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First published online September 19, 2008
Journal of Experimental Biology 211, 3059-3066 (2008)
Published by The Company of Biologists 2008
doi: 10.1242/jeb.009597

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Cellular mechanisms of Cnidarian bleaching: stress causes the collapse of symbiosis

Virginia M. Weis

Department of Zoology, Oregon State University, Corvallis, OR, 97331, USA

View larger version (139K): [in this window] [in a new window]   Fig. 1. Bleached and unbleached corals at Great Keppel Island on the Southern Great Barrier Reef in January 2002. The coral on the left appears brown and healthy whereas the colonies on the right are partially (lower right) and fully (upper right) bleached. This differential bleaching response between different coral species is commonly observed and not fully understood. Photograph courtesy of O. Hoegh-Guldberg, Centre for Marine Studies, University of Queensland.

View larger version (19K): [in this window] [in a new window]   Fig. 2. Schematic representation of oxygen handling pathways in Symbiodinium resident in host cells under ambient (A), and elevated temperature and light (B) conditions. Under ambient conditions, the photosynthetic apparatus, consisting of photosystem II (PSII) and photosystem I (PSI) on the thylakoid, operates normally and produces large quantities of oxygen that diffuse into the host. ROS that are produced are converted back to oxygen with superoxide dismutase (SOD) and ascorbate peroxidase (APX). Under stressed conditions, damage to the photosynthetic apparatus occurs in at least three places (depicted as `flashes' in the figure): the D1 protein in PSII; in the Calvin cycle; and on the thylakoid membranes. This damage acts to generate large amounts of ROS in the form of singlet oxygen (1O2) and superoxide (O2–) that overwhelm the oxygen-handling pathways. O2– is converted to both the most highly reactive hydroxyl radical (·OH) and the more stable and highly diffusible hydrogen peroxide (H2O2), which can move into host tissues. Figure adapted from Venn and colleagues (Venn et al., 2008).

View larger version (16K): [in this window] [in a new window]   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 (H2O2), 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 O2– to form highly reactive peroxynitrite (ONOO– 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.

View larger version (11K): [in this window] [in a new window]   Fig. 4. Five different types of cellular mechanisms of symbiont loss from Cnidarian host tissues. The different types are discussed in the text from top to bottom. Symbionts lost by in situ degradation die or are killed in the host cell and are either digested or expelled (not shown). Symbionts lost via exocytosis are expelled free within the gastrovascular cavity. In host cell detachment, symbionts are lost when whole host cells with their symbionts still resident within, become detached from the mesoglea and surrounding cells and are released into the gastrovascular cavity. Host cells undergoing apoptosis, shrink and form multiple apoptotic bodies and in the process release viable or degrading symbionts into the gastrovascular cavity. Host cells dying by necrosis, swell and burst, releasing their contents, including symbionts (either viable or degrading) into the gastrovascular cavity. Normal host cells (H) are anchored to the acellular mesoglea (M). Symbionts (S) are contained with host vacuoles or symbiosomes (Sy). Figure adapted from Gates and colleagues (Gates et al., 1992).

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