Worm Breeder's Gazette 11(2): 88
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.
Wild-type worms defecate by periodically activating a stereotyped series of muscle contractions. First, the posterior body muscles briefly contract (pBoc) in all four muscle quadrants, squeezing the gut contents anteriorly. When these muscles relax some of the gut contents rush back and collect in a bolus in the preanal region. Just as this relaxation is complete, the anterior body muscles contract ( aBoc) in all four muscle quadrants, driving the pharynx back into the gut and pressurizing the gut lumen. As the aBoc reaches its zenith a set of muscles in the anus contract (Exp) to expel gut contents. This motor program occurs with remarkable regularity in N2, once every 40 to 45 seconds at 23 C in the presence of bacteria. As first found by Steve McIntire for unc-25 and unc-47, most mutants defective in defecation become constipated and are readily recognized using a dissecting microscope. Using a combination of observing existing behavioral mutants and screening directly for new constipated mutants, I have been accumulating mutants defective in defecation. At latest count there are mutations in 23 genes that cause strong defects in some aspect of defecation, including 10 new genes. Viable, fertile mutants for three of the genes appear never to actively defecate, suggesting that the defecation motor program is a dispensable function (instead they appear to rarely release gut contents passively, presumably when gut lumen pressure becomes great enough to force the anus open). The mutants fall, without too much cramming, into five phenotypic classes. Three of the classes have defects specific to one or the other of the three motor steps described above, without affecting the other two. A fourth class has defects in both aBoc and Exp, but not pBoc. The fifth class has defective timing of the cycle period but the motor program, when it occurs, is normal. The most novel mutants are those that affect the cycle period. So far there are three genes in this class, cha-1, dec-1, and unc-75, and each causes the intercycle period to become much longer and more irregular in length than normal. cha-1 encodes choline acetyltransferase, and cha-1 mutants are severely deficient in acetylcholine (ACh). This result implicates ACh, directly or indirectly, in control of the cycle period. Interestingly, unc-75 seems also to be a good candidate for affecting cholinergic function: it's pumping, locomotory, and defecation defects are remarkably similar to those of strong cha-1 alleles. dec-1 mutants are not Unc and pump normally, but have a longer defecation cycle.