Format

Send to

Choose Destination
See comment in PubMed Commons below
Mutat Res. 2003 Nov 27;532(1-2):245-53.

G2 and spindle assembly checkpoint adaptation, and tetraploidy arrest: implications for intrinsic and chemically induced genomic instability.

Author information

1
Institut de Biologie Structurale J-P Ebel, CEA-CNRS-UJF, 41 rue Jules Horowitz, 38027 Grenoble Cedex 1, France.

Abstract

While checkpoints that act in S-phase are essential to the maintenance of genomic stability, these checkpoints do not act alone. Additionally, G2 DNA damage checkpoints, the spindle assembly checkpoint, and a post-mitotic G1 tetraploidy checkpoint act subsequent to DNA replication to ensure genetic fidelity in cell division. In this review, we will examine how these checkpoints cooperate in the maintenance of genomic stability in response to either DNA damage or cytoskeletal disruption. Since the G2 and spindle assembly checkpoints are subject to adaptation, we will discuss how the G1 tetraploidy checkpoint acts in concert with these checkpoints to mediate stable arrest. We will also probe the relationship of these checkpoints by exploring common features of their regulation. Finally, the consequences of malfunction of these checkpoints for both intrinsic and chemically induced genomic instability will be examined. Among these consequences are aneuploidization, extranumerary centrosomes, and micronucleation.

PMID:
14643440
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center