Epistasis or 'suppression' of a gain-of-function mutation in Drosophila. In early Drosophila development, the terminal cells differentiate from the central cells in response to signaling through the Torso protein, a receptor tyrosine kinase that is expressed on all the cells of the developing embryo. Torso signaling is confined to the termini through localized release (or processing) of Torso's ligand, which activates the receptor, resulting ultimately in transcription of the tailless gene. Tailless is a transcriptional regulator that specifies terminal cell fates and represses central cell fates. In torso loss-of-function mutants (torsolof), all cells develop as central cells. In torso gain-of-function mutants (torsogof), the receptor is constitutively active and all cells develop as terminal cells. In the double mutant, loss of tailless function masks the effect of the torso gain-of-function mutation and all the cells differentiate as central cells.
Roth et al. Journal of Biology 2009 8:35 doi:10.1186/jbiol144