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Development 129, 399-407 (2002)
© 2002 The Company of Biologists Limited

The Drosophila melanogaster gene brain tumor negatively regulates cell growth and ribosomal RNA synthesis

Deborah J. Frank*, Bruce A. Edgar and Mark B. Roth{dagger}

Division of Basic Sciences and Molecular and Cellular Biology Program, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
* Present address: Biology Department, Washington University, 1 Brookings Drive, St Louis, MO 63130, USA

{dagger}Author for correspondence (e-mail: mroth{at}fred.fhcrc.org)

Accepted 17 October 2001

The regulation of ribosome synthesis is likely to play an important role in the regulation of cell growth. Previously, we have shown that the ncl-1 gene in Caenorhabditis elegans functions as an inhibitor of cell growth and ribosome synthesis. We now indicate that the Drosophila melanogaster tumor suppressor brain tumor (brat) is an inhibitor of cell growth and is a functional homolog of the C. elegans gene ncl-1. The brat gene is able to rescue the large nucleolus phenotype of ncl-1 mutants. We also show that brat mutant cells are larger, have larger nucleoli, and have more ribosomal RNA than wild-type cells. Furthermore, brat overexpressing cells contain less ribosomal RNA than control cells. These results suggest that the tumorous phenotype of brat mutants may be due to excess cell growth and ribosome synthesis.

Key words: Drosophila, cell growth, ribosome, brain tumor


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© The Company of Biologists Ltd 2002