Drath Miriam, Kloft Nicole, Batschauer Alfred, Marin Kay, Novak Jens, Forchhammer Karl
Institut für Mikrobiologie und Molekularbiologie, Justus-Liebig-Universität Giessen, D-35392 Giessen, Germany.
Plant Physiol. 2008 May;147(1):206-15. doi: 10.1104/pp.108.117218. Epub 2008 Mar 5.
Ammonia has long been known to be toxic for many photosynthetic organisms; however, the target for its toxicity remains elusive. Here, we show that in the cyanobacterium Synechocystis sp. strain PCC 6803, ammonia triggers a rapid photodamage of photosystem II (PSII). Whereas wild-type cells can cope with this damage by turning on the FtsH2-dependent PSII repair cycle, the FtsH2-deficient mutant is highly sensitive and loses PSII activity at millimolar concentration of ammonia. Ammonia-triggered PSII destruction is light dependent and occurs already at low photon fluence rates. Experiments with monochromatic light showed that ammonia-promoted PSII photoinhibition is executed by wavebands known to directly destroy the manganese cluster in the PSII oxygen-evolving complex, suggesting that the oxygen-evolving complex may be a direct target for ammonia toxicity.
长期以来,人们一直知道氨对许多光合生物具有毒性;然而,其毒性靶点仍然难以捉摸。在此,我们表明,在蓝藻集胞藻PCC 6803菌株中,氨会引发光系统II(PSII)的快速光损伤。野生型细胞可以通过开启依赖FtsH2的PSII修复循环来应对这种损伤,而缺乏FtsH2的突变体则高度敏感,在毫摩尔浓度的氨环境下会丧失PSII活性。氨引发的PSII破坏依赖于光,且在低光子通量率下就会发生。单色光实验表明,氨促进的PSII光抑制是由已知可直接破坏PSII放氧复合体中锰簇的波段执行的,这表明放氧复合体可能是氨毒性的直接靶点。