The development of the Drosophila melanogaster wing depends on its subdivision 
into anterior and posterior compartments, which constitute two independent cell 
lineages since their origin in the embryonic ectoderm. The anterior-posterior 
compartment boundary is the place where signaling by the Hedgehog pathway takes 
place, and this requires pathway activation in anterior cells by ligand 
expressed exclusively in posterior cells. Several mechanisms ensure the 
confinement of hedgehog expression to posterior cells, including repression by 
Cubitus interruptus, the co-repressor Groucho and Master of thick veins. In this 
work we identified Kismet, a chromodomain-containing protein of the SNF2-like 
family of ATPases, as a novel component of the hedgehog transcriptional 
repression mechanism in anterior compartment cells. In kismet mutants, hedgehog 
is ectopically expressed in a domain of anterior cells close to the 
anterior-posterior compartment boundary, causing inappropriate activation of the 
pathway and changes in the development of the central region of the wing. The 
contribution of Kismet to the silencing of hedgehog expression is limited to 
anterior cells with low levels of the repressor form of Cubitus interruptus. We 
also show that knockdown of CHD8, the kismet homolog in Xenopus tropicalis, is 
also associated with ectopic sonic hedgehog expression and up-regulation of one 
of its target genes in the eye, Pax2, indicating the evolutionary conservation 
of Kismet/CHD8 function in negatively controlling hedgehog expression.