Worm Breeder's Gazette 13(2): 52 (February 1, 1994)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
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.