Rad9B responds to nucleolar stress through ATR and JNK signalling, and delays the G1-S transition.

Abstract:

:The complex formed by Rad9, Rad1 and Hus1 (9-1-1) protects against genomic instability by activating DNA damage checkpoint and DNA damage repair pathways, mainly in response to replication fork collapse and UV lesions. Here we compare the role of Rad9A (also known as Rad9) with the human paralogue Rad9B. Unlike Rad9A, overexpression of Rad9B delays cells in G1 phase. Moreover, Rad9B migrates to nucleoli after nucleolar stress in an ATR- and JNK-dependent manner, in a newly described nucleolar domain structure containing p21. Analysis of chimeras of Rad9A and Rad9B demonstrate that localisation to nucleoli and the block in G1 phase upon overexpression crucially depend on the Rad9B C-terminal tail. Taken together, data presented here show a relationship between Rad9B and pathways for checkpoints, stress response and nucleolar function.

journal_name

J Cell Sci

journal_title

Journal of cell science

authors

Pérez-Castro AJ,Freire R

doi

10.1242/jcs.091124

subject

Has Abstract

pub_date

2012-03-01 00:00:00

pages

1152-64

issue

Pt 5

eissn

0021-9533

issn

1477-9137

pii

jcs.091124

journal_volume

125

pub_type

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