The Role of Epigenetics in Evolution: The Extended Synthesis

Abstract

Coral skeletal growth anomaly (GA) is a common coral disease. It has been considered as a pathological condition comparable to abnormal tissue growth in mammals, but little is known about the molecular changes underlying coral GA. To investigate the molecular pathology of GA, we compared the proteome between normal and GA-affected tissues of the brain coral Platygyra carnosa using iTRAQ-labeling and LC-MS/MS, which quantified 818 proteins and identified 117 differentially expressed proteins (DEPs). GO analyses revealed DEPs that might be related to GA included “translational elongation”, “proteasome core complex”, “amine metabolic processes” and “lysosome”. Several proteins implicated in calcification and fluorescence were differentially expressed at both protein and mRNA level. Protein-protein interaction network suggested possible involvement of TNF receptor signaling in GA. Overall, our results provided novel insights into the molecular pathology of coral GA, which will pave the way for determination of the causative agent(s) of this coral disease.