کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2819163 | 1569906 | 2008 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Identification of genes involved in the butyrolactone autoregulator cascade that modulates secondary metabolism in Streptomyces lavendulae FRI-5 Identification of genes involved in the butyrolactone autoregulator cascade that modulates secondary metabolism in Streptomyces lavendulae FRI-5](/preview/png/2819163.png)
The γ-butyrolactone-autoregulator signalling system is widely distributed across many Streptomyces species and it controls secondary metabolism and/or morphological differentiation. IM-2 [(2R,3R,1′R)-2-1′-hydroxybutyl-3-hydroxymethyl-γ-butanolide] is a γ-butyrolactone autoregulator which, in Streptomyces lavendulae FRI-5, switches off the production of d-cycloserine, but switches on the production of several nucleoside antibiotics and blue pigment. In the IM-2 system, an IM-2 specific receptor (FarA) plays a critical role in the biosynthetic regulation of these metabolites, including IM-2 itself. Here, we identified five additional regulatory genes in the farA-flanking region and demonstrated that, in addition to farA, at least two more genes (farR1 and farR2) are involved in the IM-2/FarA system as the direct transcriptional target of FarA. The gel-shift assay revealed that FarA was bound to the upstream region of the four genes (including farR1 and farR2) in an IM-2-dependent manner. The FarA-binding sites were localized by DNase I footprinting to 27- to 33-bp palindromic structures, suggesting that FarA-binding sequences consist of two conserved hexamers separated by six nucleotides. Both farR1 and farR2 were transcribed in a growth-dependent manner, and marked expression was induced in the presence of IM-2, whereas transcripts of other two genes were not detected under the cultivation conditions used. The FarA-binding sites of farR1 and far2 overlap the promoter regions, suggesting that FarA represses the transcription of these two genes in the absence of IM-2 by inhibiting RNA polymerase access.
Journal: Gene - Volume 425, Issues 1–2, 1 December 2008, Pages 9–16