SAMS-1 is required for the normal defecation motor program in Caenorhabditis elegans.

Defecation is an ultradian rhythmic behavior in Caenorhabditis elegans . We investigated the involvement of sams family genes in regulating the defecation motor program. We found that sams-1 mutants exhibited longer cycles than wild-type animals. With aging, the sams-1 mutants also frequently skipped the expulsion (Exp) step of defecation behavior. The sams-1 knockdown is known to reduce phosphatidylcholine (PC) levels, which are reversed by choline supplementation. We examined the effect of choline supplementation on defecation cycle times and Exp steps from adult days 1-4. Although choline supplementation did not alter the longer defecation cycle times of sams-1 mutants, it restored the loss of the Exp step in sams-1 mutants on adult days 3 and 4, suggesting a link between the regulation of the Exp step in sams-1 mutants and PC production.

Dietary methionine functions in proliferative zone maintenance and production of eggs via sams-1 in Caenorhabditis elegans.

The maintenance of germ cells is critical for the prosperity of offspring. The amount of food consumption is known to be closely related to reproduction, i.e., the number of eggs decreases under calorie-restricted conditions in various organisms. Previous studies in Caenorhabditis elegans have reported that calorie restriction reduces the number of eggs and the reduction can be rescued by methionine. However, the effect of methionine on the reproductive process has not been fully understood. In this study, to assess the gonadal function of methionine metabolism, we firstly demonstrated that a depletion in dietary methionine resulted in reduced levels of S-adenosyl-l-methionine (SAM) and S-adenosyl homocysteine (SAH) in wild-type N2, but not in glp-1 mutants, which possess only a few germ cells. Second, we found no recovery in egg numbers upon methionine administration in SAM synthase (sams)-1 mutants. Furthermore, a reduced number of proliferative zone nuclei exhibited in the sams-1 mutants was not rescued via methionine. Thus, our results have shown that dietary methionine is required for the normal establishment of both the germline progenitor pool and fecundity, mediated by sams-1.