Transforming growth factor (TGF-beta) regulates normal cell proliferation, differentiation, and survival. In C. elegans, a TGF-beta-like gene,
daf-7, regulates dauer entry and longevity. Many compounds including steroids, other growth factors, and the neurotransmitter serotonin regulate the synthesis and/or the secretion of TGF-beta in mammals. These compounds often signal through heterotrimeric G proteins. We are using transgenic worm lines expressing green fluorescent protein (GFP) under the
daf-7 promoter as a tool to understand how
daf-7 transcription is regulated by the G proteins EGL-30 (similar to human Galphaq) and GOA-1 (similar to human Galphao). We have found that mutations in
goa-1 and
egl-30 caused changes in
pdaf-7::GFP expression during both the L1 and L2 stages. In addition, we have found that mutations in
goa-1 and
egl-30 altered dauer formation. We have begun to investigate the role of GOA-1 and EGL-30 in
daf-7 expression and have found they were required for normal sensitivity to dauer-related ascarosides, which modulate dauer entry1. Besides dauer entry, DAF-7 plays a role in the localization of DAF-162. We have begun to investigate whether
goa-1 and
egl-30 are also important for this function of DAF-7 as well. 1= Butcher RA, Fujita M, Schroeder FC, Clardy J. (2007). Nat Chem Biol. 3(7):420-2 2= Lee, RYN, Hench, J and Ruvkun, G. (2001) Current Biology 11:1950--1957