scholarly journals Cdc55 coordinates spindle assembly and chromosome disjunction during meiosis

2011 ◽  
Vol 193 (7) ◽  
pp. 1213-1228 ◽  
Author(s):  
Farid Bizzari ◽  
Adele L. Marston
Keyword(s):  
Protein Phosphatase ◽  
Deoxyribonucleic Acid ◽  
Nuclear Division ◽  
Spindle Assembly ◽  
Regulatory Subunit ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Phosphatase 2A ◽  
Meiosis I ◽  
Sequential Assembly

During meiosis, two consecutive nuclear divisions follow a single round of deoxyribonucleic acid replication. In meiosis I, homologues are segregated, whereas in meiosis II, sister chromatids are segregated. This requires that the sequential assembly and dissolution of specialized chromosomal factors are coordinated with two rounds of spindle assembly and disassembly. How these events are coupled is unknown. In this paper, we show, in budding yeast, that the protein phosphatase 2A regulatory subunit Cdc55 couples the loss of linkages between chromosomes with nuclear division by restraining two other phosphatases, Cdc14 and PP2ARts1. Cdc55 maintains Cdc14 sequestration in the nucleolus during early meiosis, and this is essential for the assembly of the meiosis I spindle but not for chromosomes to separate. Cdc55 also limits the formation of PP2A holocomplexes containing the alternative regulatory subunit Rts1, which is crucial for the timely dissolution of sister chromatid cohesion. Therefore, Cdc55 orders passage through the meiotic divisions by ensuring a balance of phosphatases.

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.

scholarly journals The budding yeast PP2ACdc55 protein phosphatase prevents the onset of anaphase in response to morphogenetic defects

2007 ◽  
Vol 177 (4) ◽  
pp. 599-611 ◽  
Author(s):  
Elena Chiroli ◽  
Valentina Rossio ◽  
Giovanna Lucchini ◽  
Simonetta Piatti
Keyword(s):  
Protein Phosphatase ◽  
Budding Yeast ◽  
S Phase ◽  
Yeast Cells ◽  
Regulatory Subunit ◽  
Chromosome Transmission ◽  
Anaphase Onset ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Noncanonical Pathway

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 conditions, suggesting that other factors contribute to cohesion maintainance in G2. We find that the protein phosphatase PP2A bound to its regulatory subunit Cdc55 plays a key role in this process, uncovering a new function for PP2ACdc55 in controlling a noncanonical pathway of chromatid cohesion removal.

scholarly journals Multiple pools of Protein Phosphatase 2A-B56 function to antagonize spindle assembly, promote kinetochore attachments and maintain cohesion in Drosophila Oocytes

2020 ◽  
Author(s):  
Janet K. Jang ◽  
Amy C. Gladstein ◽  
Arunika Das ◽  
Zachary L. Sisco ◽  
Kim S. McKim
Keyword(s):  
Protein Phosphatase ◽  
Protein Phosphatase 2A ◽  
Spindle Assembly ◽  
Meiotic Spindle ◽  
Aurora B ◽  
Microtubule Organizing Center ◽  
Chromosomal Passenger ◽  
Organizing Center ◽  
Phosphatase 2A ◽  
Meiosis I

AbstractMeiosis in female oocytes lack centrosomes, the major microtubule-organizing center, which makes them especially vulnerable to aneuploidy. In the acentrosomal oocytes of Drosophila, meiotic spindle assembly depends on the chromosomal passenger complex (CPC). Aurora B is the catalytic component of the CPC while the remaining subunits regulate its localization. Using an inhibitor of Aurora B activity, Binucleine 2, we found that continuous Aurora B activity is required to maintain the oocyte spindle during meiosis I, and this activity is antagonized by phosphatases acting on spindle associated proteins such as kinesins. Protein Phosphatase 2A (PP2A) exists in two varieties, B55 and B56. While both antagonize Aurora B, B55 has only minor roles in meiosis I spindle function. The B56 subunit is encoded by two partially redundant paralogs in the Drosophila genome, wdb and wrd. Knocking down both paralogs showed that the B56 subunit is critical for maintaining sister chromatid cohesion, establishing end-on microtubule attachments, and the metaphase I arrest in oocytes. We found that WDB recruitment to the centromeres depends on BUBR1, MEI-S332, and kinetochore protein SPC105R. While BUBR1 has been shown previously to stabilize microtubule attachments in Drosophila oocytes, only SPC105R is required for cohesion maintenance during meiosis I. We propose that SPC105R promotes cohesion maintenance by recruiting two proteins that recruit PP2A, MEI-S332, and the Soronin homolog Dalmatian.

Protein phosphatase 2A protects centromeric sister chromatid cohesion during meiosis I

Nature ◽  
2006 ◽  
Vol 441 (7089) ◽  
pp. 53-61 ◽  
Author(s):  
Christian G. Riedel ◽  
Vittorio L. Katis ◽  
Yuki Katou ◽  
Saori Mori ◽  
Takehiko Itoh ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Protein Phosphatase ◽  
Protein Phosphatase 2A ◽  
Sister Chromatid Cohesion ◽  
Chromatid Cohesion ◽  
Phosphatase 2A ◽  
Meiosis I

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 Meiotic nuclear divisions in budding yeast require PP2ACdc55-mediated antagonism of Net1 phosphorylation by Cdk

2011 ◽  
Vol 193 (7) ◽  
pp. 1157-1166 ◽  
Author(s):  
Gary W. Kerr ◽  
Sourav Sarkar ◽  
Katherine L. Tibbles ◽  
Mark Petronczki ◽  
Jonathan B.A. Millar ◽  
...  
Keyword(s):  
Protein Phosphatase ◽  
Deoxyribonucleic Acid ◽  
Nuclear Division ◽  
Mutant Form ◽  
Phosphorylation Sites ◽  
Cyclin Dependent Kinase ◽  
Dominant Mutant ◽  
Early Anaphase ◽  
Cdk Phosphorylation ◽  
Meiosis I

During meiosis, one round of deoxyribonucleic acid replication is followed by two rounds of nuclear division. In Saccharomyces cerevisiae, activation of the Cdc14 early anaphase release (FEAR) network is required for exit from meiosis I but does not lead to the activation of origins of replication. The precise mechanism of how FEAR regulates meiosis is not understood. In this paper, we report that premature activation of FEAR during meiosis caused by loss of protein phosphatase PP2ACdc55 activity blocks bipolar spindle assembly and nuclear divisions. In cdc55 meiotic null (cdc55-mn) cells, the cyclin-dependent kinase (Cdk)–counteracting phosphatase Cdc14 was released prematurely from the nucleolus concomitant with hyperphosphorylation of its nucleolar anchor protein Net1. Crucially, a mutant form of Net1 that lacks six Cdk phosphorylation sites rescued the meiotic defect of cdc55-mn cells. Expression of a dominant mutant allele of CDC14 mimicked the cdc55-mn phenotype. We propose that phosphoregulation of Net1 by PP2ACdc55 is essential for preventing precocious exit from meiosis I.

scholarly journals SUMOylation targets shugoshin to stabilize sister kinetochore biorientation

2019 ◽  
Author(s):  
Xue Bessie Su ◽  
Menglu Wang ◽  
Claudia Schaffner ◽  
Dean Clift ◽  
Olga O. Nerusheva ◽  
...  
Keyword(s):  
Protein Phosphatase ◽  
Cell Cycle Progression ◽  
Aurora B ◽  
Cycle Progression ◽  
Anaphase Onset ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Sister Kinetochore ◽  
Phosphatase 2A ◽  
Segregation Of Chromosomes

AbstractThe accurate segregation of chromosomes during mitosis relies on the attachment of sister chromatids to microtubules from opposite poles, called biorientation. Sister chromatid cohesion resists microtubule forces, generating tension which provides the signal that biorientation has occurred. How tension silences the surveillance pathways that prevent cell cycle progression and correct erroneous kinetochore-microtubule remains unclear. Here we identify SUMOylation as a mechanism that promotes anaphase onset upon biorientation. SUMO ligases modify the tension-sensing pericentromere-localized chromatin protein, shugoshin, to stabilize bioriented sister kinetochore-microtubule attachments. In the absence of SUMOylation, Aurora B kinase removal from kinetochores is delayed. Shugoshin SUMOylation prevents its binding to protein phosphatase 2A (PP2A) and release of this interaction is important for stabilizing sister kinetochore biorientation. We propose that SUMOylation modulates the kinase-phosphatase balance within pericentromeres to inactivate the error correction machinery, thereby allowing anaphase entry in response to biorientation.

scholarly journals SUMOylation stabilizes sister kinetochore biorientation to allow timely anaphase

2021 ◽  
Vol 220 (7) ◽  
Author(s):  
Xue Bessie Su ◽  
Menglu Wang ◽  
Claudia Schaffner ◽  
Olga O. Nerusheva ◽  
Dean Clift ◽  
...  
Keyword(s):  
Error Correction ◽  
Protein Phosphatase ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Anaphase Onset ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Sister Kinetochore ◽  
Phosphatase 2A ◽  
Chromosome Passenger Complex

During mitosis, sister chromatids attach to microtubules from opposite poles, called biorientation. Sister chromatid cohesion resists microtubule forces, generating tension, which provides the signal that biorientation has occurred. How tension silences the surveillance pathways that prevent cell cycle progression and correct erroneous kinetochore–microtubule attachments remains unclear. Here we show that SUMOylation dampens error correction to allow stable sister kinetochore biorientation and timely anaphase onset. The Siz1/Siz2 SUMO ligases modify the pericentromere-localized shugoshin (Sgo1) protein before its tension-dependent release from chromatin. Sgo1 SUMOylation reduces its binding to protein phosphatase 2A (PP2A), and weakening of this interaction is important for stable biorientation. Unstable biorientation in SUMO-deficient cells is associated with persistence of the chromosome passenger complex (CPC) at centromeres, and SUMOylation of CPC subunit Bir1 also contributes to timely anaphase onset. We propose that SUMOylation acts in a combinatorial manner to facilitate dismantling of the error correction machinery within pericentromeres and thereby sharpen the metaphase–anaphase transition.

scholarly journals Multiple pools of PP2A regulate spindle assembly, kinetochore attachments, and cohesion in Drosophila oocytes

2021 ◽  
Author(s):  
Janet K. Jang ◽  
Amy C. Gladstein ◽  
Arunika Das ◽  
Joanatta G. Shapiro ◽  
Zachary L. Sisco ◽  
...  
Keyword(s):  
Spindle Assembly ◽  
Meiotic Spindle ◽  
Aurora B ◽  
Microtubule Organizing Center ◽  
Oocyte Meiosis ◽  
Chromatid Cohesion ◽  
Chromosomal Passenger ◽  
Organizing Center ◽  
Phosphatase 2A ◽  
Meiosis I

Meiosis in female oocytes lacks centrosomes, the microtubule-organizing center. In Drosophila oocytes, meiotic spindle assembly depends on the chromosomal passenger complex (CPC). To investigate the mechanisms that regulate Aurora B activity, we examined the role of Protein Phosphatase 2A (PP2A) in oocyte meiosis. We found that both forms of PP2A, B55 and B56, antagonize the Aurora B spindle assembly function, suggesting that a balance between Aurora B and PP2A activity maintains the oocyte spindle during meiosis I. PP2A-B56, which is encoded by two partially redundant paralogs, wdb and wrd, is also required for maintaining sister chromatid cohesion, establishing end-on microtubule attachments, and the metaphase I arrest in oocytes. WDB recruitment to the centromeres depends on BUBR1, MEI-S332, and kinetochore protein SPC105R. While BUBR1 stabilizes microtubule attachments in Drosophila oocytes, it is not required for cohesion maintenance during meiosis I. We propose at least three populations of PP2A-B56 regulate meiosis, two of which depend on SPC105R and a third that is associated with the spindle.

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