Chromosome missegregation and apoptosis in mice lacking the mitotic checkpoint protein Mad2.

Abstract:

:The initiation of chromosome segregation at anaphase is linked by the spindle assembly checkpoint to the completion of chromosome-microtubule attachment during metaphase. To determine the function of the mitotic checkpoint protein Mad2 during normal cell division and when mitosis goes awry, we have knocked out Mad2 in mice. We find that E5.5 embryonic cells lacking Mad2, like mad2 yeast, grow normally but are unable to arrest in response to spindle disruption. At E6.5, the cells of the epiblast begin rapid cell division and the absence of a checkpoint results in widespread chromosome missegregation and apoptosis. In contrast, the postmitotic trophoblast giant cells survive without Mad2. Thus, the spindle assembly checkpoint is required for accurate chromosome segregation in mitotic mouse cells, and for embryonic viability, even in the absence of spindle damage.

journal_name

Cell

journal_title

Cell

authors

Dobles M,Liberal V,Scott ML,Benezra R,Sorger PK

doi

10.1016/s0092-8674(00)80875-2

subject

Has Abstract

pub_date

2000-06-09 00:00:00

pages

635-45

issue

6

eissn

0092-8674

issn

1097-4172

pii

S0092-8674(00)80875-2

journal_volume

101

pub_type

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