Aurora B regulates spindle bipolarity in meiosis in vertebrate oocytes

Shao, Hua; Ma, Chunsheng; Zhang, Xuan; Miller, Ann L.; Li, Ruizhen

doi:10.4161/cc.21016

Cited by 22 publications

(23 citation statements)

References 35 publications

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“…S1A and B), as reported. 11,[21][22][23]25 Using a well-established in vitro depolymerization assay, 14 we examined the catalytic activity of MCAK WT and its variants. As expected, MCAK WT efficiently depolymerized MTs (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…11,23 Further studies have demonstrated that MCAK phosphorylation by Aurora B is involved in the correction of merotelic attachments and interfering with these phosphorylation sites lead to mitotic defects in Xenopus leavis extracts. 21,22,24,25 Interestingly, Aurora A was also shown to phosphorylate MCAK on S196 at early mitosis to regulate aster organization in Xenopus leavis extracts. 10 In addition, the Rac1-Aurora A-MCAK signaling pathway mediated by phosphorylation of S196 promotes endothelial cell polarization and directional migration in HUVEC and MCF-7 cells.…”

Section: Introductionmentioning

confidence: 99%

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Functional analysis of phosphorylation of the mitotic centromere-associated kinesin by Aurora B kinase in human tumor cells

et al. 2015

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(2015) Functional analysis of phosphorylation of the mitotic centromere-associated kinesin by Aurora B kinase in human tumor cells, Cell Cycle, 14:23, 3755-3767, DOI: 10.1080/15384101.2015 Keywords: Aurora B, cell motility, MCAK phosphorylation, microtubule dynamics, mitotic defect Abbreviations: ACA, anti-centromere antibody; MCAK, mitotic centromere-associated kinesin; MT, microtubule; MAP, microtubule-associated protein; Plk, Polo-like kinase; Cdk, cyclin-dependent kinase; HUVEC, human umbilical vein endothelial cell; PAK, p21-activated kinase.Mitotic centromere-associated kinesin (MCAK) is the best characterized member of the kinesin-13 family and plays important roles in microtubule dynamics during mitosis. Its activity and subcellular localization is tightly regulated by an orchestra of mitotic kinases, such as Aurora B. It is well known that serine 196 of MCAK is the major phosphorylation site of Aurora B in Xenopus leavis extracts and that this phosphorylation regulates its catalytic activity and subcellular localization. In the current study, we have addressed the conserved phosphorylation site serine 192 in human MCAK to characterize its function in more depth in human cancer cells. Our data confirm that S192 is the major phosphorylation site of Aurora B in human MCAK and that this phosphorylation has crucial roles in regulating its catalytic activity and localization at the kinetochore/centromere region in mitosis. Interfering with this phosphorylation leads to a delayed progression through prometa-and metaphase associated with mitotic defects in chromosome alignment and segregation. We show further that MCAK is involved in directional migration and invasion of tumor cells, and interestingly, interference with the S192 phosphorylation affects this capability of MCAK. These data provide the first molecular explanation for clinical observation, where an overexpression of MCAK was associated with lymphatic invasion and lymph node metastasis in gastric and colorectal cancer patients.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Functional analysis of phosphorylation of the mitotic centromere-associated kinesin by Aurora B kinase in human tumor cells

et al. 2015

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“…14 Aurora B is a multi-functional protein that plays many different roles in mitosis; 15 Aurora B is also subjected to phosphorylation and polyubiquitination during mitotic progression. 16,17 Aurora B activation also requires binding to its cofactor inner centromere protein (INCENP); 18 autophosphorylation at Thr 232 within its activation loop is required for kinase activity, and enzyme dephosphorylation is inhibitory.…”

Section: Introductionmentioning

confidence: 99%

Calmodulin protects Aurora B on the midbody to regulate the fidelity of cytokinesis

et al. 2013

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“…22 Meiosis I in human oocytes is error-prone primarily due to premature separation of sister chromatids (PSSC) (as appose to whole chromosome non-disjunction) 1,23 caused by premature loss of centromeric cohesin, 8 an error not likely recognized by SAC, which surveys kinetochore-microtubule interaction and tension. 33 In addition, animal oocytes lack centrosomes and assemble a bipolar spindle from multiple microtubule-organizing centers; 11,41,44 in acentrosomal spindles, kinetochore microtubules are entirely absent in some species 45,48 or, in other species, are relatively scarce and only discernable after experimental destruction of non-kinetochore microtubules. 2,6,12,18,20,36,44 Finally, the essence of SAC is the ability of the spindle to control the biochemistry of cytoplasmic proteins (Cdc20, cyclin B, securin, etc.).…”

Section: Introductionmentioning

confidence: 98%

“…33 In addition, animal oocytes lack centrosomes and assemble a bipolar spindle from multiple microtubule-organizing centers; 11,41,44 in acentrosomal spindles, kinetochore microtubules are entirely absent in some species 45,48 or, in other species, are relatively scarce and only discernable after experimental destruction of non-kinetochore microtubules. 2,6,12,18,20,36,44 Finally, the essence of SAC is the ability of the spindle to control the biochemistry of cytoplasmic proteins (Cdc20, cyclin B, securin, etc.). It seems that the mechanism would be quite different in somatic cells and large animal eggs, where the spindles are similar in size but the cytoplasm volumes are different by thousands-to millions-fold.…”

Section: Introductionmentioning

confidence: 98%

Meiosis I inXenopusoocytes is not error-prone despite lacking spindle assembly checkpoint

et al. 2014

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The spindle assembly checkpoint, SAC, is a surveillance mechanism to control the onset of anaphase during cell division. SAC prevents anaphase initiation until all chromosome pairs have achieved bipolar attachment and aligned at the metaphase plate of the spindle. In doing so, SAC is thought to be the key mechanism to prevent chromosome nondisjunction in mitosis and meiosis. We have recently demonstrated that Xenopus oocyte meiosis lacks SAC control. This prompted the question of whether Xenopus oocyte meiosis is particularly error-prone. In this study, we have karyotyped a total of 313 Xenopus eggs following in vitro oocyte maturation. We found no hyperploid egg, out of 204 metaphase II eggs with countable chromosome spreads. Therefore, chromosome nondisjunction is very rare during Xenopus oocyte meiosis I, despite the lack of SAC.

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Aurora B regulates spindle bipolarity in meiosis in vertebrate oocytes

Cited by 22 publications

References 35 publications

Functional analysis of phosphorylation of the mitotic centromere-associated kinesin by Aurora B kinase in human tumor cells

Functional analysis of phosphorylation of the mitotic centromere-associated kinesin by Aurora B kinase in human tumor cells

Calmodulin protects Aurora B on the midbody to regulate the fidelity of cytokinesis

Meiosis I inXenopusoocytes is not error-prone despite lacking spindle assembly checkpoint

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