Takahashi Shunichi, Whitney Spencer, Itoh Shigeru, Maruyama Tadashi, Badger Murray
Australian Research Council Center of Excellence in Plant Energy Biology, Research School of Biological Sciences, Australian National University, Australian Capital Territory, Canberra, Australia.
Proc Natl Acad Sci U S A. 2008 Mar 18;105(11):4203-8. doi: 10.1073/pnas.0708554105. Epub 2008 Mar 5.
Coral bleaching, caused by heat stress, is accompanied by the light-induced loss of photosynthetic pigments in in situ symbiotic dinoflagellate algae (Symbiodinium spp.). However, the molecular mechanisms responsible for pigment loss are poorly understood. Here, we show that moderate heat stress causes photobleaching through inhibition of the de novo synthesis of intrinsic light-harvesting antennae [chlorophyll a-chlorophyll c(2)-peridinin-protein complexes (acpPC)] in cultured Symbiodinium algae and that two Clade A Symbiodinium species showing different thermal sensitivities of photobleaching also show differential sensitivity of this key protein synthesis process. Photoinhibition of photosystem II (PSII) and subsequent photobleaching were observed at temperatures of >31 degrees C in cultured Symbiodinium CS-73 cells grown at 25-34 degrees C, but not in cultures of the more thermally tolerant control Symbiodinium species OTcH-1. We found that bleaching in CS-73 is associated with loss of acpPC, which is a major antennae protein in Symbiodinium. In addition, the thermally induced loss of this protein is light-dependent, but does not coincide directly with PSII photoinhibition and is not caused by stimulated degradation of acpPC. In cells treated at 34 degrees C over 24 h, the steady-state acpPC mRNA pool was modestly reduced, by approximately 30%, whereas the corresponding synthesis rate of acpPC was diminished by >80%. Our results suggest that photobleaching in Symbiodinium is consequentially linked to the relative susceptibility of PSII to photoinhibition during thermal stress and occurs, at least partially, because of the loss of acpPC via undefined mechanism(s) that hamper the de novo synthesis of acpPC primarily at the translational processing step.
由热应激引起的珊瑚白化，伴随着原位共生双鞭毛藻（共生藻属）光合色素因光照而损失。然而，色素损失的分子机制仍知之甚少。在此，我们表明适度的热应激通过抑制培养的共生藻中内在光捕获天线[叶绿素a - 叶绿素c₂ - 多甲藻素 - 蛋白质复合物（acpPC）]的从头合成导致光漂白，并且两种表现出不同光漂白热敏感性的A类共生藻物种在这个关键蛋白质合成过程中也表现出不同的敏感性。在25 - 34℃生长的培养共生藻CS - 73细胞中，当温度高于31℃时观察到光系统II（PSII）的光抑制及随后的光漂白，但在热耐受性更强的对照共生藻物种OTcH - 1的培养物中未观察到。我们发现CS - 73中的漂白与acpPC的损失有关，acpPC是共生藻中的一种主要天线蛋白。此外，这种蛋白质的热诱导损失是光依赖性的，但与PSII光抑制并不直接一致，也不是由acpPC的刺激降解引起的。在34℃处理24小时的细胞中，稳态acpPC mRNA库适度减少，约30%，而acpPC的相应合成速率降低超过80%。我们的结果表明，共生藻中的光漂白与热应激期间PSII对光抑制的相对敏感性相关，并且至少部分是由于通过未明确的机制导致acpPC损失，这些机制主要在翻译加工步骤阻碍了acpPC的从头合成。
