The intracellular coral–dinoflagellate symbiosis is the engine that underpins the success of coral reefs, one of the most diverse ecosystems on the planet. However, the breakdown of the symbiosis and the loss of the microalgal symbiont (i.e. coral bleaching) due to environmental changes are resulting in the rapid degradation of coral reefs globally. There is an urgent need to understand the cellular physiology of coral bleaching at the mechanistic level to help develop solutions to mitigate the coral reef crisis. Here, at an unprecedented scope, we present novel models that integrate putative mechanisms of coral bleaching within a common framework according to the triggers (initiators of bleaching, e.g. heat, cold, light stress, hypoxia, hyposalinity), cascades (cellular pathways, e.g. photoinhibition, unfolded protein response, nitric oxide), and endpoints (mechanisms of symbiont loss, e.g. apoptosis, necrosis, exocytosis/vomocytosis). The models are supported by direct evidence from cnidarian systems, and indirectly through comparative evolutionary analyses from non-cnidarian systems. With this approach, new putative mechanisms have been established within and between cascades initiated by different bleaching triggers. In particular, the models provide new insights into the poorly understood connections between bleaching cascades and endpoints and highlight the role of a new mechanism of symbiont loss, i.e. ‘symbiolysosomal digestion’, which is different from symbiophagy. This review also increases the approachability of bleaching physiology for specialists and non-specialists by mapping the vast landscape of bleaching mechanisms in an atlas of comprehensible and detailed mechanistic models. We then discuss major knowledge gaps and how future research may improve the understanding of the connections between the diverse cascade of cellular pathways and the mechanisms of symbiont loss (endpoints).

中文翻译：

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触发点、级联和终点：连接珊瑚白化机制的各个点

细胞内珊瑚-甲藻共生是支撑珊瑚礁成功的引擎，珊瑚礁是地球上最多样化的生态系统之一。然而，由于环境变化导致共生关系的崩溃和微藻共生体的丧失（即珊瑚白化），导致全球珊瑚礁迅速退化。迫切需要从机制层面了解珊瑚白化的细胞生理学，以帮助制定缓解珊瑚礁危机的解决方案。在这里，我们在前所未有的范围内提出了新的模型，根据触发因素（白化的引发因素，例如热、冷、光应激、缺氧、低盐度）、级联（细胞途径，例如光抑制、未折叠蛋白反应、一氧化氮）和终点（共生体丧失机制，例如细胞凋亡、坏死、胞吐作用/胞吐作用）。这些模型得到来自刺胞动物系统的直接证据的支持，以及来自非刺胞动物系统的比较进化分析的间接支持。通过这种方法，在不同漂白触发因素引发的级联内部和级联之间建立了新的假定机制。特别是，这些模型为漂白级联和终点之间的联系提供了新的见解，并强调了一种新的共生体损失机制的作用，即“共生溶酶体消化”，它不同于共生自噬。这篇综述还通过在可理解和详细的机制模型图谱中绘制漂白机制的广阔图景，增加了专家和非专家对漂白生理学的了解。然后，我们讨论主要的知识差距以及未来的研究如何提高对细胞途径的不同级联与共生体损失机制（端点）之间联系的理解。