Abstract
Coral reefs are of major ecological and socio-economic interest. They are threatened by global warming and natural pressures such as solar ultraviolet radiation. While great efforts have been made to understand the physiological response of corals to these stresses, the signalling pathways involved in the immediate cellular response exhibited by corals remain largely unknown. Here, we demonstrate that c-Jun N-terminal kinase (JNK) activation is involved in the early response of corals to thermal and UV stress. Furthermore, we found that JNK activity is required to repress stress-induced reactive oxygen species (ROS) accumulation in both the coral Stylophora pistillata and human skin cells. We also show that inhibiting JNK activation under stress conditions leads to ROS accumulation, subsequent coral bleaching and cell death. Taken together, our results suggest that an ancestral response, involving the JNK pathway, is remarkably conserved from corals to human, protecting cells from the adverse environmental effects.
Highlights
Leads to coral bleaching, i.e. the loss of coral algal symbionts and/or photosynthetic pigments[23,24], resulting in a drop in photosynthesis and calcification[25], and possibly leading to coral death
A sequence showing 89%, 74% and 64% homology with the protein sequences of A. digitifera (Ad-Jun N-terminal kinase (JNK)), H. vulgaris (Hv-JNK) and the human MAPK8/JNK1 (Hs-JNK1), respectively, was identified in S. pistillata. This sequence contains both the conserved kinase domains[43] and the TPY motif unique for JNK orthologs[15], like Ad-JNK, Hv-JNK and Hs-JNK sequences (Fig. 1). These results suggest that a single ortholog of JNK is present in S. pistillata, as opposed to the three genes encoding several JNK isoforms in the human genome[44]
While the physiological response of corals to ultra-violet radiation (UVR) or thermal stress has been well studied[27,28], the intracellular signalling that allows corals to rapidly respond to these stresses is still unknown
Summary
Leads to coral bleaching, i.e. the loss of coral algal symbionts and/or photosynthetic pigments[23,24], resulting in a drop in photosynthesis and calcification[25], and possibly leading to coral death. An increasing number of studies indicate that corals express genes encoding MAPKs, including those encoding JNK29–34. This suggests the presence of a conserved stress response between coral and human cells at the molecular level, the phylum cnidaria diverged from bilateria 550 million years ago[35]. Under thermal stress and following wounding[34,36,37] Such induction may be specific to corals since post-translational and not transcriptional regulation of JNK signalling is most often observed in mammalian cells[38]. Taking advantage of the amino acid sequence conservation of coral and human JNK orthologs, in particular the phosphorylatable TPY motif contained in the kinase domain, we used commercially available antibodies to analyse JNK activation upon thermal and UVR stress in both corals and human skin fibroblasts. We endeavoured to link the JNK pathway activation to the defence against stress-induced ROS production in both models
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