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 Scijournal_title
Journal of cell scienceauthors
Pérez-Castro AJ,Freire Rdoi
10.1242/jcs.091124subject
Has Abstractpub_date
2012-03-01 00:00:00pages
1152-64issue
Pt 5eissn
0021-9533issn
1477-9137pii
jcs.091124journal_volume
125pub_type
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