首页> 美国卫生研究院文献>Plant Physiology >Genetic Enhancement of the Ability to Tolerate Photoinhibition by Introduction of Unsaturated Bonds into Membrane Glycerolipids.
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Genetic Enhancement of the Ability to Tolerate Photoinhibition by Introduction of Unsaturated Bonds into Membrane Glycerolipids.

机译:通过将不饱和键引入膜甘油脂中来提高光耐受能力的遗传增强。

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摘要

Strong light leads to damage to photosynthetic machinery, particularly at low temperatures, and the main site of the damage is the D1 protein of the photosystem II (PSII) complex. Here we describe that transformation of Synechococcus sp. PCC 7942 with the desA gene for a [delta]12 desaturase increased unsaturation of membrane lipids and enhanced tolerance to strong light. To our knowledge, this is the first report of the successful genetic enhancement of tolerance to strong light. Analysis of the light-induced inactivation and of the subsequent recovery of the activity of the PSII complex revealed that the recovery process was markedly accelerated by the genetic transformation. Labeling experiments with [35S]L-methionine also revealed that the synthesis of the D1 protein de novo at low temperature, which was a prerequisite for the restoration of the PSII complex, was much faster in the transformed cells than in the wild-type cells. These findings demonstrate that the ability of membrane lipids to desaturate fatty acids is important for the photosynthetic organisms to tolerate strong light, by accelerating the synthesis of the D1 protein de novo.
机译:强光会导致光合作用机制受损,尤其是在低温下,损害的主要部位是光系统II(PSII)复合体的D1蛋白。在这里,我们描述了Synechococcus sp。的转化。具有用于Δ12去饱和酶的desA基因的PCC 7942增加了膜脂质的不饱和度并增强了对强光的耐受性。据我们所知,这是首次成功遗传增强了对强光耐受性的报道。对光诱导的失活以及随后PSII复合物活性的恢复的分析表明,遗传转化显着促进了恢复过程。 [35S] L-蛋氨酸的标记实验还表明,低温下从头合成D1蛋白是PSII复合物恢复的前提条件,在转化的细胞中其合成速度比在野生型细胞中快得多。这些发现表明,通过加速从头合成D1蛋白,膜脂质使脂肪酸去饱和的能力对于光合生物耐受强光很重要。

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