Potassium channels are present in all cell types of C. elegans. The channels perform functions that include shaping dynamic electrical signaling and setting resting potentials. The most common type of potassium channel in C. elegans has four transmembrane domains; one such channel is the
sup-9 two-pore potassium channel. Genetic evidence suggests that SUP-9 functions in a channel complex with putative regulatory membrane proteins, SUP-10 and UNC-93. Sup-9 was originally identified as a suppressor of
unc-93 gain-of-function alleles. Gain-of-function mutations in these three proteins cause defective muscle function, including egg-laying and defecation defects and rubberband paralysis. Rubberband paralysis is flaccid paralysis characterized by ineffective backing ability from touch stimulus on the head. Loss-of-function mutations in any one of these three proteins result in worms with no visible defect as well as suppression of gain-of-function mutations in the other two proteins. In addition to suppressing egg-laying and motility defects, certain missense
sup-9 alleles confer an additional male mating defect in an
unc-93(gf) background: either via synergistic effects between the two mutant proteins or by incomplete suppression of the
unc-93(gf) phenotype. Mating is one of the most complex behaviors of C. elegans and involves 41 male specific muscles and additional dimorphic muscles in males. Abnormal charge gradients generated from SUP-9 mutant channels in the cell membranes of male muscles could lead to decreased contractility or coordination of male-specific muscles and structures necessary for mating. This research aims to identify the tissues expressing
sup-9 in males in order to better understand the relationship between the male mating defect and the SUP-9 potassium channel. We have used a transcriptional fusion of the
sup-9 promoter and GFP to identify cells expressing
sup-9. Consistent expression of
sup-9 was seen in 12 of 15 male-specific or dimorphic muscle types. Visualization of
sup-9 expression was not possible in the remaining three muscle types, the outer longitudinal muscles (aol, pol, and cdl), because their location overlaps that of
sup-9-expressing body wall muscle. Our research also failed to demonstrate expression of the transgene in any male specific neurons. We believe that the male mating deficiency generated from specific missense
sup-9 mutations in an
unc-93(gf) background is caused by disruption in normal muscle function of the male tail. We have designed further experiments to test this hypothesis. .