A novel gene, pmgA, specifically regulates photosystem stoichiometry in the cyanobacterium Synechocystis species PCC 6803 in response to high light

A novel gene, pmgA, specifically regulates photosystem stoichiometry in the cyanobacterium Synechocystis species PCC 6803 in response to high light
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DOI:
10.1104/pp.117.4.1205
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发表时间:
1998-08-01
期刊:
影响因子:
7.4
通讯作者:
Ikeuchi, M
Ikeuchi, M
中科院分区:
生物学1区
文献类型:
--
作者:
Hihara, Y;Sonoike, K;Ikeuchi, M

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在此之前,我们发现了一个新的基因pmgA,作为支持聚囊藻物种PCC 6803光自养生长的重要因子,并报道了pmgA缺失的菌株在光自养条件下比野生型生长得更好。为了深入了解pmgA的作用,我们详细研究了pmgA的突变表型。当弱光生长(20 μ E m(-2) s(-1))细胞转移到强光(HL [200 μ E m(-2) s(-1)])时,pmgA突变体未能以通常与聚胞菌相关的方式产生反应。具体来说,突变体失去了抑制叶绿素和光系统I积累的能力,因此不能调节光系统的化学计量。这些表型似乎导致短期暴露于HL的光合作用和生长速率提高。此外,混合培养实验清楚地表明,pmgA功能的丧失在长期暴露于HL中是选择性的,这表明pmgA参与了对HL胁迫的抗性获得。最后,通过逆转录- pcr检测到pmgA在向HL转变时的早期诱导表达,使我们得出结论,pmgA是我们所知的第一个被鉴定为HL驯化的特定调节因子的基因。
Previously, we identified a novel gene, pmgA, as an essential factor to support photomixotrophic growth of Synechocystis species PCC 6803 and reported that a strain in which pmgA was deleted grew better than the wild type under photoautotrophic conditions. To gain insight into the role of pmgA, we investigated the mutant phenotype of pmgA in detail. When low-light-grown (20 mu E m(-2) s(-1)) cells were transferred to high light (HL [200 mu E m(-2) s(-1)]), pmgA mutants failed to respond in the manner typically associated with Synechocystis. Specifically, mutants lost their ability to suppress accumulation of chlorophyll and photosystem I and, consequently, could not modulate photosystem stoichiometry. These phenotypes seem to result in enhanced rates of photosynthesis and growth during short-term exposure to HL. Moreover, mixed-culture experiments clearly demonstrated that loss of pmgA function was selected against during longer-term exposure to HL, suggesting that pmgA is involved in acquisition of resistance to HL stress. Finally, early induction of pmgA expression detected by reverse transcriptase-PCR upon the shift to HL led us to conclude that pmgA is the first gene identified, to our knowledge, as a specific regulatory factor for HL acclimation.