ナカムラ　マサキ   Nakamura Masaki   中村　真樹    所属   東邦大学  医学部 医学科    職種   助教
論文種別	原著
言語種別	英語
査読の有無	査読なし
表題	Reciprocal Expression of PCY1 and CYC6 in Pseudopediastrum boryanum and Pediastrum duplex (Chlorophyceae) is Regulated via a Common Transcription Mechanism under Copper-Deficient Condition
掲載誌名	正式名：Toho Liberal Arts Review ISSNコード：03877566
掲載区分	国内
巻・号・頁	50,pp.81-97
著者・共著者	Masaki Nakamura
担当区分	筆頭著者,責任著者
発行年月	2019/02/27
概要	I report here that the reciprocal expression of the genes encoding plastocyanin （PCY1） and cytochrome c6 （CYC6） in Pseudopediastrum boryanum （Turpin） E. Hegewald and Pediastrum duplex Meyen （Hydrodictyaceae） is regulated via a common upregulation mechanism under a copper-deficient condition. In the presence of copper, transcription of full-length PCY1 mRNA starts at the regular transcription start site. On the other hand, under a copper-deficient condition, an alternative start site approximately 150 bp downstream from the regular start site becomes dominant to produce untranslatable short mRNA, thereby downregulating protein synthesis by the translatable full-length mRNA. I determined the structure of PCY1 and CYC6 in both P. boryanum and P. duplex, compared the 5’ region sequences, and performed RNA analysis to examine copper responsiveness. The GTAC motif has been shown to be a core sequence of copper responsiveness in Chlamydomonas reinhardtii. I found that PCY1 and CYC6 of both species carry three GTAC motifs in a region proximal to the transcription start site. Furthermore, the distance between this GTAC cluster and the transcription start site specific to a copper-deficient condition is conserved in PCY1 and CYC6. These findings strongly suggest that both genes mediated by the mechanism that enhances transcription in the absence of copper. Therefore, I propose a model for reciprocal expression of PCY1 and CYC6 in Pediastrum, wherein copper deficiency induces transcription of the genes via a common mechanism, but results in upregulation of CYC6 mRNA synthesis and downregulation of translatable full-length PCY1 mRNA synthesis.