S-adenosylmethionine (SAM) is the main methyl donor and the common point between the three principal metabolic pathways: polyamine synthesis, transmethylation, and transsulfuration. The synthesis of SAM is catalyzed by SAM synthetase (SAMS), which transfers the adenosyl portion of ATP to methionine. Here, we investigate the physiological roles of the SAMS proteins in C. elegans by using loss-of-function mutants of sams genes,
sams-1, -3, -4 and -5. Among sams mutants, only
sams-1 mutant exhibited a marked reduction in brood size. To investigate the role of SAMS-1 in the regulation of brood size, we examined the expression pattern of
sams-1 using transgenic worms expressing GFP proteins under control of endogenous
sams-1 promoter. Unexpectedly,
sams-1 was expressed abundantly in the intestine and the body wall muscle, but not in the germline. Next, we examined whether SAM synthetic activity of
sams-1 is involved in the regulation of brood size. The reduction of brood size in
sams-1 mutant was efficiently rescued by over-expressing wild-type SAMS-1, but not an enzymatically inactive one. These results indicate that the brood size was modulated in SAM synthetic activity-dependent manner. Collectively, these data raise the possibility that SAM in the intestine and the body wall muscle might play an important role in maintaining the brood size in C. elegans.