scholarly journals The microtubule catastrophe promoter Sentin delays stable kinetochore–microtubule attachment in oocytes

2015 ◽  
Vol 211 (6) ◽  
pp. 1113-1120 ◽  
Author(s):  
A. Agata Głuszek ◽  
C. Fiona Cullen ◽  
Wenjing Li ◽  
Rachel A. Battaglia ◽  
Sarah J. Radford ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Spindle Assembly ◽  
Aurora B ◽  
Spindle Formation ◽  
Homologous Chromosomes ◽  
Critical Step ◽  
Mouse Oocytes ◽  
Microtubule Attachment

The critical step in meiosis is to attach homologous chromosomes to the opposite poles. In mouse oocytes, stable microtubule end-on attachments to kinetochores are not established until hours after spindle assembly, and phosphorylation of kinetochore proteins by Aurora B/C is responsible for the delay. Here we demonstrated that microtubule ends are actively prevented from stable attachment to kinetochores until well after spindle formation in Drosophila melanogaster oocytes. We identified the microtubule catastrophe-promoting complex Sentin-EB1 as a major factor responsible for this delay. Without this activity, microtubule ends precociously form robust attachments to kinetochores in oocytes, leading to a high proportion of homologous kinetochores stably attached to the same pole. Therefore, regulation of microtubule ends provides an alternative novel mechanism to delay stable kinetochore–microtubule attachment in oocytes.

scholarly journals Aurora-C Kinase Deficiency Causes Cytokinesis Failure in Meiosis I and Production of Large Polyploid Oocytes in Mice

2010 ◽  
Vol 21 (14) ◽  
pp. 2371-2383 ◽  
Author(s):  
Kuo-Tai Yang ◽  
Shu-Kuei Li ◽  
Chih-Chieh Chang ◽  
Chieh-Ju C. Tang ◽  
Yi-Nan Lin ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Female Mouse ◽  
Histone H3 ◽  
Aurora B ◽  
Binding Motif ◽  
Mouse Oocytes ◽  
Microtubule Attachment ◽  
H3 Phosphorylation ◽  
Histone H3 Phosphorylation ◽  
Meiosis I

We previously isolated Aurora-C/Aie1 in a screen for kinases expressed in mouse sperm and eggs. Here, we show the localization of endogenous Aurora-C and examine its roles during female mouse meiosis. Aurora-C was detected at the centromeres and along the chromosome arms in prometaphase I–metaphase I and was concentrated at centromeres at metaphase II, in which Aurora-C also was phosphorylated at Thr171. During the anaphase I–telophase I transition, Aurora-C was dephosphorylated and relocalized to the midzone and midbody. Microinjection of the kinase-deficient Aurora-C (AurC-KD) mRNA into mouse oocytes significantly inhibited Aurora-C activity and caused multiple defects, including chromosome misalignment, abnormal kinetochore–microtubule attachment, premature chromosome segregation, and cytokinesis failure in meiosis I. Furthermore, AurC-KD reduced Aurora-C and histone H3 phosphorylation and inhibited kinetochore localization of Bub1 and BubR1. Similar effects also were observed in the oocytes injected with INCNEP-delIN mRNAs, in which the Aurora-C binding motif was removed. The most dramatic effect observed in AurC-KD–injected oocytes is cytokinesis failure in meiosis I, resulting in producing large polyploid oocytes, a pattern similar to Aurora-C deficiency human spermatozoa. Surprisingly, we detected no Aurora-B protein in mouse oocytes. We propose that Aurora-C, but not Aurora-B, plays essential roles in female mouse meiosis.

Nek2 and its substrate, centrobin/Nip2, are required for proper meiotic spindle formation of the mouse oocytes

Zygote ◽  
2010 ◽  
Vol 19 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Seongkeun Sonn ◽  
Goo Taeg Oh ◽  
Kunsoo Rhee
Keyword(s):  
Spindle Assembly ◽  
Early Embryogenesis ◽  
Mouse Oocyte ◽  
Meiotic Spindle ◽  
Biological Functions ◽  
Spindle Formation ◽  
Mouse Oocytes ◽  
Early Embryos ◽  
Pericentriolar Material ◽  
Meiotic Spindles

SummaryA typical centrosome consists of a pair of centrioles embedded in a proteinous matrix called pericentriolar material. However, the centrosomes in the mouse oocytes and early embryos lack centrioles, but consist of the γ-tubulin-enriched vesicle aggregates. We previously revealed that Nek2 and centrobin/Nip2, a centrosomal substrate of Nek2, is critical for the mouse early embryogenesis, especially at the step of spindle assembly during mitosis. In order to expand our understanding of the biological functions of Nek2, we examined expression and knockdown phenotypes of Nek2 and its substrates, centrobin and C-Nap1, in the mouse oocyte. Nek2, centrobin and C-Nap1 in the mouse oocytes were also centrosomal. Suppression of Nek2 and its substrates did not affect meiotic resumption of the oocytes. However, meiosis of the Nek2- and centrobin-suppressed oocytes was not completed, but arrested with defects in spindle assembly. No visible phenotype was observed in the C-Nap1-suppressed oocytes. These results indicate that Nek2 is critical for proper assembly of the meiotic spindles. Centrobin may be a possible substrate of Nek2 responsible for the meiotic spindle assembly in the mouse oocytes.

scholarly journals Spindle assembly and cytokinesis in the absence of chromosomes during Drosophila male meiosis

2003 ◽  
Vol 160 (7) ◽  
pp. 993-999 ◽  
Author(s):  
Elisabetta Bucciarelli ◽  
Maria Grazia Giansanti ◽  
Silvia Bonaccorsi ◽  
Maurizio Gatti
Keyword(s):  
Chromosome Segregation ◽  
Spindle Assembly ◽  
Male Meiosis ◽  
Aurora B ◽  
Aurora B Kinase ◽  
Spindle Formation ◽  
Central Spindle ◽  
Morphological Transformations ◽  
Bipolar Spindles ◽  
Drosophila Mutants

Alarge body of work indicates that chromosomes play a key role in the assembly of both acentrosomal and centrosome-containing spindles. In animal systems, the absence of chromosomes either prevents spindle formation or allows the assembly of a metaphase-like spindle that fails to evolve into an ana-telophase spindle. Here, we show that Drosophila secondary spermatocytes can assemble morphologically normal spindles in the absence of chromosomes. The Drosophila mutants fusolo and solofuso are severely defective in chromosome segregation and produce secondary spermatocytes that are devoid of chromosomes. The centrosomes of these anucleated cells form robust asters that give rise to bipolar spindles that undergo the same ana-telophase morphological transformations that characterize normal spindles. The cells containing chromosome-free spindles are also able to assemble regular cytokinetic structures and cleave normally. In addition, chromosome-free spindles normally accumulate the Aurora B kinase at their midzones. This suggests that the association of Aurora B with chromosomes is not a prerequisite for its accumulation at the central spindle, or for its function during cytokinesis.

scholarly journals Deubiquitylase UCHL3 drives error correction at kinetochores and chromosome segregation independent of spindle assembly checkpoint

2020 ◽  
Author(s):  
Katerina Jerabkova ◽  
Yongrong Liao ◽  
Charlotte Kleiss ◽  
Sadek Fournane ◽  
Matej Durik ◽  
...  
Keyword(s):  
Error Correction ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Cellular Transformation ◽  
Aurora B ◽  
Mitotic Kinase ◽  
Daughter Cells ◽  
Microtubule Attachment ◽  
Anaphase Onset ◽  
Segregation Of Chromosomes

AbstractEqual segregation of chromosomes during mitosis ensures euploidy of daughter cells. Defects in this process may result in imbalance in chromosomal composition and cellular transformation. Two surveillance pathways, the spindle assembly checkpoint (SAC) and the error-correction (EC), exist at kinetochores that monitor microtubule attachment and faithful segregation of chromosomes at the metaphase to anaphase transition. However, the molecular understanding of the interplay between EC and SAC signaling remains limited. Here we describe a role of deubiquitylase UCHL3 in the regulation of EC pathway during mitosis. Downregulation or inhibition of UCHL3 leads to improper attachments of chromosomes to spindle microtubules and to chromosome alignment defects during metaphase. Frequent segregation errors during anaphase and consequently aneuploidy is also observed upon inactivation of UCHL3. Surprisingly, UCHL3 is not involved in SAC signaling as both recruitment of SAC proteins to kinetochores and timely anaphase onset are not perturbed in UCHL3-deficient cells. Mechanistically, UCHL3 interacts with and deubiquitylates the mitotic kinase Aurora B known to drive both SAC and EC signaling. UCHL3 promotes interaction of Aurora B with MCAK, important EC factor but does not regulate Aurora B binding to other interacting partners or subcellular localization of Aurora B. Our results thus suggest that UCHL3-mediated deubiquitylation functionally separates EC from SAC signaling during mitosis and is critical for maintenance of euploidy in human cells.

scholarly journals Catch and release: 14-3-3 controls Ncd in meiotic spindles

2017 ◽  
Vol 216 (10) ◽  
pp. 3003-3005
Author(s):  
Mary Dasso
Keyword(s):  
Drosophila Melanogaster ◽  
Spindle Assembly ◽  
Aurora B ◽  
Catch And Release ◽  
Cell Biol ◽  
Microtubule Motor ◽  
Meiotic Spindles ◽  
The Right

During Drosophila melanogaster oogenesis, spindle assembly occurs without centrosomes and relies on signals from chromosomes. Beaven et al. (2017. J. Cell. Biol. https://doi.org/10.1083/jcb.201704120) show that 14-3-3 proteins bind and inhibit a key microtubule motor, Ncd, during oogenesis, but Aurora B releases Ncd inhibition near chromosomes, allowing Ncd to work in the right time and place.

scholarly journals A novel transvection phenomenon affecting the white gene of Drosophila melanogaster.

Genetics ◽  
1990 ◽  
Vol 126 (1) ◽  
pp. 167-176
Author(s):  
D Gubb ◽  
M Ashburner ◽  
J Roote ◽  
T Davis
Keyword(s):  
Drosophila Melanogaster ◽  
Homologous Chromosome ◽  
Tandem Duplication ◽  
Gamma Ray ◽  
Insertion Site ◽  
Hairpin Loop ◽  
Homologous Chromosomes ◽  
Inverted Order ◽  
In Trans ◽  
In Cis

Abstract The zeste mutation of Drosophila melanogaster suppresses the expression of white genes in the eye. This suppression is normally dependent on there being two copies of w+ located close to each other in the genome--they may either be in cis (as in a tandem duplication of w+) or in trans, i.e. on homologous chromosomes. Duplicated w+ genes carried by a giant transposing element, TE146(Z), are suppressed by z whether they are in direct (tandem) or inverted order. The tandem form of the TE is very sensitive to a rearrangement on the homologous chromosome--many rearrangements with breakpoints "opposite" the TE's insertion site prevent the interaction between the white genes on a z background. These aberrations act as dominant suppressors of zeste that are specific to the tandemly duplicated form of TE146(Z). The inverted form of the TE146(Z) presumably pairs as a hairpin loop; this is more stable than the tandem form by the criterion that its zeste phenotype is unaffected by any of the aberrations. This effect of rearrangements has been used as the basis for a screen, gamma-ray induced aberrations with at least one breakpoint opposite the TE site were recovered by their suppression of the zeste phenotype.

scholarly journals WHAMM is essential for spindle formation and spindle actin polymerization in maturing mouse oocytes

Cell Cycle ◽  
2021 ◽  
pp. 1-11
Author(s):  
Yu-Jin Jo ◽  
Jeongwoo Kwon ◽  
Zhe-Long Jin ◽  
Suk Namgoong ◽  
Taeho Kwon ◽  
...  
Keyword(s):  
Actin Polymerization ◽  
Spindle Formation ◽  
Mouse Oocytes
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