文献类型：期刊文献

英文题名：A preliminary study of the mechanism of nitrate-stimulated remarkable increase of rifamycin production in Amycolatopsis mediterranei U32 by RNA-seq

作者：Shao, Zhi Hui[1];Ren, Shuang Xi[1];Liu, Xin Qiang[1];Xu, Jian[2];Yan, Han[1];Zhao, Guo Ping[1,3,4,5,6,7];Wang, Jin[1]

机构：[1]Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Plant Physiol & Ecol, CAS Key Lab Synthet Biol, Shanghai 20032, Peoples R China;[2]E China Univ Sci & Technol, New World Inst Biotechnol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[3]Fudan Univ, Sch Life Sci, Dept Microbiol & Microbial Engn, State Key Lab Genet Engn, Shanghai 200032, Peoples R China;[4]Fudan Univ, Sch Life Sci, Dept Microbiol & Microbial Engn, Ctr Synthet Biol, Shanghai 200032, Peoples R China;[5]Chinese Natl Human Genome Ctr Shanghai, Shanghai MOST Key Lab Dis & Hlth Genom, Shanghai 201203, Peoples R China;[6]Chinese Univ Hong Kong, Prince Wales Hosp, Dept Microbiol, Hong Kong, Hong Kong, Peoples R China;[7]Chinese Univ Hong Kong, Prince Wales Hosp, Li KaShing Inst Hlth Sci, Hong Kong, Hong Kong, Peoples R China

年份：2015

卷号：14

外文期刊名：MICROBIAL CELL FACTORIES

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000355511800001)】；

基金：This work was supported by the National Basic Research Program of China [2012CB721102] and National Natural Science Foundation of China [31200021, 31121001 and 31300031]. We acknowledge Shanghai Biotechnology Corporation for their assistance in RNA-seq work.

语种：英文

外文关键词：Amycolatopsis mediterranei; Rifamycin SV; Nitrate; RNA-seq; Transcriptome

摘要：Background: Rifamycin is an important antibiotic for the treatment of infectious disease caused by Mycobacteria tuberculosis. It was found that in Amycolatopsis mediterranei U32, an industrial producer for rifamycin SV, supplementation of nitrate into the medium remarkably stimulated the yield of rifamycin SV. However, the molecular mechanism of this nitrate-mediated stimulation remains unknown. Results: In this study, RNA-sequencing (RNA-seq) technology was employed for investigation of the genome-wide differential gene expression in U32 cultured with or without nitrate supplementation. In the presence of nitrate, U32 maintained a high transcriptional level of genes both located in the rifamycin biosynthetic cluster and involved in the biosynthesis of rifamycin precursors, including 3-amino-5-dihydroxybenzoic acid, malonyl-CoA and (S)-methylmalonyl- CoA. However, when nitrate was omitted from the medium, the transcription of these genes declined sharply during the transition from the mid-logarithmic phase to the early stationary phase. With these understandings, one may easily propose that nitrate stimulates the rifamycin SV production through increasing both the precursors supply and the enzymes for rifamycin biosynthesis. Conclusion: It is the first time to thoroughly illustrate the mechanism of the nitrate-mediated stimulation of rifamycin production at the transcriptional level, which may facilitate improvement of the industrial production of rifamycin SV, e. g. through optimizing the global rifamycin biosynthetic pathways on the basis of RNA-seq data.