ATM is required for rapid degradation of cyclin D1 in response to gamma-irradiation.

Abstract:

:The cellular response to DNA damage induced by gamma-irradiation activates cell-cycle arrest to permit DNA repair and to prevent replication. Cyclin D1 is the key molecule for transition between the G1 and S phases of the cell-cycle, and amplification or overexpression of cyclin D1 plays pivotal roles in the development of several human cancers. To study the regulation of cyclin D1 in the DNA-damaged condition, we analyzed the proteolytic regulation of cyclin D1 expression upon gamma-irradiation. Upon gamma-irradiation, a rapid reduction in cyclin D1 levels was observed prior to p53 stabilization, indicating that the stability of cyclin D1 is controlled in a p53-independent manner. Further analysis revealed that irradiation facilitated ubiquitination of cyclin D1 and that a proteasome inhibitor blocked cyclin D1 degradation under the same conditions. Interestingly, after mutation of threonine residue 286 of cyclin D1, which is reported to be the GSK-3beta phosphorylation site, the mutant protein showed resistance to irradiation-induced proteolysis although inhibitors of GSK-3beta failed to prevent cyclin D1 degradation. Rather, ATM inhibition markedly prevented cyclin D1 degradation induced by gamma-irradiation. Our data indicate that communication between ATM and cyclin D1 may be required for maintenance of genomic integrity achieved by rapid arrest of the cell-cycle, and that disruption of this crosstalk may increase susceptibility to cancer.

authors

Choo DW,Baek HJ,Motoyama N,Cho KH,Kim HS,Kim SS

doi

10.1016/j.bbrc.2008.11.132

subject

Has Abstract

pub_date

2009-01-23 00:00:00

pages

847-50

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(08)02371-1

journal_volume

378

pub_type

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