Publication: Mad2 and spindle assembly checkpoint function during meiosis I in mammalian oocytes
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Date
2006
Authors
Homer, H.A.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
During mammalian mitosis, a proofreading
network called the spindle assembly checkpoint (SAC)
is indispensable for ensuring the fidelity of chromosome
segregation. An inhibitory SAC signal is deputed to
inhibits mitotic cell-cycle progression in response to
misaligned chromosomes until such imperfections are
rectified thereby ensuring equitable chromosome
partitioning to daughter cells. Amongst the cast of SAC
proteins, mitotic arrest deficient 2 (Mad2) plays a
leading role in transducing the SAC signal. The
aneuploidy and cancer predispositions of individuals
who harbour genetic mutations in SAC genes emphasise
the in vivo significance of this surveillance mechanism.
In humans, congenital aneuploidies such as Down’s
syndrome demonstrate an exponential increase with
advancing female age. Although largely the result of
female meiosis I errors, the molecular entities that
succumb with age in oocytes remain elusive. Declining
oocyte SAC function could plausibly contribute to such
errors. Until recently however, convincing evidence for a
functional SAC in mammalian oocytes during meiosis I
was unforthcoming. Here I review the evidence
regarding the SAC in female mammalian meiosis I and
how our understanding of this system has evolved in
recent years. This review will focus on Mad2 as this is
the SAC protein that has been most comprehensively
investigated.
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