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First published online January 25, 2006
doi: 10.1242/10.1242/dev.02235

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URI-1 is required for DNA stability in C. elegans

Christine T. Parusel¹, Ekaterini A. Kritikou^2,*, Michael O. Hengartner², Wilhelm Krek^1, and Monica Gotta^3,

¹ Eidgenoessische Technische Hochschule Zuerich, Institute of Cell Biology, CH-8093 Zuerich, Switzerland.
² University of Zuerich, Institute of Molecular Biology, CH-8057 Zuerich, Switzerland.
³ Eidgenoessische Technische Hochschule Zuerich, Institute of Biochemistry, CH-8093 Zuerich, Switzerland.

Authors for correspondence (e-mail: monica.gotta{at}bc.biol.ethz.ch; wilhelm.krek{at}cell.biol.ethz.ch)

Accepted 5 December 2005

Unconventional prefoldin RPB5 interactor (URI), an evolutionary conserved member of the prefoldin family of molecular chaperones, plays a central role in the regulation of nutrient-sensitive, TOR (target-of-rapamycin)-dependent gene expression programs in yeast. Mammalian URI has been shown to associate with key components of the transcriptional machinery, including RPB5, a shared subunit of all three RNA polymerases, the ATPases TIP48 and TIP49, which are present in various chromatin remodeling complexes, and human PAF1 and parafibromin, which are components of a transcription elongation complex. Here, we provide the first functional characterization of a URI-1 homolog in a multicellular organism and show that the C. elegans gene uri-1 is essential for germ cell proliferation. URI-1-deficient cells exhibit cell cycle arrest and display DNA breaks as evidenced by TUNEL staining and the appearance of HUS-1::GFP foci formation. In addition, uri-1(lf) mutants and uri-1(RNAi) worms show a p53-dependent increase in germline apoptosis. Our findings indicate that URI-1 has an important function in the mitotic and meiotic cell cycles. Furthermore, they imply that URI-1 participates in a pathway(s) that is associated with the suppression of endogenous genotoxic DNA damage and highlight a role for URI-1 in the control of genome integrity.

Key words: DNA damage, Germline, Prefoldin, Proliferation

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