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首页> 外文期刊>Photochemistry and Photobiology: An International Journal >Dunaliella tertiolecta (Chlorophyta) Avoids Cell Death Under Ultraviolet Radiation By Triggering Alternative Photoprotective Mechanisms
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Dunaliella tertiolecta (Chlorophyta) Avoids Cell Death Under Ultraviolet Radiation By Triggering Alternative Photoprotective Mechanisms

机译:杜氏杜氏藻(Chlorophyta)通过触发其他光保护机制避免了紫外线辐射下的细胞死亡。

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The effect of different ultraviolet radiation (UVR) treatments combining PAR (P), UVA (A) and UVB (B) on the molecular physiology of Dunaliella tertiolecta was studied during 6 days to assess the response to chronic UVR exposure. UVR reduced cell growth but did not cause cell death, as shown by the absence of SYTOX Green labeling and cellular morphology. However, caspase-like enzymatic activities (CLs), (regarded as cell death proteases), were active even though the cells were not dying. Maximal quantum yield of fluorescence (F-v/F-m) and photosynthetic electron transport rate (ETR) dropped. Decreased nonphotochemical quenching (NPQ) paralleled a drop in xanthophyll cycle de-epoxidation under UVB. Reactive oxygen species (ROS) and D1 protein accumulation were inversely correlated. PAB exhibited elevated ROS production at earlier times. Once ROS decayed, D1 protein recovered two-fold compared with P and PA at later stages. Therefore, PsbA gene was still transcribed, suggesting ROS involvement in D1 recovery by its direct effect on mRNA-translation. We add evidence of an UVB-induced positive effect on the cells when P is present, providing photoprotection and resilience, by means of D1 repair. This allowed cells to survive. The photoprotective mechanisms described here (which are counterintuitive in principle) conform to an important ecophysiological response regarding light stress acclimation.
机译:在6天内研究了结合PAR(P),UVA(A)和UVB(B)的不同紫外线(UVR)处理对杜氏杜氏藻的分子生理的影响,以评估对慢性UVR暴露的反应。 UVR减少了细胞生长,但没有引起细胞死亡,这是由于缺少SYTOX Green标记和细胞形态所显示的。然而,即使细胞没有死亡,类似胱天蛋白酶的酶活性(CLs)(被认为是细胞死亡蛋白酶)也具有活性。荧光的最大量子产率(F-v / F-m)和光合电子传输速率(ETR)下降。非光化学淬灭(NPQ)的减少与UVB下叶黄素循环脱环氧化的下降平行。活性氧(ROS)与D1蛋白积累呈负相关。 PAB在较早的时间表现出较高的ROS产生。 ROS降解后,D1蛋白在后期恢复到P和PA的两倍。因此,PsbA基因仍被转录,表明ROS通过直接影响mRNA的翻译而参与了D1的恢复。我们添加了证据,证明当P存在时,UVB诱导的对细胞的积极作用,通过D1修复提供光保护和回弹力。这使细胞得以存活。这里描述的光保护机制(原则上是违反直觉的)符合关于光应力适应的重要生态生理响应。

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