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.