scholarly journals Xenopus oocyte meiosis lacks spindle assembly checkpoint control

2013 ◽  
Vol 201 (2) ◽  
pp. 191-200 ◽  
Author(s):  
Hua Shao ◽  
Ruizhen Li ◽  
Chunqi Ma ◽  
Eric Chen ◽  
X. Johné Liu
Keyword(s):  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Xenopus Laevis Oocytes ◽  
Checkpoint Control ◽  
Oocyte Meiosis ◽  
Complete Disruption ◽  
Spindle Microtubules ◽  
Surveillance Mechanism ◽  
Mammalian Eggs ◽  
Mitosis And Meiosis

The spindle assembly checkpoint (SAC) functions as a surveillance mechanism to detect chromosome misalignment and to delay anaphase until the errors are corrected. The SAC is thought to control mitosis and meiosis, including meiosis in mammalian eggs. However, it remains unknown if meiosis in the eggs of nonmammalian vertebrate species is also regulated by SAC. Using a novel karyotyping technique, we demonstrate that complete disruption of spindle microtubules in Xenopus laevis oocytes did not affect the bivalent-to-dyad transition at the time oocytes are undergoing anaphase I. These oocytes also acquired the ability to respond to parthenogenetic activation, which indicates proper metaphase II arrest. Similarly, oocytes exhibiting monopolar spindles, via inhibition of aurora B or Eg5 kinesin, underwent monopolar anaphase on time and without additional intervention. Therefore, the metaphase-to-anaphase transition in frog oocytes is not regulated by SAC.

scholarly journals Novel roles for BicD in pronuclear fusion and meiosis II progression via localization of the CHC/TACC/Msps complex to MII spindles

2020 ◽  
Author(s):  
Paula Vazquez-Pianzola ◽  
Dirk Beuchle ◽  
Gabriela Saro ◽  
Greco Hernández ◽  
Giovanna Maldonado ◽  
...  
Keyword(s):  
Heavy Chain ◽  
Spindle Assembly Checkpoint ◽  
Coiled Coil ◽  
Spindle Assembly ◽  
Meiotic Spindle ◽  
C Elegans ◽  
Spindle Apparatus ◽  
Spindle Microtubules ◽  
Mitosis And Meiosis ◽  
Overexpressed Gene

ABSTRACTVertebrate Clathrin heavy chain (Chc) plays a moonlighting function during mitosis. Chc forms a complex with TACC3 (Transforming Acidic Coiled Coil 3) and ch-TOG (colonic hepatic tumor overexpressed gene) at the spindle microtubules, forming inter microtubule bridges that stabilize the K-fibers. Since Drosophila Chc is a cargo of the dynein adaptor Bicaudal-D (BicD), we investigated whether BicD regulates Clathrin function at the spindle. We found that BicD localizes, like Chc, to centrosomes and spindles during mitosis and meiosis II, and that Chc interacts with Drosophila TACC (D-TACC). Using deGradFP to reduce the activity of BicD in mature eggs and very young embryos, we uncovered a novel function of BicD in meiosis II. The affected meiosis II products underwent abnormal rounds of additional replications and failed to carry out pronuclear fusion. Pointing to a mechanism, we found that the localization of Clathrin/D-TACC/Minispindles (Msps, homolog of ch-TOG) to the meiosis II spindles was impaired upon BicD knockdown. Furthermore, the meiotic products showed abnormal staining for PH3 and reduced recruitment of spindle assembly checkpoint (SAC) components. Altogether, our results support the notion that BicD performs a key activity in assembling the meiotic spindle apparatus. This function of BicD seems conserved in evolution because C. elegans embryos with reduced activities of these genes developed comparable phenotypes.

Spindle assembly checkpoint regulation of chromosome segregation in mammalian oocytes

2013 ◽  
Vol 25 (3) ◽  
pp. 472 ◽  
Author(s):  
Zbigniew Polanski
Keyword(s):  
Chromosome Segregation ◽  
Spindle Assembly Checkpoint ◽  
Cell Cycle Control ◽  
Genetic Material ◽  
Spindle Assembly ◽  
Female Meiosis ◽  
Mammalian Oocyte ◽  
Oocyte Meiosis ◽  
Surveillance Mechanism

The spindle assembly checkpoint (SAC) is a surveillance mechanism that monitors the quality of the spindle during division and blocks anaphase entry in the presence of anomalies that could result in erroneous segregation of the chromosomes. Because human aneuploidy is mainly linked to the erroneous segregation of genetic material in oocytes, the issue of the effectiveness of the SAC in female meiosis is especially important. The present review summarises our understanding of the SAC control of mammalian oocyte meiosis, including its possible impact on the incidence of embryonic aneuploidy. Owing to the peculiarities of cell cycle control in female meiosis, the integration of the SAC within such a specific environment results in several unusual situations, which are also discussed.

scholarly journals Caenorhabditis elegans oocytes detect meiotic errors in the absence of canonical end-on kinetochore attachments

2017 ◽  
Vol 216 (5) ◽  
pp. 1243-1253 ◽  
Author(s):  
Amanda C. Davis-Roca ◽  
Christina C. Muscat ◽  
Sarah M. Wignall
Keyword(s):  
Caenorhabditis Elegans ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Aurora B ◽  
C Elegans ◽  
Dividing Cells ◽  
Spindle Microtubules ◽  
Surveillance Mechanism ◽  
Key Events

Mitotically dividing cells use a surveillance mechanism, the spindle assembly checkpoint, that monitors the attachment of spindle microtubules to kinetochores as a means of detecting errors. However, end-on kinetochore attachments have not been observed in Caenorhabditis elegans oocytes and chromosomes instead associate with lateral microtubule bundles; whether errors can be sensed in this context is not known. Here, we show that C. elegans oocytes delay key events in anaphase, including AIR-2/Aurora B relocalization to the microtubules, in response to a variety of meiotic defects, demonstrating that errors can be detected in these cells and revealing a mechanism that regulates anaphase progression. This mechanism does not appear to rely on several components of the spindle assembly checkpoint but does require the kinetochore, as depleting kinetochore components prevents the error-induced anaphase delays. These findings therefore suggest that in this system, kinetochores could be involved in sensing meiotic errors using an unconventional mechanism that does not use canonical end-on attachments.

scholarly journals CENP-V is required for proper chromosome segregation through interaction with spindle microtubules in mouse oocytes

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Dalileh Nabi ◽  
Hauke Drechsler ◽  
Johannes Pschirer ◽  
Franz Korn ◽  
Nadine Schuler ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Spindle Assembly Checkpoint ◽  
Polar Body ◽  
Spindle Assembly ◽  
V Protein ◽  
Oocyte Meiosis ◽  
Spindle Microtubules ◽  
Polar Body Extrusion ◽  
Metaphase I

AbstractProper chromosome segregation is essential to avoid aneuploidy, yet this process fails with increasing age in mammalian oocytes. Here we report a role for the scarcely described protein CENP-V in oocyte spindle formation and chromosome segregation. We show that depending on the oocyte maturation state, CENP-V localizes to centromeres, to microtubule organizing centers, and to spindle microtubules. We find that Cenp-V−/− oocytes feature severe deficiencies, including metaphase I arrest, strongly reduced polar body extrusion, increased numbers of mis-aligned chromosomes and aneuploidy, multipolar spindles, unfocused spindle poles and loss of kinetochore spindle fibres. We also show that CENP-V protein binds, diffuses along, and bundles microtubules in vitro. The spindle assembly checkpoint arrests about half of metaphase I Cenp-V−/− oocytes from young adults only. This finding suggests checkpoint weakening in ageing oocytes, which mature despite carrying mis-aligned chromosomes. Thus, CENP-V is a microtubule bundling protein crucial to faithful oocyte meiosis, and Cenp-V−/− oocytes reveal age-dependent weakening of the spindle assembly checkpoint.

scholarly journals OLA1 is responsible for normal spindle assembly and SAC activation in mouse oocytes

2019 ◽  
Author(s):  
Di Xie ◽  
Juan Zhang ◽  
JinLi Ding ◽  
Jing Yang ◽  
Yan Zhang
Keyword(s):  
Spindle Assembly Checkpoint ◽  
Polar Body ◽  
Germinal Vesicle ◽  
Spindle Assembly ◽  
Mouse Oocyte ◽  
Immunofluorescent Staining ◽  
Germinal Vesicle Breakdown ◽  
Oocyte Meiosis ◽  
Polar Body Extrusion ◽  
Spread Analysis

Background. OLA1 is a member of the GTPase protein family, unlike other members, it can bind and hydrolyze ATP more efficiently than GTP. OLA1 participates in cell proliferation, oxidative response and tumorigenesis. However, whether OLA1 is also required for oocyte meiosis is still unknown. Methods. In this study, the localization, expression, and functions of OLA1 in the mouse oocyte meiosis were examined. Immunofluorescent and confocal microscopy were used to explore the location pattern of OLA1 in the mouse oocyte. Moreover, nocodazole treatment was used to confirm the spindle-like location of OLA1 during mouse meiosis. Western blot was used to explore the expression pattern of OLA1 in the mouse oocyte. Microinjection of siRNA was used to explore the OLA1 functions in the mouse oocyte meiosis. In addition, chromosome spreading was used to investigate the spindle assembly checkpoint (SAC) activity. Results. Immunofluorescent staining showed that OLA1 evenly distributed in the cytoplasm at germinal vesicle (GV) stage. After meiosis resumption (GVBD), OLA1 co-localized with spindles, which was further identified by nocodazole treatment experiments. Knockdown of OLA1 impaired the germinal vesicle breakdown progression and finally resulted in a lower polar body extrusion rate. Immunofluorescence analysis indicated that knockdown of OLA1 led to abnormal spindle assembly, which was evidenced by multipolar spindles in OLA1-RNAi-oocytes. After 6 h post-GVBD in culture, an increased proportion of oocyte which has precociously entered into anaphase/telephase I (A/TI) was observed in OLA1-knockdown oocytes, suggesting that loss of OLA1 resulted in the premature segregation of homologous chromosomes. In addition, the chromosome spread analysis suggested that OLA1 knockdown induced premature anaphase onset was due to the precocious inactivation of SAC. Taken together, we concluded that OLA1 plays important role in GVBD, spindle assembly and SAC activation maintenance in oocyte meiosis.

scholarly journals Uncoupling Anaphase-Promoting Complex/Cyclosome Activity from Spindle Assembly Checkpoint Control by Deregulating Polo-Like Kinase 1

2005 ◽  
Vol 25 (5) ◽  
pp. 2031-2044 ◽  
Author(s):  
Barbara C. M. van de Weerdt ◽  
Marcel A. T. M. van Vugt ◽  
Catherine Lindon ◽  
Jos J. W. Kauw ◽  
Marieke J. Rozendaal ◽  
...  
Keyword(s):  
Double Mutant ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Mitotic Catastrophe ◽  
Anaphase Promoting Complex ◽  
Checkpoint Control ◽  
Mitotic Progression ◽  
Specific Antibodies ◽  
Mitotic Entry

ABSTRACT Polo-like kinase 1 (Plk1) plays a role in numerous events in mitosis, but how the multiple functions of Plk1 are separated is poorly understood. We studied regulation of Plk1 through two putative phosphorylation residues, Ser-137 and Thr-210. Using phospho-specific antibodies, we found that Thr-210 phosphorylation precedes Ser-137 phosphorylation in vivo, the latter occurring specifically in late mitosis. We show that expression of two activating mutants of these residues, S137D and T210D, results in distinct mitotic phenotypes. Whereas expression of both phospho-mimicking mutants as well as of the double mutant leads to accelerated mitotic entry, further progression through mitosis is dramatically different: the T210D mutant causes a spindle assembly checkpoint-dependent delay, whereas the expression of the S137D mutant or the double mutant results in untimely activation of the anaphase-promoting complex/cyclosome (APC/C) and frequent mitotic catastrophe. Using nonphosphorylatable Plk1-S137A and Plk1-T210A mutants, we show that both sites contribute to proper mitotic progression. Based on these observations, we propose that Plk1 function is altered at different stages of mitosis through consecutive posttranslational events, e.g., at Ser-137 and Thr-210. Furthermore, our data show that uncontrolled Plk1 activation can uncouple APC/C activity from spindle assembly checkpoint control.

Evidence that the spindle assembly checkpoint does not regulate APCFzy activity in Drosophila female meiosis

Genome ◽  
2012 ◽  
Vol 55 (1) ◽  
pp. 63-67 ◽  
Author(s):  
Osamah Batiha ◽  
Andrew Swan
Keyword(s):  
Chromosome Segregation ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Cyclin B ◽  
Meiotic Spindle ◽  
Loss Of Function ◽  
Female Meiosis ◽  
Chromosome Attachment ◽  
Spindle Microtubules ◽  
Made In

The spindle assembly checkpoint (SAC) plays an important role in mitotic cells to sense improper chromosome attachment to spindle microtubules and to inhibit APCFzy-dependent destruction of cyclin B and Securin; consequent initiation of anaphase until correct attachments are made. In Drosophila , SAC genes have been found to play a role in ensuring proper chromosome segregation in meiosis, possibly reflecting a similar role for the SAC in APCFzy inhibition during meiosis. We found that loss of function mutations in SAC genes, Mad2, zwilch, and mps1, do not lead to the predicted rise in APCFzy-dependent degradation of cyclin B either globally throughout the egg or locally on the meiotic spindle. Further, the SAC is not responsible for the inability of APCFzy to target cyclin B and promote anaphase in metaphase II arrested eggs from cort mutant females. Our findings support the argument that SAC proteins play checkpoint independent roles in Drosophila female meiosis and that other mechanisms must function to control APC activity.

Sign in / Sign up

Export Citation Format

Share Document