Meeting Abstract
Coral reefs have experienced precipitous declines during the Anthropocene, in large part due to coral diseases and hyperthermic bleaching, which is the loss of the obligate algal symbiont. Intense research efforts have been undertaken to establish links between coral pathologies and cellular mechanics. Up to now the intermediary cellular pathways linking the coral host’s response to heat and pathogen stress have not been functionally validated. A recently characterized cellular pathway, the mitochondrial unfolded protein response (mtUPR) is a potent pro-survival mechanism mediating a wide array of effector responses. The key pathways up-regulated by the mtUPR known to be important in coral stress responses include: antioxidant elements, heat shock proteins and anti-microbial compounds. Up to now the mtUPR has only been investigated in humans and the model nematode Caenorhabditis elegans (C. elegans) for its role in numerous human diseases. In the first study to utilize transgenesis in corals, we validated the existence of the mtUPR in Orbicella faveolata (O. faveolata) mediated by the coral cyclic AMP-dependent Activating Transcription Factor 5 (cATF5). Microinjection of the cATF5 gene construct was able to rescue a genetic knockout model of C. elegans harboring a mtUPR reporter construct. cATF5 was demonstrated to be up-regulated during both temperature and pathogenic stress in O. faveolata. Using qPCR and bioinformatic methods we were able to demonstrate the coral mtUPR shares functional homology to the human and C. elegans mtUPR, by being able to increase transcription of Heat Shock proteins 60 and 70, as well as superoxide dismutase. This pathway has the potential to enhance understanding of coral stress responses at the cellular level in a changing climate.
