The coral immune response facilitates protection against microbes during tissue regeneration

Mol Ecol. 2015 Jul;24(13):3390-404. doi: 10.1111/mec.13257. Epub 2015 Jun 19.

Abstract

Increasing physical damage on coral reefs from predation, storms and anthropogenic disturbances highlights the need to understand the impact of injury on the coral immune system. In this study, we examined the regulation of the coral immune response over 10 days following physical trauma artificially inflicted on in situ colonies of the coral Acropora aspera, simultaneously with bacterial colonization of the lesions. Corals responded to injury by increasing the expression of immune system-related genes involved in the Toll-like and NOD-like receptor signalling pathways and the lectin-complement system in three phases (<2, 4 and 10 days post-injury). Phenoloxidase activity was also significantly upregulated in two phases (<3 and 10 days post-injury), as were levels of non-fluorescent chromoprotein. In addition, green fluorescent protein expression was upregulated in response to injury from 4 days post-injury, while cyan fluorescent protein expression was reduced. No shifts in the composition of coral-associated bacterial communities were evident following injury based on 16S rRNA gene amplicon pyrosequencing. Bacteria-specific fluorescence in situ hybridization also showed no evidence of bacterial colonization of the wound or regenerating tissues. Coral tissues showed near-complete regeneration of lesions within 10 days. This study demonstrates that corals exhibit immune responses that support rapid recovery following physical injury, maintain coral microbial homeostasis and prevent bacterial infestation that may compromise coral fitness.

Keywords: bacteria; coral; gene expression; immunity; injury.

MeSH terms

  • Animals
  • Anthozoa / immunology*
  • Anthozoa / microbiology*
  • Bacteria / isolation & purification
  • Bacteria / pathogenicity*
  • Immunity, Innate
  • Nod Signaling Adaptor Proteins / genetics
  • Regeneration*
  • Signal Transduction
  • Toll-Like Receptors / genetics

Substances

  • Nod Signaling Adaptor Proteins
  • Toll-Like Receptors