Suppression of the lethality of high light to a quadruple HLI mutant by the inactivation of the regulatory protein PfsR in Synechocystis PCC 6803
Suppression of the lethality of high light to a quadruple HLI mutant by the inactivation of the regulatory protein PfsR in Synechocystis PCC 6803
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DOI：
10.1074/jbc.m606252200
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发表时间：
2006-10-13
影响因子：
4.8
通讯作者：
He, Qingfang
中科院分区：
文献类型：
--
作者：
Jantaro, Saowarath;Ali, Quaisar;He, Qingfang
通过对集胞藻PCC 6803进行遗传筛选，发现了一个调控基因，命名为pfsR（photosynthesis，Fe homeostasis and stress-response regulator）。从缺少四个hli基因的高光敏感菌株（4Xhli）中缺失该基因恢复了在强光条件下亲本菌株的活力。pfsR（-）/4Xhli突变体在强光条件下保持了与野生型相似的光系统II和放氧能力。两个bfr基因（编码细菌铁蛋白）的转录本被发现是组成性上调，而ho 1基因（编码血红素加氧酶）的转录本被大大下调，在高光下删除pfsR。在中等高强度光下，pfsR缺失菌株积累的类胡萝卜素和叶绿素a显着高于其相应的亲本菌株的水平。在高光驯化的早期几个小时期间氧释放的加剧的瞬时增加和在4Xhli菌株中观察到的光系统II介导的氧释放的稳态水平的稍微增加被带回到野生型水平后，从菌株中删除pfsR。发现pfsR缺失突变体在低光条件下对铁限制不太敏感，并且在暴露于强光下后遭受较少的脂质过氧化。因此，PfsR的失活导致更严格的控制铁的可用性，这反过来又减少了在强光下光合作用过程中的氧化应激。这些研究揭示了PfsR在调节铁稳态和应激反应中的关键作用。
A regulatory gene, designated pfsR ( photosynthesis, Fe homeostasis and stress-response regulator), was discovered by a genetic screen in Synechocystis PCC 6803. Deletion of the gene from a high light-sensitive strain lacking four hli genes (4Xhli) restored viability to the parental strain under high light conditions. The quintuple mutant pfsR(-)/4Xhli retained photosystem-II and oxygen evolution capacity at levels similar to the wild-type levels under high light conditions. The transcripts of the two bfr genes ( encoding bacterioferritin) were found to be constitutively up-regulated, whereas the transcripts of ho1 gene ( encoding a heme oxygenase) were greatly down-regulated in high light upon deletion of pfsR. Under intermediate high intensity light, the pfsR deletion strains accumulated carotenoids and chlorophyll a to a significantly higher level than their corresponding parental strains. An exacerbated, transient increase in oxygen evolution during the early hours of high light acclimation and a somewhat increased steady-state level of photosystem-II-mediated oxygen evolution observed in the 4Xhli strain were brought back to the wild-type levels upon deletion of pfsR from the strain. The pfsR deletion mutants were found to be less sensitive to iron limitation under low light conditions and to suffer less lipid peroxidation following exposure to high light. Therefore, inactivation of PfsR resulted in tighter control of iron availability, which in turn reduced oxidative stress during photosynthesis in high light. These studies have revealed a critical role of PfsR in regulation of iron homeostasis and stress response.