Abstract
Here we show that in the nematode Caenorhabditis elegans mutational inactivation of two autophagy genes unc-51/atg1 and bec-1/atg6/beclin1 results in small body size without affecting cell number. Furthermore, loss-of-function mutations in unc-51 and bec-1 suppress the giant phenotype of mutant animals with aberrant insulin-like growth factor-1 (insulin/IGF-1) or transforming growth factor-beta (TGF-beta) signaling. This function for unc-51 and bec-1 in cell size control and their interaction with these two growth modulatory pathways may represent a link between the hormonal and nutritional regulation of cell growth.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Autophagy*
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Caenorhabditis elegans / cytology
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Caenorhabditis elegans / growth & development*
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Caenorhabditis elegans / metabolism
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Caenorhabditis elegans Proteins / physiology*
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Cell Size*
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Mutation
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Phenotype
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Protein Serine-Threonine Kinases / physiology*
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Somatomedins / metabolism
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Transforming Growth Factor beta / metabolism
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Vesicular Transport Proteins
Substances
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Caenorhabditis elegans Proteins
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Somatomedins
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Transforming Growth Factor beta
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Vesicular Transport Proteins
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bec-1 protein, C elegans
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UNC-51 protein, C elegans
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Protein Serine-Threonine Kinases