TNF signaling leads to apoptosis and coenosarc degradation
The significant enrichment of GO terms apoptotic process andextrinsic apoptotic signaling pathway in our transcriptomic data (Table 1) supports the hypothesis of apoptosis-induced coenosarc degradation proposed in previous studies (Kvitt et al., 2015; Wecker et al., 2018). The extrinsic apoptotic signaling pathway, comprising signals mediated by the TNF receptor family and a caspase cascade initiated by caspase-8, is highly conserved among animals and was proposed in polyp bail-out (Quistad et al., 2014; Wecker et al., 2018). Interestingly, even with significant enrichment of the TNF signaling pathway in our transcriptomic data and upregulation of the FAS receptor gene in the qPCR assay, no overexpression of TNF was found during the polyp bail-out induction in this study, either in the transcriptomic or qPCR analysis. Similar to our finding, in Wecker et al. (2018) TNF overexpression was found with a delayed spike compared to that of caspase and TNF receptor genes. It is possible that signals triggering the TNF pathway during polyp bail-out came from symbiotic microorganisms in the corals, which were filtered out during our data processing step. Since changing the culture environment can substantially alter the composition of coral-associated microbes (Littman, Willis, & Bourne, 2011; Webster et al., 2013), initiation of polyp bail-out may be attributable to shift of chemical signals provided from microbes to the coral host. In fact, it was recently reported that polyp bail-out inP. damicornis can be induced by inoculation with the coral pathogen, Vibrio coralliilyticus (Gavish, Shapiro, Kramarsky-Winter, & Vardi, 2018). Our results thus add further evidence for involvement of the TNF receptor-mediated extrinsic apoptotic signaling pathway in polyp bail-out and point to a possibly role of symbiotic microbes in this stress response (Fig. 4).