Keiko HIROTA    Department   School of Medicine, School of Medicine    Position   Assistant Professor
Article types	Original article
Language	English
Peer review	Peer reviewed
Title	Conserved SAMS function in regulating egg-laying in C. elegans.
Journal	Formal name：Journal of receptor and signal transduction research Abbreviation：J. Recept. Signal Transduct. Res. ISSN code：10799893
Domestic / Foregin	Foregin
Volume, Issue, Page	33(1),pp.56-62
Author and coauthor	TAMIYA Hiroko†, HIROTA Keiko, TAKAHASHI Yuta, DAITOKU Hiroaki, KANEKO Yuta, SAKUTA Genki, IIZUKA Kei, WATANABE Satoshi, ISHII Naoaki, FUKAMIZU Akiyoshi*
Authorship	Lead author
Publication date	2013
Summary	S-adenosyl-L-methionine (SAM) is an intermediate metabolite of methionine and serves as the methyl donor for many biological methylation reactions. The synthesis of SAM is catalyzed by SAM synthetase (SAMS), which transfers the adenosyl moiety of adenosine-5'-triphosphate to methionine. In the nematode Caenorhabditis elegans, four sams family genes, sams-1, -3, -4 and -5, are predicted to encode SAMS proteins. However, their physiological roles remain unclear. Here we show that the four predicted SAMS proteins in fact have the ability to catalyze the formation of SAM in vitro, and revealed that only sams-1 mutant animals among the family genes exhibited a significant reduction in egg-laying. Using transgenic animals carrying a transcriptional reporter for each sams gene promoter, we observed that each sams promoter confers a distinct expression pattern with respect to tissue, time of expression and expression level (i.e. promoter specificity). Promoter-swap experiments revealed that the ectopic expression of SAMS-3, -4 or -5 driven by the sams-1 promoter completely rescued egg-laying in sams-1 mutants. These data indicate that SAMS protein function is conserved throughout the entire family.
DOI	10.3109/10799893.2012.756896.