Abstract
Polyp bailout is a drastic response to acute stress where coral coloniality breaks down and polyps detach. We induced polyp bailout in Pocillopora acuta with heat stress and tested for differential gene expression using RNAseq and a qPCR assay. Furthermore, we induced polyp bailout with hypersalinity and compared the results to identify stressor-independent signals and pathways active during polyp bailout. Both stressors led to the onset of polyp bailout and the detachment of vital polyps. We observed activation of microbe-associated molecular pattern receptors and downstream signaling pathways of the innate immune system. Further, we detected growth factors and genes active during Wnt-signaling potentially contributing to wound healing, regeneration, and proliferation. Upregulation of several genes encoding for matrix metalloproteinases and the fibroblast growth factor signaling pathway are the most likely involved in the remodeling of the extracellular matrix, as well as in the detachment of polyps from the calcareous skeleton during polyp bailout. Expression of genes of interest in our qPCR assay of vital polyps from our heat-stress experiment, showed a trend for a normalization of gene expression after polyp bailout. Our results provide new insights into the signaling cascades leading to the observed physiological responses during polyp bailout. Comparison between the two stressors showed that certain signaling pathways are independent of the stressor and suggested that polyp bailout is a general response of corals to acute stress. Furthermore, immune system responses during polyp bailout indicate that microbe-associated partners of corals may lead to the polyp bailout response.
Highlights
Polyp bailout is a drastic response to acute stress where coral coloniality breaks down and polyps detach
To determine which genes are involved only in the polyp bailout response, we identified genes significantly differentially expressed in both experiments. 2130 differentially expressed genes (DEG) were identified in the analysis of both experiments and clustering of the transcripts led to the formation of four distinct clusters (Fig. 2c)
Among upregulated DEGs in the hypersalinity stress (Salinity Cluster 1), we found Gene ontology (GO) categories already described for polyp bailout in this stressor (Chuang and Mitarai 2020), such as tumor necrosis factor (TNF)-mediated signaling pathway, fibroblast growth factor (FGF) receptor signaling pathway, extrinsic apoptotic signaling pathway, and proteolysis, which were significantly enriched (p \ 0.05)
Summary
Polyp bailout is a drastic response to acute stress where coral coloniality breaks down and polyps detach. We induced polyp bailout with hypersalinity and compared the results to identify stressor-independent signals and pathways active during polyp bailout. Both stressors led to the onset of polyp bailout and the detachment of vital polyps. Based on the results of Kvitt et al (2015), Shapiro et al (2016), and Wecker et al (2018), a recent study used hypersalinity to induce polyp bailout in Pocillopora acuta and added further information about the signaling pathways. Beyond upregulation of apoptosis and proteolysis, P. acuta showed significant activation of tumor necrosis factor and fibroblast growth factor, which probably led to the polyp bailout response (Chuang and Mitarai 2020)
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