◈ Topic : Calcium binding proteins in C. elegans development and behavior
◈ Speaker : Joo hong Ahnn (Hanyang University)
◈ Date/Time : PM 4:00/Mar. 5/2010
◈ Place : Postech Biotech Center auditorium
◈ Information : Seung Jae Lee (279-2351)
◈ Abstract
Ca2+/calmodulin-dependent calcineurin has been shown to have important roles in various Ca2+ signaling pathways. We have previously reported that cnb-1 mutants, null mutants of a regulatory B subunit, displayed pleiotropic defects including uncoordinated movement and delayed egg laying in C. elegans. Interestingly, gain-of-function mutants of a catalytic A subunit showed exactly opposite phenotypes to those of cnb-1 mutants providing an excellent genetic model to define calcium-mediated signaling pathway at the organism level. Furthermore, calcineurin is also important for normal cuticle formation, which is required for maintenance of normal body size in C. elegans. Genetic interactions between tax-6 and several mutants including egl-30 and egl-10 which are known to be involved in G-protein signaling pathway suggest that calcineurin indeed regulates locomotion and serotonin-mediated egg laying through goa-1(Goα) and egl-30(Gqα). Our results indicate that, along with CaMKII, calcineurin regulates G-protein-coupled phosphorylation signaling pathways in C. elegans.
The enteric muscle contraction (EMC) is the last step of the defecation behavior which occurs every 50 seconds in C. elegans. This EMC is regulated by intestinal and anal depressor muscles, which are innervated by GABA motor neurons. Our data show that calcineurin (tax-6) is expressed in intestinal muscle and anal depressor muscle, and the gain-of-function mutant of calcineurin, tax-6(jh107), shows defects in enteric muscle contractions. In addition, exogenous GABA failed to rescue the EMC defects of tax-6(jh107) indicating that calcineurin functions in postsynaptic muscles rather than presynaptic neurons regulating EMC, which could be rescued by exogenous GABA treatment. Genetic epistasis with exp-1 mutant, which encodes an excitatory GABA receptor, suggests that calcineurin functions as a negative regulator of exp-1 in excitatory GABA signaling.
