Abstract
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.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Brain / cytology
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Brain / metabolism
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Caenorhabditis elegans Proteins*
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Carrier Proteins / metabolism
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Cell Division / physiology*
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Cell Size
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DNA-Binding Proteins*
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Drosophila Proteins / genetics
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Drosophila Proteins / metabolism
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Drosophila melanogaster / cytology
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Drosophila melanogaster / genetics*
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Drosophila melanogaster / physiology
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Flow Cytometry
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Genes, Insect
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Genes, Tumor Suppressor
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Green Fluorescent Proteins
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In Situ Hybridization
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Insect Proteins / genetics*
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Insect Proteins / metabolism*
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Luminescent Proteins / genetics
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Luminescent Proteins / metabolism
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Mutation
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RNA, Ribosomal / biosynthesis*
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RNA-Binding Proteins
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Recombinant Fusion Proteins / metabolism
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Ribosomal Proteins / metabolism
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Transgenes
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Wings, Animal / physiology
Substances
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Caenorhabditis elegans Proteins
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Carrier Proteins
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DNA-Binding Proteins
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Drosophila Proteins
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Insect Proteins
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Luminescent Proteins
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RNA, Ribosomal
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RNA-Binding Proteins
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Recombinant Fusion Proteins
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Ribosomal Proteins
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brat protein, Drosophila
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ncl-1 protein, C elegans
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Green Fluorescent Proteins