Negative regulation of male development in Caenorhabditis elegans by a protein-protein interaction between TRA-2A and FEM-3

The tra-2 gene of the nematode Caenorhabditis elegans encodes a predicted membrane protein, TRA-2A, that promotes XX hermaphrodite development. Genetic analysis suggests that tra-2 is a negative regulator of three genes that are required for male development: fem-1, fem-2, and fem-3. We report that...

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Bibliographic Details
Published in:Genes & development 1999-06, Vol.13 (11), p.1453-1463
Main Authors: Mehra, A, Gaudet, J, Heck, L, Kuwabara, P E, Spence, A M
Format: Article
Language:English
Subjects:
Animals
Binding Sites
Caenorhabditis elegans
Caenorhabditis elegans - genetics
Caenorhabditis elegans - physiology
Caenorhabditis elegans Proteins
Cell Cycle Proteins - genetics
Cell Cycle Proteins - metabolism
Cloning, Molecular
Female
Heat-Shock Response
Helminth Proteins - genetics
Helminth Proteins - metabolism
Male
Membrane Proteins - genetics
Membrane Proteins - metabolism
Phosphoprotein Phosphatases
Research Paper
Saccharomyces cerevisiae
Sex Differentiation - genetics
Transgenes
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Summary:The tra-2 gene of the nematode Caenorhabditis elegans encodes a predicted membrane protein, TRA-2A, that promotes XX hermaphrodite development. Genetic analysis suggests that tra-2 is a negative regulator of three genes that are required for male development: fem-1, fem-2, and fem-3. We report that the carboxy-terminal region of TRA-2A interacts specifically with FEM-3 in the yeast two-hybrid system and in vitro. Consistent with the idea that FEM-3 is a target of negative regulation, we find that excess FEM-3 can overcome the feminizing effect of tra-2 and cause widespread masculinization of XX somatic tissues. In turn, we show that the masculinizing effects of excess FEM-3 can be suppressed by overproduction of the carboxy-terminal domain of TRA-2A. A FEM-3 fragment that retains TRA-2A-binding activity can masculinize fem-3(+) animals, but not fem-3 mutants, suggesting that it is possible to release and to activate endogenous FEM-3 by titrating TRA-2A. We propose that TRA-2A prevents male development by interacting directly with FEM-3 and that a balance between the opposing activities of TRA-2A and FEM-3 determines sex-specific cell fates in somatic tissues. When the balance favors FEM-3, it acts through or with the other FEM proteins to promote male cell fates.
ISSN:0890-9369
DOI:10.1101/gad.13.11.1453