ヒロタ　ケイコ   Keiko HIROTA   廣田　恵子    所属   医学部 医学科    職種   講師
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Conserved SAMS function in regulating egg-laying in C. elegans.
掲載誌名	正式名：Journal of receptor and signal transduction research 略　 称：J. Recept. Signal Transduct. Res. ISSNコード：10799893
掲載区分	国外
巻・号・頁	33(1),pp.56-62
著者・共著者	TAMIYA Hiroko†, HIROTA Keiko, TAKAHASHI Yuta, DAITOKU Hiroaki, KANEKO Yuta, SAKUTA Genki, IIZUKA Kei, WATANABE Satoshi, ISHII Naoaki, FUKAMIZU Akiyoshi*
担当区分	筆頭著者
発行年月	2013
概要	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.