Department of Biological Chemistry, The Hebrew University of Jerusalem 91904, Edmond J. Safra campus, Givat Ram, Jerusalem, Israel.
Physiol Plant. 2011 May;142(1):79-86. doi: 10.1111/j.1399-3054.2011.01466.x.
We briefly review the main mechanisms proposed for photodamage to photosystem II (PSII), at the donor and acceptor sides, and then discuss the mechanism whereby filamentous cyanobacteria inhabiting biological sand crusts such as Microcoleus sp. are able to avoid serious damage to their photosynthetic machinery. We show that the decline in fluorescence following exposure to excess light does not reflect a reduction in PSII activity but rather the activation of a non-radiative charge recombination in PSII. Furthermore, we show that the difference in the thermoluminescent peak temperature intensities in these organisms, in the presence and absence of inhibitors such as dichlorophenyl-dimethylurea (DCMU), is smaller than observed in model organisms suggesting that the redox gap between Q(A)⁻ and P₆₈₀+ is smaller. On the basis of these data, we propose that this could enable an alternative, pheophytin-independent recombination, thereby minimizing the damaging ¹O₂ production associated with radiative recombination.
我们简要回顾了光系统 II(PSII)供体和受体侧光损伤的主要机制,然后讨论了丝状蓝细菌如何避免其光合作用机制受到严重损伤,这些丝状蓝细菌栖息在生物沙壳中,如微鞘藻属。我们表明,过量光照后荧光的下降并不反映 PSII 活性的降低,而是 PSII 中无辐射电荷复合的激活。此外,我们表明,在存在和不存在二氯苯基-二甲基脲(DCMU)等抑制剂的情况下,这些生物体的热致发光峰温强度差异小于在模式生物中观察到的差异,这表明 Q(A)⁻和 P₆₈₀+之间的氧化还原间隙更小。基于这些数据,我们提出这可能允许替代的、与叶绿素无关的复合,从而最小化与辐射复合相关的破坏性 ¹O₂ 产生。