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Formation of the dorsal–ventral axis of the  Drosophila  wing depends on activity of the LIM–homeodomain protein Apterous (Ap). Here we report that Ap activity levels are modulated by dLMO, the protein encoded by the  Beadex  ( Bx ) gene. Overexpression of dLMO in  Bx  mutants interferes with Apterous function. Conversely, Bx  loss-of-function mutants fail to down-regulate Apterous activity at late stages of wing development. Biochemical analysis shows that dLMO protein competes for binding of Apterous to its cofactor Chip. These data suggest that Apterous activity depends on formation of a functional complex with Chip and that the relative levels of dLMO, Apterous, and Chip determine the level of Apterous activity. The dominant interference mechanism of dLMO action may serve as a model for the mechanism by which  LMO  oncogenes cause cancer when misexpressed in T cells.

genes and development

Beadex encodes an LMO protein that regulates Apterous LIM–homeodomain activity in Drosophila wing development: a model for LMO oncogene function