We identified the homeodomain factor, CEH-22, as a candidate regulator of the pharyngeal myosin gene,
myo-2. CEH-22 binds to one site that contributes to
myo-2 enhancer function, and it is expressed in pharyngeal muscle precursors before differentiation. To ask directly if CEH-22 activates pharyngeal muscle-specific genes, we expressed CEH-22 under control of the
unc-54 promoter. Body wall muscle expression of CEH-22 can activate both the pharyngeal myosin genes
myo-2 and
myo-1. In contrast, two early markers of pharyngeal muscle differentiation, an antigen recognized by MAb 3NB12 and a
ceh-22::lacZ fusion, are not activated. Therefore CEH-22 is sufficient to induce aspects of pharyngeal muscle differentiation in body wall muscle, but it does not result in a complete transformation to pharyngeal muscle. We have isolated a
ceh-22 mutant by insertion and imprecise excision of Tc1.
ceh-22(
cc8266) contains a deletion that removes a coding exon but leaves the homeobox intact. These homozygotes have defects in pharyngeal muscle morphology and function that result in a partially penetrant larval lethal phenotype.
ceh-22 mutants have defects in pharyngeal muscle gene expression. An enhancer consisting of CEH-22 binding sites, which is highly active in wild type, is inactive in the mutant. However, these mutants express the endogenous
myo-2 gene similarly to wild type. This is consistent with previous results indicating
myo-2 contains multiple regulatory elements that may be sufficient for expression. Our working model is that CEH-22 is one of several factors regulating
myo-2 and other pharyngeal muscle genes. In the absence of CEH-22, these other factors activate sufficient gene expression to make a partially functional pharynx. The
ceh-22 phenotype might result from either subtle defects in myosin expression or defects in expression of other downstream targets.