Abstract
The Anthropocene will be characterized by increased environmental disturbances, leading to the survival of stress-tolerant organisms, particularly in the oceans, where novel marine diseases and elevated temperatures are re-shaping ecosystems. These environmental changes underscore the importance of identifying mechanisms which promote stress tolerance in ecologically important non-model species such as reef-building corals. Mitochondria are central regulators of cellular stress and have dedicated recovery pathways including the mitochondrial unfolded protein response, which increases the transcription of protective genes promoting protein homeostasis, free radical detoxification and innate immunity. In this investigation, we identify a mitochondrial unfolded protein response in the endangered Caribbean coral Orbicella faveolata, by performing in vivo functional replacement using a transcription factor (Of-ATF5) originating from a coral in the model organism Caenorhabditis elegans. In addition, we use RNA-seq network analysis and transcription factor-binding predictions to identify a transcriptional network of genes likely to be regulated by Of-ATF5 which is induced during the immune challenge and temperature stress. Overall, our findings uncover a conserved cellular pathway which may promote the ability of reef-building corals to survive increasing levels of environmental stress.
Highlights
Coral reefs have recently experienced massive declines [1,2], primarily driven by marine diseases [3,4] and thermally induced mass coral bleaching [5,6]
By using transgenesis of a genetic reporter line of UPRmt activity in C. elegans, we show that O. faveolata possesses a gene which is able to rescue a loss of function mutation of the UPRmt mediator ATFS-1 in vivo
We were unable to locate an obvious ATFS-1 homologue in the genome of O. faveolata; a subsequent search revealed a putative homologue of Hs-ATF5 in the O. faveolata genome that contains a basic leucine zipper (bZIP) domain and a weakly predicted mitochondrial targeting sequence (MTS) termed Of-ATF5
Summary
Coral reefs have recently experienced massive declines [1,2], primarily driven by marine diseases [3,4] and thermally induced mass coral bleaching [5,6]. As the UPRmt regulates many of the elements thought to be important in coral stress responses including production of heat shock proteins (HSP) and antioxidants, and that the regulatory pathways in coral remain largely obscure, we sought to characterize a possible UPRmt in the reef-building coral Orbicella faveolata In this investigation, we demonstrate the existence of a pathway in O. faveolata which bears high similarity to the described UPRmt. By using transgenesis of a genetic reporter line of UPRmt activity in C. elegans, we show that O. faveolata possesses a gene which is able to rescue a loss of function mutation of the UPRmt mediator ATFS-1 in vivo. To investigate if the genes identified by our weighted gene co-expression network analysis (WGCNA) module possessed Hs-ATF5 binding motifs within their regulatory regions, we extracted 1000 bp upstream of the start codon for all annotated genes in the O. faveolata genome (ofav_dov_v1, GenBank: MZGG00000000.1) using a custom Python script and BEDTOOLS [46]. All statistical analysis including DESeq, WGCNA and GOMWU was performed in the R programming environment [51]
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