Ectoine and hydroxyectoine are excellent compatible solutes for bacteria to deal with environmental osmotic stress and temperature damages. The biosynthesis cluster of ectoine and hydroxyectoine is widespread among microorganisms, and its expression is activated by high salinity and temperature changes. So far, little is known about the mechanism of the regulation of the transcription of ect genes and only two MarR family regulators (EctR1 in methylobacteria and the EctR1-related regulator CosR in Vibrio cholerae) have been found to negatively regulate the expression of ect genes. Here, we characterize GlnR, the global regulator for nitrogen metabolism in actinomycetes, as a negative regulator for the transcription of ectoine/hydroxyectoine biosynthetic genes (ect operon) in Streptomyces coelicolor. The physiological role of this transcriptional repression by GlnR is proposed to protect the intracellular glutamate pool, which acts as a key nitrogen donor for both the nitrogen metabolism and the ectoine/hydroxyectoine biosynthesis. IMPORTANCE High salinity is deleterious, and cells must evolve sophisticated mechanisms to cope with this osmotic stress. Although production of ectoine and hydroxyectoine is one of the most frequently adopted strategies, the in-depth mechanism of regulation of their biosynthesis is less understood. So far, only two MarR family negative regulators, EctR1 and CosR, have been identified in methylobacteria and Vibrio, respectively. Here, our work demonstrates that GlnR, the global regulator for nitrogen metabolism, is a negative transcriptional regulator for ect genes in Streptomyces coelicolor. Moreover, a close relationship is found between nitrogen metabolism and osmotic resistance, and GlnR-mediated regulation of ect transcription is proposed to protect the intracellular glutamate pool. Meanwhile, the work reveals the multiple roles of GlnR in bacterial physiology.
[1]Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Plant Physiol & Ecol, CAS Key Lab Synthet Biol, Shanghai, Peoples R China.
[2]Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Key Lab Med Reprogramming Technol, Shenzhen, Peoples R China.
[3]Fudan Univ, State Key Lab Genet Engn, Shanghai 200433, Peoples R China.
[4]Fudan Univ, Sch Life Sci, Dept Microbiol & Microbial Engn, Ctr Synthet Biol, Shanghai 200433, Peoples R China.
[5]Chinese Univ Hong Kong, Dept Microbiol, Shatin, Hong Kong, Peoples R China.
[6]Chinese Univ Hong Kong, Prince Wales Hosp, Li KaShing Inst Hlth Sci, Shatin, Hong Kong, Peoples R China.
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