Abstract
Mammalian oocytes are particularly error prone in chromosome segregation during two successive meiotic divisions. The proper kinetochore-microtubule attachment is a prerequisite for faithful chromosome segregation during meiosis. Here, we report that Spc24 localizes at the kinetochores during mouse oocyte meiosis. Depletion of Spc24 using specific siRNA injection caused defective kinetochore-microtubule attachments and chromosome misalignment, and accelerated the first meiosis by abrogating the kinetochore recruitment of spindle assembly checkpoint protein Mad2, leading to a high incidence of aneuploidy. Thus, Spc24 plays an important role in genomic stability maintenance during oocyte meiotic maturation.
Highlights
Maintenance of genomic stability is a key prerequisite for all multicellular organisms
In the GV oocytes, Spc24 was primarily distributed in the germinal vesicles
It is revealed that Spc24 may involve in the K-MT attachment as a component of the kinetochore in mouse oocyte meiosis
Summary
Maintenance of genomic stability is a key prerequisite for all multicellular organisms. Abnormalities in chromosome number have been associated with human diseases, and maternally-derived aneuploidies are problematic [1, 2]. Mammalian oocytes are error prone in segregating chromosomes during two successive meiotic divisions. Most aneuploidies appear to be caused by mis-segregation of a bivalent in the first meiotic division [3, 4]. One of the most common viable aneuploidies is trisomy 21 resulting from mis-segregation of chromosome 21 during the first meiosis [2]. There has been much interest in understanding how chromosome segregation is controlled in meiosis I
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