scholarly journals BubR1 is a spindle assembly checkpoint protein regulating meiotic cell cycle progression of mouse oocyte

Cell Cycle ◽  
2010 ◽  
Vol 9 (6) ◽  
pp. 1112-1121 ◽  
Author(s):  
Liang Wei ◽  
Xing-Wei Liang ◽  
Qing-Hua Zhang ◽  
Mo Li ◽  
Ju Yuan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Mouse Oocyte ◽  
Meiotic Cell ◽  
Cycle Progression ◽  
Checkpoint Protein ◽  
Spindle Assembly Checkpoint Protein

scholarly journals CNOT 6L couples the selective degradation of maternal transcripts to meiotic cell cycle progression in mouse oocyte

2018 ◽  
Vol 37 (24) ◽  
Author(s):  
Qian‐Qian Sha ◽  
Jia‐Li Yu ◽  
Jing‐Xin Guo ◽  
Xing‐Xing Dai ◽  
Jun‐Chao Jiang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Mouse Oocyte ◽  
Meiotic Cell ◽  
Cycle Progression ◽  
Selective Degradation ◽  
Maternal Transcripts

scholarly journals Bub3 Is a Spindle Assembly Checkpoint Protein Regulating Chromosome Segregation during Mouse Oocyte Meiosis

PLoS ONE ◽  
2009 ◽  
Vol 4 (11) ◽  
pp. e7701 ◽  
Author(s):  
Mo Li ◽  
Sen Li ◽  
Ju Yuan ◽  
Zhen-Bo Wang ◽  
Shao-Chen Sun ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Mouse Oocyte ◽  
Checkpoint Protein ◽  
Oocyte Meiosis ◽  
Spindle Assembly Checkpoint Protein

scholarly journals TheSac3Homologueshd1Is Involved in Mitotic Progression in Mammalian Cells

2004 ◽  
Vol 279 (44) ◽  
pp. 46182-46190 ◽  
Author(s):  
Sefat-e- Khuda ◽  
Mikoto Yoshida ◽  
Yan Xing ◽  
Tatsuya Shimasaki ◽  
Motohiro Takeya ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mammalian Cells ◽  
Cell Cycle Progression ◽  
Spindle Assembly Checkpoint ◽  
Fluorescent Protein ◽  
Spindle Assembly ◽  
Centrosome Duplication ◽  
Cycle Progression ◽  
M Phase ◽  
Green Fluorescent

SaccharomycesSac3 required for actin assembly was shown to be involved in DNA replication. Here, we studied the function of a mammalian homologue SHD1 in cell cycle progression. SHD1 is localized on centrosomes at interphase and at spindle poles and mitotic spindles, similar to α-tubulin, at M phase. RNA interference suppression of endogenousshd1caused defects in centrosome duplication and spindle formation displaying cells with a single apparent centrosome and down-regulated Mad2 expression, generating increased micronuclei. Conversely, increased expression of SHD1 by DNA transfection withshd1-green fluorescent protein (gfp) vector for a fusion protein of SHD1 and GFP caused abnormalities in centrosome duplication displaying cells with multiple centrosomes and deregulated spindle assembly with up-regulated Mad2 expression until anaphase, generating polyploidy cells. These results demonstrated thatshd1is involved in cell cycle progression, in particular centrosome duplication and a spindle assembly checkpoint function.

scholarly journals Centromeric CENP-A loading requires accurate mitotic timing, which is linked to checkpoint proteins

2018 ◽  
Author(s):  
Anne Laure Pauleau ◽  
Andrea Bergner ◽  
Janko Kajtez ◽  
Sylvia Erhardt
Keyword(s):  
Cell Cycle ◽  
Spindle Assembly Checkpoint ◽  
Cultured Cells ◽  
Histone H3 ◽  
Spindle Assembly ◽  
Checkpoint Proteins ◽  
Checkpoint Protein ◽  
Histone H3 Variant ◽  
Metaphase Stage ◽  
Spindle Assembly Checkpoint Protein

AbstractA defining feature of centromeres is the presence of the histone H3 variant CENP-A that replaces H3 in a subset of centromeric nucleosomes. In Drosophila cultured cells CENP-A deposition at centromeres takes place during the metaphase stage of the cell cycle and strictly depends on the presence of its specific chaperone CAL1. How CENP-A loading is restricted to mitosis is unknown. We found that overexpression of CAL1 is associated with increased CENP-A levels at centromeres and completely uncouples CENP-A loading from mitosis. Moreover, CENP-A levels inversely correlate with mitosis duration. We found that CAL1 interacts with the spindle assembly checkpoint protein and RZZ complex component Zw10 and thus constitutes the anchor for the recruitment of RZZ. Therefore, CAL1 controls CENP-A incorporation at centromeres both quantitatively and temporally, connecting it to the spindle assembly checkpoint to ensure mitotic fidelity.

scholarly journals Distinct responses to reduplicated chromosomes require distinct Mad2 responses

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Benjamin M Stormo ◽  
Donald T Fox
Keyword(s):  
Cell Cycle ◽  
Cancer Progression ◽  
Sister Chromatid ◽  
Spindle Assembly Checkpoint ◽  
Polytene Chromosomes ◽  
Spindle Assembly ◽  
Tissue Development ◽  
Checkpoint Protein ◽  
Independent Mechanism ◽  
Spindle Assembly Checkpoint Protein

Duplicating chromosomes once each cell cycle produces sister chromatid pairs, which separate accurately at anaphase. In contrast, reduplicating chromosomes without separation frequently produces polytene chromosomes, a barrier to accurate mitosis. Chromosome reduplication occurs in many contexts, including: polytene tissue development, polytene tumors, and following treatment with mitosis-blocking chemotherapeutics. However, mechanisms responding to or resolving polyteny during mitosis are poorly understood. Here, using Drosophila, we uncover two distinct reduplicated chromosome responses. First, when reduplicated polytene chromosomes persist into metaphase, an anaphase delay prevents tissue malformation and apoptosis. Second, reduplicated polytene chromosomes can also separate prior to metaphase through a spindle-independent mechanism termed Separation-Into-Recent-Sisters (SIRS). Both reduplication responses require the spindle assembly checkpoint protein Mad2. While Mad2 delays anaphase separation of metaphase polytene chromosomes, Mad2’s control of overall mitotic timing ensures efficient SIRS. Our results pinpoint mechanisms enabling continued proliferation after genome reduplication, a finding with implications for cancer progression and prevention.

scholarly journals Extracellular Signal-regulated Kinase 1/2 Activity Is Not Required in Mammalian Cells during Late G2 for Timely Entry into or Exit from Mitosis

2006 ◽  
Vol 17 (12) ◽  
pp. 5227-5240 ◽  
Author(s):  
Mio Shinohara ◽  
Alexei V. Mikhailov ◽  
Julio A. Aguirre-Ghiso ◽  
Conly L. Rieder
Keyword(s):  
Cell Cycle ◽  
Mammalian Cells ◽  
Cell Cycle Progression ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Live Cells ◽  
Cycle Progression ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Sustained Inhibition

Extracellular signal-regulated kinase (ERK)1/2 activity is reported to be required in mammalian cells for timely entry into and exit from mitosis (i.e., the G2-mitosis [G2/M] and metaphase-anaphase [M/A] transitions). However, it is unclear whether this involvement reflects a direct requirement for ERK1/2 activity during these transitions or for activating gene transcription programs at earlier stages of the cell cycle. To examine these possibilities, we followed live cells in which ERK1/2 activity was inhibited through late G2 and mitosis. We find that acute inhibition of ERK1/2 during late G2 and through mitosis does not affect the timing of the G2/M or M/A transitions in normal or transformed human cells, nor does it impede spindle assembly, inactivate the p38 stress-activated checkpoint during late G2 or the spindle assembly checkpoint during mitosis. Using CENP-F as a marker for progress through G2, we also show that sustained inhibition of ERK1/2 transiently delays the cell cycle in early/mid-G2 via a p53-dependent mechanism. Together, our data reveal that ERK1/2 activity is required in early G2 for a timely entry into mitosis but that it does not directly regulate cell cycle progression from late G2 through mitosis in normal or transformed mammalian cells.

scholarly journals Distinct Responses to Reduplicated Chromosomes Require Distinct Mad2 Responses

2016 ◽  
Author(s):  
Benjamin M. Stormo ◽  
Donald T. Fox
Keyword(s):  
Cell Cycle ◽  
Cancer Progression ◽  
Sister Chromatid ◽  
Spindle Assembly Checkpoint ◽  
Polytene Chromosomes ◽  
Spindle Assembly ◽  
Tissue Development ◽  
Checkpoint Protein ◽  
Spindle Assembly Checkpoint Protein

ABSTRACTDuplicating chromosomes once each cell cycle produces sister chromatid pairs, which separate accurately at anaphase. In contrast, reduplicating chromosomes without separation frequently produces polytene chromosomes, a barrier to accurate mitosis. Chromosome reduplication occurs in many contexts, including: polytene tissue development, polytene tumors, and following treatment with mitosis-blocking chemotherapeutics. However, mechanisms responding to or resolving polyteny during mitosis are poorly understood. Here, using Drosophila, we uncover two distinct reduplicated chromosome responses. First, when reduplicated polytene chromosomes persist into metaphase, an anaphase delay prevents tissue malformation and apoptosis. Second, reduplicated polytene chromosomes can also separate prior to metaphase through a spindlePindependent mechanism termed Separation-Into-Recent-Sisters (SIRS). Both reduplication responses require the spindle assembly checkpoint protein Mad2. While Mad2 delays anaphase separation of metaphase polytene chromosomes, Mad2’s control of overall mitotic timing ensures efficient SIRS. Our results pinpoint mechanisms enabling continued proliferation after genome reduplication, a finding with implications for cancer progression and prevention.

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