiotic Cell ◽  
Homologous Chromosomes ◽  
Cell Divisions ◽  
Sister Chromatids ◽  
Sister Kinetochore ◽  
A Minor ◽  
Meiosis I

Chromosome segregation must be executed accurately during both mitotic and meiotic cell divisions. Sgo1 plays a key role in ensuring faithful chromosome segregation in at least two ways. During meiosis this protein regulates the removal of cohesins, the proteins that hold sister chromatids together, from chromosomes. During mitosis, Sgo1 is required for sensing the absence of tension caused by sister kinetochores not being attached to microtubules emanating from opposite poles. Here we describe a differential requirement for Sgo1 in the segregation of homologous chromosomes and sister chromatids. Sgo1 plays only a minor role in segregating homologous chromosomes at meiosis I. In contrast, Sgo1 is important to bias sister kinetochores toward biorientation. We suggest that Sgo1 acts at sister kinetochores to promote their biorientation.

scholarly journals Chiasmata and the kinetochore component Dam1 are crucial for elimination of erroneous chromosome attachments and centromere oscillation at meiosis I

Open Biology ◽  
2021 ◽  
Vol 11 (2) ◽  
Author(s):  
Misuzu Wakiya ◽  
Eriko Nishi ◽  
Shinnosuke Kawai ◽  
Kohei Yamada ◽  
Kazuhiro Katsumata ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Spindle Pole ◽  
Oriented Attachment ◽  
Aurora B ◽  
Correction Factors ◽  
Homologous Chromosomes ◽  
Spindle Poles ◽  
Sister Chromatids ◽  
Potential Link ◽  
Meiosis I

Establishment of proper chromosome attachments to the spindle requires elimination of erroneous attachments, but the mechanism of this process is not fully understood. During meiosis I, sister chromatids attach to the same spindle pole (mono-oriented attachment), whereas homologous chromosomes attach to opposite poles (bi-oriented attachment), resulting in homologous chromosome segregation. Here, we show that chiasmata that link homologous chromosomes and kinetochore component Dam1 are crucial for elimination of erroneous attachments and oscillation of centromeres between the spindle poles at meiosis I in fission yeast. In chiasma-forming cells, Mad2 and Aurora B kinase, which provides time for attachment correction and destabilizes erroneous attachments, respectively, caused elimination of bi-oriented attachments of sister chromatids, whereas in chiasma-lacking cells, they caused elimination of mono-oriented attachments. In chiasma-forming cells, in addition, homologous centromere oscillation was coordinated. Furthermore, Dam1 contributed to attachment elimination in both chiasma-forming and chiasma-lacking cells, and drove centromere oscillation. These results demonstrate that chiasmata alter attachment correction patterns by enabling error correction factors to eliminate bi-oriented attachment of sister chromatids, and suggest that Dam1 induces elimination of erroneous attachments. The coincidental contribution of chiasmata and Dam1 to centromere oscillation also suggests a potential link between centromere oscillation and attachment elimination.

scholarly journals Spo13 prevents premature cohesin cleavage during meiosis

2019 ◽  
Vol 4 ◽  
pp. 29 ◽  
Author(s):  
Stefan Galander ◽  
Rachael E. Barton ◽  
David A. Kelly ◽  
Adèle L. Marston
Keyword(s):  
Regulatory Subunit ◽  
Homologous Chromosomes ◽  
Sister Chromatids ◽  
Functional Homolog ◽  
Sister Kinetochore ◽  
Phosphatase 2A ◽  
Cohesin Subunit ◽  
Yeast Meiosis ◽  
Mitosis And Meiosis ◽  
Meiosis I

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. Methods: Here we investigate the effects of loss of SPO13 on cohesion during meiosis I using a live-cell imaging approach. Results: Unlike wild type, cells lacking SPO13 fail to maintain the meiosis-specific cohesin subunit, Rec8, at centromeres and segregate sister chromatids to opposite poles during anaphase I. We show that the cohesin-destabilizing factor, Wpl1, is not primarily responsible for the loss of cohesion during meiosis I. Instead, premature loss of centromeric cohesin during anaphase I in spo13Δ cells relies on separase-dependent cohesin cleavage. Further, cohesin loss in spo13Δ anaphase I cells is blocked by forcibly tethering the regulatory subunit of protein phosphatase 2A, Rts1, to Rec8. Conclusions: Our findings indicate that separase-dependent cleavage of phosphorylated Rec8 causes premature cohesin loss in spo13Δ cells.

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 Spo13 prevents premature cohesin cleavage during meiosis

2018 ◽  
Author(s):  
Stefan Galander ◽  
Rachael E Barton ◽  
David A Kelly ◽  
Adele L Marston
Keyword(s):  
Regulatory Subunit ◽  
Homologous Chromosomes ◽  
Sister Chromatids ◽  
Functional Homolog ◽  
Sister Kinetochore ◽  
Phosphatase 2A ◽  
Cohesin Subunit ◽  
Yeast Meiosis ◽  
Mitosis And Meiosis ◽  
Meiosis I

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. Here we investigate the effects of loss of SPO13 on cohesion during meiosis I. Unlike wild type, cells lacking SPO13 fail to maintain the meiosis-specific cohesin subunit, Rec8, at centromeres and segregate sister chromatids to opposite poles during anaphase I. We show that the cohesin-destabilizing factor, Wpl1, is not primarily responsible for the loss of cohesion during meiosis I. Instead, premature loss of centromeric cohesin during anaphase I in spo13Δ cells relies on separase-dependent cohesin cleavage. Further, cohesin loss in spo13Δ anaphase I cells is blocked by forcibly tethering the regulatory subunit of protein phosphatase 2A, Rts1, to Rec8. Our findings indicate that separase-dependent cleavage of phosphorylated Rec8 causes premature cohesin loss in spo13Δ cells.

scholarly journals Direct evaluation of cohesin-mediated sister kinetochore associations at meiosis I in fission yeast

2021 ◽  
Author(s):  
Masashi Nambu ◽  
Atsuki Kishikawa ◽  
Takatomi Yamada ◽  
Kento Ichikawa ◽  
Yunosuke Kira ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Chromosome Segregation ◽  
Mitotic Chromosomes ◽  
Direct Evaluation ◽  
Homologous Chromosomes ◽  
Sister Chromatids ◽  
Pheromone Signaling ◽  
Sister Kinetochore ◽  
Novel Method ◽  
Meiosis I

Kinetochores drive chromosome segregation by mediating chromosome interactions with the spindle. In higher eukaryotes, sister kinetochores are separately positioned on opposite sides of sister centromeres during mitosis, but associate with each other during meiosis I. Kinetochore association facilitates the attachment of sister chromatids to the same pole, enabling the segregation of homologous chromosomes toward opposite poles. In the fission yeast, Schizosaccharomyces pombe, Rec8-containing meiotic cohesin is suggested to establish kinetochore associations by mediating cohesion of the centromere cores. However, cohesin-mediated kinetochore associations on intact chromosomes have never been demonstrated directly. Here, we describe a novel method for the direct evaluation of kinetochore associations on intact chromosomes in live S. pombe cells, and demonstrate that sister kinetochores and the centromere cores are positioned separately on mitotic chromosomes but associate with each other on meiosis I chromosomes. Furthermore, we demonstrate that kinetochore association depends on meiotic cohesin and the cohesin regulators, Moa1 and Mrc1, and requires mating-pheromone signaling for its establishment. These results confirm cohesin-mediated kinetochore association and its regulatory mechanisms, along with the usefulness of the developed method for its analysis.

scholarly journals The Reduction of Chromosome Number in Meiosis Is Determined by Properties Built into the Chromosomes

2000 ◽  
Vol 150 (6) ◽  
pp. 1223-1232 ◽  
Author(s):  
Leocadia V. Paliulis ◽  
R. Bruce Nicklas
Keyword(s):  
Chromosome Number ◽  
Meiotic Division ◽  
Spindle Pole ◽  
The Other ◽  
Whole Cell ◽  
Sister Chromatids ◽  
Meiosis I

In meiosis I, two chromatids move to each spindle pole. Then, in meiosis II, the two are distributed, one to each future gamete. This requires that meiosis I chromosomes attach to the spindle differently than meiosis II chromosomes and that they regulate chromosome cohesion differently. We investigated whether the information that dictates the division type of the chromosome comes from the whole cell, the spindle, or the chromosome itself. Also, we determined when chromosomes can switch from meiosis I behavior to meiosis II behavior. We used a micromanipulation needle to fuse grasshopper spermatocytes in meiosis I to spermatocytes in meiosis II, and to move chromosomes from one spindle to the other. Chromosomes placed on spindles of a different meiotic division always behaved as they would have on their native spindle; e.g., a meiosis I chromosome attached to a meiosis II spindle in its normal fashion and sister chromatids moved together to the same spindle pole. We also showed that meiosis I chromosomes become competent meiosis II chromosomes in anaphase of meiosis I, but not before. The patterns for attachment to the spindle and regulation of cohesion are built into the chromosome itself. These results suggest that regulation of chromosome cohesion may be linked to differences in the arrangement of kinetochores in the two meiotic divisions.

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