Aklujkar Muktak, Prince Roger C, Beatty J Thomas
Department of Microbiology and Immunology, University of British Columbia, 300-6174 University Blvd., Vancouver, BC, Canada V6T 1Z3.
Arch Biochem Biophys. 2005 May 15;437(2):186-98. doi: 10.1016/j.abb.2005.03.012. Epub 2005 Mar 25.
A conserved orf of previously unknown function (herein designated as puhE) is located 3' of the reaction centre H (puhA) gene in purple photosynthetic bacteria, in the order puhABCE in Rhodobacter capsulatus. Disruptions of R. capsulatus puhE resulted in a long lag in the growth of photosynthetic cultures inoculated with cells grown under high aeration, and increased the level of the peripheral antenna, light-harvesting complex 2 (LH2). The amount of the photosynthetic reaction centre (RC) and its core antenna, light-harvesting complex 1 (LH1), was reduced; however, there was no decrease in expression of a lacZ reporter fused to the puf (RC and LH1) promoter, in RC assembly in the absence of LH1, or in LH1 assembly in the absence of the RC. In strains that lack LH2, disruption of puhE increased the in vivo absorption at 780 nm, which we attribute to excess bacteriochlorophyll a (BChl) pigment production. This effect was seen in the presence and absence of PufQ, a protein that stimulates BChl biosynthesis. Expression of puhE from a plasmid reduced A(780) production in puhE mutants. We suggest that PuhE modulates BChl biosynthesis independently of PufQ, and that the presence of excess BChl in PuhE(-)LH2(+) strains results in excess LH2 assembly and also interferes with the adaptation of cells during the transition from aerobic respiratory to anaerobic photosynthetic growth.
在紫色光合细菌中,一个功能未知的保守开放阅读框(在此命名为puhE)位于反应中心H(puhA)基因的3'端,在荚膜红细菌中其排列顺序为puhABCE。荚膜红细菌puhE的缺失导致接种在高通气条件下生长的细胞的光合培养物生长出现长时间延迟,并增加了外周天线捕光复合物2(LH2)的水平。光合反应中心(RC)及其核心天线捕光复合物1(LH1)的量减少;然而,与puf(RC和LH1)启动子融合的lacZ报告基因的表达、在没有LH1时的RC组装或在没有RC时的LH1组装均未降低。在缺乏LH2的菌株中,puhE的缺失增加了780 nm处的体内吸收,我们将其归因于过量的细菌叶绿素a(BChl)色素产生。在存在和不存在刺激BChl生物合成的蛋白质PufQ的情况下均观察到这种效应。从质粒表达puhE可降低puhE突变体中A(780)的产生。我们认为PuhE独立于PufQ调节BChl生物合成,并且在PuhE(-)LH2(+)菌株中过量BChl的存在导致过量LH2组装,并且还干扰细胞从有氧呼吸生长向厌氧光合生长转变期间的适应过程。