Braatsch Stephan, Moskvin Oleg V, Klug Gabriele, Gomelsky Mark
Institut für Mikrobiologie und Molekularbiologie, Universität Giessen, Giesse, Germany.
J Bacteriol. 2004 Nov;186(22):7726-35. doi: 10.1128/JB.186.22.7726-7735.2004.
Exposure to blue light of the facultative phototrophic proteobacterium Rhodobacter sphaeroides grown semiaerobically results in repression of the puc and puf operons involved in photosystem formation. To reveal the genome-wide effects of blue light on gene expression and the underlying photosensory mechanisms, transcriptome profiles of R. sphaeroides during blue-light irradiation (for 5 to 135 min) were analyzed. Expression of most photosystem genes was repressed upon irradiation. Downregulation of photosystem development may be used to prevent photooxidative damage occurring when the photosystem, oxygen, and high-intensity light are present simultaneously. The photoreceptor of the BLUF-domain family, AppA, which belongs to the AppA-PpsR antirepressor-repressor system, is essential for maintenance of repression upon prolonged irradiation (S. Braatsch et al., Mol. Microbiol. 45:827-836, 2002). Transcriptome data suggest that the onset of repression is also mediated by the AppA-PpsR system, albeit via an apparently different sensory mechanism. Expression of several genes, whose products may participate in photooxidative damage defense, including deoxypyrimidine photolyase, glutathione peroxidase, and quinol oxidoreductases, was increased. Among the genes upregulated were genes encoding two sigma factors: sigmaE and sigma38. The consensus promoter sequences for these sigma factors were predicted in the upstream sequences of numerous upregulated genes, suggesting that coordinated action of sigmaE and sigma38 is responsible for the upregulation. Based on the dynamics of upregulation, the anti-sigmaE factor ChrR or its putative upstream partner is proposed to be the primary sensor. The identified transcriptome responses provided a framework for deciphering blue-light-dependent signal transduction pathways in R. sphaeroides.
兼性光合细菌球形红杆菌在半好氧条件下暴露于蓝光会导致参与光系统形成的puc和puf操纵子受到抑制。为了揭示蓝光对基因表达的全基因组影响以及潜在的光感受机制，分析了球形红杆菌在蓝光照射期间（5至135分钟）的转录组图谱。照射后大多数光系统基因的表达受到抑制。光系统发育的下调可能用于防止在光系统、氧气和高强度光同时存在时发生的光氧化损伤。属于AppA-PpsR抗阻遏物-阻遏物系统的BLUF结构域家族的光感受器AppA对于长时间照射后维持抑制作用至关重要（S. Braatsch等人，《分子微生物学》45:827-836，2002）。转录组数据表明，抑制作用的起始也由AppA-PpsR系统介导，尽管是通过一种明显不同的光感受机制。几个基因的表达增加，其产物可能参与光氧化损伤防御，包括脱氧嘧啶光解酶、谷胱甘肽过氧化物酶和喹啉氧化还原酶。上调的基因中包括编码两个sigma因子的基因：sigmaE和sigma38。在许多上调基因的上游序列中预测了这些sigma因子的共有启动子序列，表明sigmaE和sigma38的协同作用负责上调。基于上调的动力学，提出抗sigmaE因子ChrR或其假定的上游伙伴是主要传感器。所确定的转录组反应为解读球形红杆菌中蓝光依赖性信号转导途径提供了一个框架。
