Floriano B, Bibb M
John Innes Centre, Norwich Research Park, Colney, UK.
Mol Microbiol. 1996 Jul;21(2):385-96. doi: 10.1046/j.1365-2958.1996.6491364.x.
The N-terminal region of AfsR, a putative pleiotropic regulatory protein for antibiotic production in Streptomyces coelicolor A3(2), is homologous to RedD and Actil-ORF4, pathway-specific regulatory proteins required for the production of the antibiotics undecylprodigiosin (Red) and actinorhodin (Act), respectively. The recent identification of afsS, which lies immediately 3' of afsR and which stimulates antibiotic production when cloned at high copy number, questioned whether afsR was a pleiotropic regulatory gene. In this study we demonstrate that multiple copies of afsR can stimulate both Act and Red production and that, despite its homology, it cannot substitute for the pathway-specific regulatory genes. Moreover, an in-frame deletion that removed most of the afsR coding sequence resulted in loss of Act and Red production, and a marked reduction in the synthesis of the calcium-dependent antibiotic (CDA), but only under some (non-permissive) nutritional conditions. Although additional copies of afsR resulted in elevated levels of the actII-ORF4 and redD transcripts, transcription of the pathway-specific regulatory genes under non-permissive conditions was unaffected by deletion of afsR. While afsR may operate independently of the pathway-specific regulatory proteins to influence antibiotic production, the activity of ActII-ORF4 and of RedD under non-permissive conditions could depend on interaction with, or modification by, AfsR.
天蓝色链霉菌A3(2)中假定的多效调控蛋白AfsR的N端区域,分别与产抗生素十一烷基灵菌红素(Red)和放线紫红素(Act)所需的途径特异性调控蛋白RedD和ActII-ORF4同源。最近发现afsS位于afsR的紧邻3'端,以高拷贝数克隆时可刺激抗生素产生,这对afsR是否为多效调控基因提出了质疑。在本研究中,我们证明多个拷贝的afsR可同时刺激Act和Red的产生,并且尽管它具有同源性,但不能替代途径特异性调控基因。此外,一个缺失大部分afsR编码序列的读码框内缺失导致Act和Red产生丧失,以及钙依赖性抗生素(CDA)合成显著减少,但仅在某些(非允许)营养条件下如此。尽管额外拷贝的afsR导致actII-ORF4和redD转录本水平升高,但在非允许条件下途径特异性调控基因的转录不受afsR缺失的影响。虽然afsR可能独立于途径特异性调控蛋白发挥作用以影响抗生素产生,但在非允许条件下ActII-ORF4和RedD的活性可能取决于与AfsR的相互作用或被其修饰。