Survival of polyps after polyp bail-out
Interestingly, in our transcriptomic data, no significant difference in
caspase gene expression was found between coenosarc-containing coral
tissue (T24-1) and detached solitary polyps (T24-2) collected at the
same time. We therefore hypothesize that tissue-specific apoptosis in
polyp bail-out is mediated at the post-transcriptional level. In support
of this hypothesis, in our transcriptomic data we identified significant
enrichment of protein ubiquitination and upregulation of XIAP gene,
which both have been shown to regulate caspase activities and cell death
(Bader & Steller, 2009; Chen & Qiu, 2013; Deveraux, Takahashi,
Salvesen, & Reed, 1997). It was proposed that the anti-apoptotic
response is induced by a delayed TNF signal after polyp bail-out (Wecker
et al., 2018). However, in our transcriptomic data, GO terms such asJNK cascade , negative regulation of cell death , andI-κB kinase/NF-κB signaling were significantly enriched during
the experiments (Table 1), indicating earlier activation of
anti-apoptotic/cell survival signaling (Karin & Lin, 2002; Roulston,
Reinhard, Amiri, & Williams, 1998; Van Antwerp, Martin, Kafri, Green,
& Verma, 1996). Our qPCR results further showed concurrent expression
profiles of the NFKB1, XIAP, and JNK genes, suggesting possible
association of these survival and anti-apoptotic signals in the polyp
bail-out repsonse. In mammalian cell models, association of XIAP and
activation of the JNK and NF-κB signaling has been illustrated (Lu et
al., 2007; Nakano, 2004; Tang et al., 2001). Accordingly, our results
suggest that the tissue-specificity of apoptosis in polyp bail-out may
be attributed to spatial variation in anti-apoptotic signals, leading to
inhibition of caspase activity in coral polyps and to their subsequent
survival (Fig. 3). The ultimate trigger of these anti-apoptotic/cell
survial signals and their functional involvement in polyp bail-out,
however, requires further investigation.