ARC Centre of Excellence for Coral Reef Studies, School of Biological Sciences, University of Queensland, Brisbane, Australia.
PLoS One. 2012;7(7):e39024. doi: 10.1371/journal.pone.0039024. Epub 2012 Jul 16.
The symbiotic relationship between cnidarians and their dinoflagellate symbionts, Symbiodinium spp, which underpins the formation of tropical coral reefs, can be destabilized by rapid changes to environmental conditions. Although some studies have concluded that a breakdown in the symbiosis begins with increased reactive oxygen species (ROS) generation within the symbiont due to a decoupling of photosynthesis, others have reported the release of viable symbionts via a variety of host cell derived mechanisms. We explored an alternative model focused upon changes in host cnidarian mitochondrial integrity in response to thermal stress. Mitochondria are often likened to being batteries of the cell, providing energy in the form of ATP, and controlling cellular pathway activation and ROS generation. The overall morphology of host mitochondria was compared to that of associated symbionts under an experimental thermal stress using confocal and electron microscopy. The results demonstrate that hyperthermic stress induces the degradation of cnidarian host mitochondria that is independent of symbiont cellular deterioration. The potential sites of host mitochondrial disruption were also assessed by measuring changes in the expression of genes associated with electron transport and ATP synthesis using quantitative RT-PCR. The primary site of degradation appeared to be downstream of complex III of the electron transport chain with a significant reduction in host cytochrome c and ATP synthase expression. The consequences of reduced expression could limit the capacity of the host to mitigate ROS generation and maintain both organelle integrity and cellular energy supplies. The disruption of host mitochondria, cellular homeostasis, and subsequent cell death irrespective of symbiont integrity highlights the importance of the host response to thermal stress and in symbiosis dysfunction that has substantial implications for understanding how coral reefs will survive in the face of climate change.
刺胞动物与其共生的甲藻（Symbiodinium spp）之间的共生关系是热带珊瑚礁形成的基础，但这种共生关系会因环境条件的快速变化而不稳定。虽然一些研究得出的结论是，由于光合作用的解耦，共生体中活性氧（ROS）的产生增加会导致共生关系的破裂，但也有其他研究报告称，通过各种宿主细胞衍生的机制释放有活力的共生体。我们探索了一种替代模型，该模型专注于宿主刺胞动物线粒体完整性因热应激而发生的变化。线粒体通常被比作细胞的电池，以 ATP 的形式提供能量，并控制细胞途径的激活和 ROS 的产生。使用共聚焦和电子显微镜，比较了宿主线粒体在实验热应激下的整体形态与相关共生体的形态。结果表明，高温应激诱导宿主刺胞动物线粒体的降解，而与共生体细胞的恶化无关。通过定量 RT-PCR 测量与电子传递和 ATP 合成相关的基因表达变化，还评估了宿主线粒体破坏的潜在部位。降解的主要部位似乎在电子传递链复合物 III 的下游，宿主细胞色素 c 和 ATP 合酶的表达显著减少。表达减少的后果可能会限制宿主减轻 ROS 产生和维持细胞器完整性和细胞能量供应的能力。无论共生体完整性如何，宿主线粒体、细胞内稳态和随后的细胞死亡的破坏都强调了宿主对热应激的反应以及共生功能障碍的重要性，这对理解珊瑚礁如何在气候变化面前生存具有重要意义。
