Abstract:
:The level of Sirt2 protein is reduced in oocytes from aged mice, while exogenous expression of Sirt2 could ameliorate the maternal age-associated meiotic defects. To date, the underlying mechanism remains unclear. Here, we confirmed that specific depletion of Sirt2 disrupts maturational progression and spindle/chromosome organization in mouse oocytes, with compromised kinetochore-microtubule attachments. Candidate screening revealed that acetylation state of lysine 243 on BubR1 (BubR1-K243, an integral part of the spindle assembly checkpoint complex) functions during oocyte meiosis, and acetylation-mimetic mutant BubR1-K243Q results in the very similar phenotypes as Sirt2-knockdown oocytes. Furthermore, we found that nonacetylatable-mimetic mutant BubR1-K243R partly prevents the meiotic deficits in oocytes depleted of Sirt2. Importantly, BubR1-K243R overexpression in oocytes derived from aged mice markedly suppresses spindle/chromosome anomalies and thereupon lowers the incidence of aneuploid eggs. In sum, our data suggest that Sirt2-dependent BubR1 deacetylation involves in the regulation of meiotic apparatus in normal oocytes and mediates the effects of advanced maternal age on oocyte quality.
journal_name
Aging Celljournal_title
Aging cellauthors
Qiu D,Hou X,Han L,Li X,Ge J,Wang Qdoi
10.1111/acel.12698subject
Has Abstractpub_date
2018-02-01 00:00:00issue
1eissn
1474-9718issn
1474-9726journal_volume
17pub_type
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