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Fig. 3. Model of cell signaling pathways in the host cell that lead to bleaching by host cell apoptosis. Generation of ROS in the symbiont is described in Fig. 2. Although oxygen-handling pathways including superoxide dismutases (SOD) and catalase are present, they become overwhelmed by the high concentrations of ROS. In one pathway, high concentrations of superoxide (O₂^–), generated from host mitochondrial membrane damage (depicted as a `flash' in the figure), and hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), coming from both symbiont and host, trigger the activation of the innate immunity gatekeeper transcription factor NF-B. It, in turn, activates apoptosis directly and/or induces the expression of inducible nitric oxide synthase (iNOS) that produces nitric oxide (NO). In another pathway, NO is produced directly by the symbiont and diffuses into the host. NO combines with O<sub>2</sub><sup>–</sup> to form highly reactive peroxynitrite (ONOO<sup>–</sup> that damages the mitochondrial membrane (depicted as a `flash' in the figure). This damage releases potent pro-apoptotic molecules such as apoptosis inducing factor (AIF) and cytochrome c (not shown) that activate caspases, the proteases responsible for carrying out apoptosis. In another pathway, NO activates p53, a pro-apoptotic transcription factor, which in turn activates caspases and apoptosis. There is direct evidence in Cnidarian–dinoflagellate symbioses for pathways depicted in red, indirect evidence for those depicted in blue and evidence only in other metazoans and host–microbe interactions for those depicted in green. See text for details.

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