期刊
SCIENCE
卷 326, 期 5955, 页码 991-994出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1175326
关键词
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资金
- Medical Research Council [082587/Z/07/Z]
- MRC [G0400530] Funding Source: UKRI
- Medical Research Council [G0400530] Funding Source: researchfish
Two critical stages of mammalian oocyte regulation are prophase I arrest, which is important for sustaining the oocyte pool, and the progression through meiosis I (MI) to produce fertilizable eggs. We have found that the spindle assembly checkpoint protein BubR1 regulates both stages in mouse oocytes. We show that oocytes depleted of BubR1 cannot sustain prophase I arrest and readily undergo germinal vesicle breakdown, a marker for reentry into MI. BubR1-depleted oocytes then arrest before completing MI, marked by failure of polar body extrusion. Both meiotic defects in BubR1-depleted oocytes are due to reduced activity of the master regulator known as the anaphase-promoting complex (APC), brought about through diminished levels of the APC coactivator Cdh1.
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