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).