Meiotic Spindle Assembly and Chromosome Segregation in Oocytes

Oogenesis ◽  
2010 ◽  
pp. 267-290 ◽  
Author(s):  
Julien Dumont ◽  
Stéphane Brunet
2004 ◽  
Vol 15 (1) ◽  
pp. 121-131 ◽  
Author(s):  
Rita Gandhi ◽  
Silvia Bonaccorsi ◽  
Diana Wentworth ◽  
Stephen Doxsey ◽  
Maurizio Gatti ◽  
...  

We have performed a mutational analysis together with RNA interference to determine the role of the kinesin-like protein KLP67A in Drosophila cell division. During both mitosis and male meiosis, Klp67A mutations cause an increase in MT length and disrupt discrete aspects of spindle assembly, as well as cytokinesis. Mutant cells exhibit greatly enlarged metaphase spindle as a result of excessive MT polymerization. The analysis of both living and fixed cells also shows perturbations in centrosome separation, chromosome segregation, and central spindle assembly. These data demonstrate that the MT plus end-directed motor KLP67A is essential for spindle assembly during mitosis and male meiosis and suggest that the regulation of MT plus-end polymerization is a key determinant of spindle architecture throughout cell division.


Genome ◽  
2012 ◽  
Vol 55 (1) ◽  
pp. 63-67 ◽  
Author(s):  
Osamah Batiha ◽  
Andrew Swan

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.


2015 ◽  
Vol 27 (12) ◽  
pp. 3367-3382 ◽  
Author(s):  
Baixiao Niu ◽  
Liudan Wang ◽  
Liangsheng Zhang ◽  
Ding Ren ◽  
Ren Ren ◽  
...  

2004 ◽  
Vol 15 (6) ◽  
pp. 2895-2906 ◽  
Author(s):  
Ryoma Ohi ◽  
Tanuj Sapra ◽  
Jonathan Howard ◽  
Timothy J. Mitchison

The KinI kinesin MCAK is a microtubule depolymerase important for governing spindle microtubule dynamics during chromosome segregation. The dynamic nature of spindle assembly and chromosome-microtubule interactions suggest that mechanisms must exist that modulate the activity of MCAK, both spatially and temporally. In Xenopus extracts, MCAK associates with and is stimulated by the inner centromere protein ICIS. The inner centromere kinase Aurora B also interacts with ICIS and MCAK raising the possibility that Aurora B may regulate MCAK activity as well. Herein, we demonstrate that recombinant Aurora B-INCENP inhibits Xenopus MCAK activity in vitro in a phosphorylation-dependent manner. Substituting endogenous MCAK in Xenopus extracts with the alanine mutant XMCAK-4A, which is resistant to inhibition by Aurora B-INCENP, led to assembly of mono-astral and monopolar structures instead of bipolar spindles. The size of these structures and extent of tubulin polymerization in XMCAK-4A extracts indicate that XM-CAK-4A is not defective for microtubule dynamics regulation throughout the cytoplasm. We further demonstrate that the ability of XMCAK-4A to localize to inner centromeres is abolished. Our results show that MCAK regulation of cytoplasmic and spindle-associated microtubules can be differentiated by Aurora B-dependent phosphorylation, and they further demonstrate that this regulation is required for bipolar meiotic spindle assembly.


Gene ◽  
2020 ◽  
Vol 741 ◽  
pp. 144495
Author(s):  
Changquan Zhang ◽  
Lei Zhao ◽  
Lizhi Leng ◽  
Qinwei Zhou ◽  
Shuoping Zhang ◽  
...  

2016 ◽  
Vol 215 (5) ◽  
pp. 611-619 ◽  
Author(s):  
Isma Bennabi ◽  
Marie-Emilie Terret ◽  
Marie-Hélène Verlhac

Oocytes accumulate maternal stores (proteins, mRNAs, metabolites, etc.) during their growth in the ovary to support development after fertilization. To preserve this cytoplasmic maternal inheritance, they accomplish the difficult task of partitioning their cytoplasm unequally while dividing their chromosomes equally. Added to this complexity, most oocytes, for reasons still speculative, lack the major microtubule organizing centers that most cells use to assemble and position their spindles, namely canonical centrosomes. In this review, we will address recent work on the mechanisms of meiotic spindle assembly and chromosome alignment/segregation in female gametes to try to understand the origin of errors of oocyte meiotic divisions. The challenge of oocyte divisions appears indeed not trivial because in both mice and humans oocyte meiotic divisions are prone to chromosome segregation errors, a leading cause of frequent miscarriages and congenital defects.


2015 ◽  
Vol 210 (6) ◽  
pp. 917-932 ◽  
Author(s):  
Amy A. Connolly ◽  
Kenji Sugioka ◽  
Chien-Hui Chuang ◽  
Joshua B. Lowry ◽  
Bruce Bowerman

During oocyte meiotic cell division in many animals, bipolar spindles assemble in the absence of centrosomes, but the mechanisms that restrict pole assembly to a bipolar state are unknown. We show that KLP-7, the single mitotic centromere–associated kinesin (MCAK)/kinesin-13 in Caenorhabditis elegans, is required for bipolar oocyte meiotic spindle assembly. In klp-7(−) mutants, extra microtubules accumulated, extra functional spindle poles assembled, and chromosomes frequently segregated as three distinct masses during meiosis I anaphase. Moreover, reducing KLP-7 function in monopolar klp-18(−) mutants often restored spindle bipolarity and chromosome segregation. MCAKs act at kinetochores to correct improper kinetochore–microtubule (k–MT) attachments, and depletion of the Ndc-80 kinetochore complex, which binds microtubules to mediate kinetochore attachment, restored bipolarity in klp-7(−) mutant oocytes. We propose a model in which KLP-7/MCAK regulates k–MT attachment and spindle tension to promote the coalescence of early spindle pole foci that produces a bipolar structure during the acentrosomal process of oocyte meiotic spindle assembly.


2011 ◽  
Vol 44 (5) ◽  
pp. 391-400 ◽  
Author(s):  
P. Silva ◽  
J. Barbosa ◽  
A. V. Nascimento ◽  
J. Faria ◽  
R. Reis ◽  
...  

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