RNA-Seq of the Caribbean reef-building coral Orbicella faveolata (Scleractinia-Merulinidae) under bleaching and disease stress expands models of coral innate immunity.

David A Anderson,Ernesto Weil,Marcus E Walz,Matthew C Smith,Peter Tonellato

doi:10.7717/peerj.1616

Abstract

Climate change-driven coral disease outbreaks have led to widespread declines in coral populations. Early work on coral genomics established that corals have a complex innate immune system, and whole-transcriptome gene expression studies have revealed mechanisms by which the coral immune system responds to stress and disease. The present investigation expands bioinformatic data available to study coral molecular physiology through the assembly and annotation of a reference transcriptome of the Caribbean reef-building coral, Orbicella faveolata. Samples were collected during a warm water thermal anomaly, coral bleaching event and Caribbean yellow band disease outbreak in 2010 in Puerto Rico. Multiplex sequencing of RNA on the Illumina GAIIx platform and de novo transcriptome assembly by Trinity produced 70,745,177 raw short-sequence reads and 32,463 O. faveolata transcripts, respectively. The reference transcriptome was annotated with gene ontologies, mapped to KEGG pathways, and a predicted proteome of 20,488 sequences was generated. Protein families and signaling pathways that are essential in the regulation of innate immunity across Phyla were investigated in-depth. Results were used to develop models of evolutionarily conserved Wnt, Notch, Rig-like receptor, Nod-like receptor, and Dicer signaling. O. faveolata is a coral species that has been studied widely under climate-driven stress and disease, and the present investigation provides new data on the genes that putatively regulate its immune system.

Highlights

IntroductionCoral reefs are experiencing a dramatic decline in coral cover and reef biodiversity, reports of which have been documented as early as the 1970s (Alemu & Clement, 2014; Altizer et al, 2013; Antonius, 1973; Bastidas et al, 2012; Bruno et al, 2007; Ducklow & Mitchell, 1979; Glynn, Peters & Muscatine, 1985; Glynn, 1983; Harvell et al, 1999; Tracy et al, 2015; Weil & Rogers, 2011; Weil, Smith & Gil-Agudelo, 2006)
The reference transcriptome generated here was annotated with gene ontologies, KEGG orthologies, and KEGG pathways
Sequence accuracy was high with reference transcriptome sequences sharing 96% identity with corresponding O. faveolata expression sequence tags (EST) in NCBI (Supplemental Information 6)

Summary

Introduction

Coral reefs are experiencing a dramatic decline in coral cover and reef biodiversity, reports of which have been documented as early as the 1970s (Alemu & Clement, 2014; Altizer et al, 2013; Antonius, 1973; Bastidas et al, 2012; Bruno et al, 2007; Ducklow & Mitchell, 1979; Glynn, Peters & Muscatine, 1985; Glynn, 1983; Harvell et al, 1999; Tracy et al, 2015; Weil & Rogers, 2011; Weil, Smith & Gil-Agudelo, 2006). Climate change-driven stress can lead to disease outbreaks by shifting coral-associated microbial communities from symbiont and commensal-dominated to pathogen-dominated (Bourne et al, 2009; Rosenberg et al, 2007), and the molecular and cellular responses of coral to disease and environmental stress are well established (Ocampo et al, 2015; Palmer & Traylor-Knowles, 2012; Pinzon et al, 2015; Weiss et al, 2013). Orbicella faveolata is an important Caribbean and Atlantic reef-building coral It has experienced recent population declines and is classified as a threatened species under the federal endangered species act (NOAA, 2014). To better understand the biological mechanisms of this decline, transcriptomics has been used to define changes in gene expression of this coral and commensal microbiota in response to environmental stress during larval development, the establishment of symbiosis, and the maintenance of homeostasis (Aranda et al, 2012; Borger & Colley, 2010; Closek et al, 2014; Croquer et al, 2013; Desalvo et al, 2008; Kimes et al, 2010; Pinzon et al, 2015; Roder et al, 2014; Schwarz et al, 2008; Sunagawa et al, 2009; Voolstra et al, 2009)

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Results

Conclusion