Eraso J M, Kaplan S
Department of Microbiology and Molecular Genetics, University of Texas Medical School, Houston 77030.
J Bacteriol. 1994 Jan;176(1):32-43. doi: 10.1128/jb.176.1.32-43.1994.
A new locus, prrA, involved in the regulation of photosynthesis gene expression in response to oxygen, has been identified in Rhodobacter sphaeroides. Inactivation of prrA results in the absence of photosynthetic spectral complexes. The prrA gene product has strong homology to response regulators associated with signal transduction in other prokaryotes. When prrA is present in multiple copies, cells produce light-harvesting complexes under aerobic growth conditions, suggesting that prrA affects photosynthesis gene expression positively in response to oxygen deprivation. Analysis of the expression of puc::lacZ fusions in wild-type and PrrA- cells revealed a substantial decrease in LacZ expression in the absence of prrA under all conditions of growth, especially when cells were grown anaerobically in the dark in the presence of dimethyl sulfoxide. Northern (RNA) and slot blot hybridizations confirmed the beta-galactoside results for puc and revealed additional positive regulation of puf, puhA, and cycA by PrrA. The effect of truncated PrrA on photosynthesis gene expression in the presence of low oxygen levels can be explained by assuming that PrrA may be effective as a multimer. PrrA was found to act on the downstream regulatory sequences (J. K. Lee and S. Kaplan, J. Bacteriol. 174:1146-1157, 1992) of the puc operon regulatory region. Finally, two spontaneous prrA mutations that abolish prrA function by changing amino acids in the amino-terminal domain of the protein were isolated.
在球形红杆菌中发现了一个新的基因座prrA，它参与光合作用基因表达对氧气的响应调节。prrA失活导致光合光谱复合物缺失。prrA基因产物与其他原核生物中与信号转导相关的响应调节因子具有很强的同源性。当prrA以多拷贝形式存在时，细胞在有氧生长条件下会产生光捕获复合物，这表明prrA在缺氧时对光合作用基因表达有正向影响。对野生型和PrrA-细胞中puc::lacZ融合基因表达的分析表明，在所有生长条件下，尤其是当细胞在黑暗中厌氧生长且存在二甲基亚砜时，缺失prrA会导致LacZ表达大幅下降。Northern（RNA）杂交和狭缝杂交证实了puc的β-半乳糖苷结果，并揭示了PrrA对puf、puhA和cycA的额外正向调节。在低氧水平下，截短的PrrA对光合作用基因表达的影响可以通过假设PrrA可能作为多聚体起作用来解释。发现PrrA作用于puc操纵子调节区域的下游调节序列（J. K. Lee和S. Kaplan，《细菌学杂志》174:1146 - 1157，1992）。最后，分离出了两个自发的prrA突变，它们通过改变蛋白质氨基末端结构域中的氨基酸来消除prrA的功能。
