egl-30 encodes the C. elegans homologue of the mammalian heterotrimeric G protein alpha subunit, Gq. Reduction-of-function and loss-of-function mutations in
egl-30 affect diverse behaviors in C. elegans. These include: viability, egg-laying, pharyngeal pumping, movement, and spicule protraction. In a screen for suppressors of the reduction-of-function mutation,
egl-30(
md186), two intragenic suppressor mutations were recovered. One of the mutations lies in a region in close proximity to residues involved in guanine ring binding. The other mutation is in a region that might affect receptor interaction, and is not expected to make contacts with the region that contains the original
egl-30(
md186) mutation. These mutants phenotypically resemble worms that overexpress
egl-30, and have been used as a tool to characterize genes that function in a pathway with
egl-30. From these studies, it is clear that EGL-30 regulates egg laying via downstream signaling pathways distinct from downstream pathways so far defined that control movement (1), viability (2), and spicule protraction (3). A rescuing gfp::
egl-30 transgene confirms that
egl-30 is coexpressed in some cells with
egl-8 and
lfe-1/itr-1/dec-4, two genes that encode signaling molecules defined as downstream of Gq in mammalian systems, and that appear to be downstream of
egl-30 with respect to movement and viability, respectively (1,2). However,
egl-30 is also uniquely localized and expressed in some cells. To determine the basis for the differences in genetic interactions with respect to different behaviors, we are develooping a system to characterize cell-type-specific molecular interactions with EGL-30 in vivo . 1. Lackner MR, Nurrish SJ, Kaplan JM; Neuron 24: 335-346 1999 2. Hajdu-Cronin YM and Sternberg PW, personal communication 3. Garcia LR and Sternberg PW, personal communication