Mutations in
eat-6 cause a distinctive pharyngeal phenotype consisting of incomplete or delayed relaxations of the corpus and terminal bulb and a reduction or lack of negative transients in the electropharyngeogram (EPG)(fig. 1). We have mapped
eat-6 to the right of
lin-25 by three point mapping and left of arP3 by its failure to complement arDf1 .
spa-1 ,which encodes a Na/K ATPase, had been cloned by Doug Fambrough and Delores Sommerville based on its homology to vertebrate ATPases and was mapped to this region of the physical map. This caused us to wonder whether the defect in
eat-6 could be a failure of the ATPase to maintain a proper resting potential and thereby to repolarize properly at the end of an action potential. To determine what effect a defect in Na/K ATPase function might have on pumping, we applied the inhibitor ouabain to dissected N2 pharynxes and recorded EPG's. This drug phenocopied the
eat-6 phenotype fairly well (fig.1). Based on these results, we concentrated on injecting the cosmid R07B8 ,which should contain the entire
spa-1 gene. We obtained two stably rescued lines. We have obtained several lambda clones from a genomic library using probes obtained from D. Sommerville and D. Fambrough and plan to inject these soon. Although not yet proven, it seems likely based on the phenotypes, pharmacology and molecular data that
eat-6 is
spa-1 and that the failure of the pharynx to repolarize following a pump is due to a reduction of the Na+ and K+ gradients across the muscle membranes.