Slavov Chavdar, Schrameyer Verena, Reus Michael, Ralph Peter J, Hill Ross, Büchel Claudia, Larkum Anthony W D, Holzwarth Alfred R
Max Planck Institute for Chemical Energy Conversion, Mülheim a.d. Ruhr D-45470, Germany; Institute of Physical and Theoretical Chemistry, Goethe University, Frankfurt D-60438, Germany.
Plant Functional Biology and Climate Change Cluster (C3), School of the Environment, University of Technology, Sydney, NSW 2007, Australia.
Biochim Biophys Acta. 2016 Jun;1857(6):840-7. doi: 10.1016/j.bbabio.2016.02.002. Epub 2016 Feb 8.
The global rise in sea surface temperatures causes regular exposure of corals to high temperature and high light stress, leading to worldwide disastrous coral bleaching events (loss of symbiotic dinoflagellates (Symbiodinium) from reef-building corals). Our picosecond chlorophyll fluorescence experiments on cultured Symbiodinium clade C cells exposed to coral bleaching conditions uncovered the transformations of the alga's photosynthetic apparatus (PSA) that activate an extremely efficient non-photochemical "super-quenching" mechanism. The mechanism is associated with a transition from an initially heterogeneous photosystem II (PSII) pool to a homogeneous "spillover" pool, where nearly all excitation energy is transferred to photosystem I (PSI). There, the inherently higher stability of PSI and high quenching efficiency of P(700)(+) allow dumping of PSII excess excitation energy into heat, resulting in almost complete cessation of photosynthetic electron transport (PET). This potentially reversible "super-quenching" mechanism protects the PSA against destruction at the cost of a loss of photosynthetic activity. We suggest that the inhibition of PET and the consequent inhibition of organic carbon production (e.g. sugars) in the symbiotic Symbiodinium provide a trigger for the symbiont expulsion, i.e. bleaching.
全球海平面温度上升导致珊瑚经常暴露于高温和高光胁迫之下，引发了全球范围内灾难性的珊瑚白化事件（造礁珊瑚失去共生双鞭毛虫（共生藻））。我们对暴露于珊瑚白化条件下的培养共生藻C系细胞进行的皮秒叶绿素荧光实验，揭示了藻类光合机构（PSA）的转变，这种转变激活了一种极其高效的非光化学“超级猝灭”机制。该机制与从最初异质性的光系统II（PSII）池向均一的“溢出”池的转变有关，在“溢出”池中，几乎所有激发能都转移到了光系统I（PSI）。在那里，PSI固有的更高稳定性和P(700)(+)的高猝灭效率，使得PSII多余的激发能以热的形式耗散，导致光合电子传递（PET）几乎完全停止。这种潜在可逆的“超级猝灭”机制以光合活性丧失为代价，保护了PSA不被破坏。我们认为，共生共生藻中PET的抑制以及随之而来的有机碳生产（如糖类）的抑制，为共生体的排出即白化提供了触发因素。
