Project description:Scleractinian corals acquire autotrophic nutrients via the photosynthetic activity of their symbionts and the subsequent transfer of photosynthates. Zooplankton predation by the animal (heterotrophy) is an additional food source. Under stress events, corals loose their symbionts, a phenomena known as bleaching, which eventually leads to starvation, unless corals increase their heterotrophic capacities. Molecular mechanisms by which heterotrophy sustains metabolism in stressed corals remain elusive. Here for the first time, we identify specific genes expressed in heterotrophically fed and unfed corals maintained under normal and light-stress conditions inducing bleaching. Physiological parameters and gene expression profiling showed ominously that fed corals better resisted the stress than unfed corals, by presenting less oxidative damage and protein/DNA degradation. Light stressed and unfed/starved corals (HLS) up-regulated by 140 and 13 times two genes (CP2U1 and CP1A2), which belong to the Cytochrome P450 superfamily, while these genes remained almost unchanged in fed corals (HLF). Other genes of redox regulation, DNA damage response, molecular chaperones, and protein degradation were also up-regulated in HLS corals, presenting higher bleaching, and strong decrease of the photosynthesis performance compared to HLF corals. Several pivotal genes associated with the calcification apparatus such as carbonic anhydrases, calcium-transporting ATPase, calcium channel subunit, and bone morphogenetic proteins (BMPs), were significantly down-regulated only in HLS corals. A parallel decrease in the calcification rates of these later corals was also observed. All together, these results show clearly that heterotrophy helps preventing oxidative stress in corals, and thus avoid the cascade of metabolic problems downstream this stress.
Project description:Over the past several decades, corals worldwide have been affected by global warming, experiencing severe bleaching events that have often lead to coral death. The symbiotic Red Sea coral Stylophora pistillata is considered an opportunistic ‘r’ strategist, thriving in relatively unstable and unpredictable environments, and it is considered a stress-tolerant species. This study aimed to examine S. pistillata gene expression and to clarify the cellular pathways that are active during short-term heat stress caused by an increase from 24°C to 34°C over a 10-day period. Total RNA was extracted from heat-stressed coral fragments, labeled and hybridized against a designated S. pistillata custom microarray containing approximately 12,000 genes. Our results show that the heat stress reaction was sighted from 32°C and intensified significantly after 34°C treatment. Protein interaction networks of up- and down-regulated genes were constructed. The main clustering groups of up-regulated genes were ER stress and ER protein folding, cell cycle, ubiquitin-mediated proteolysis, cell death and cell death regulation and cellular stress response genes. These genes were enriched in cellular pathways related to the unfolded protein response (UPR) in the ER, ER-associated degradation (ERAD) and ubiquitin-mediated proteolysis. An analysis of the down-regulated genes yielded different clusters of genes related to extracellular matrix and actin organization, collagen, negative regulation of cell death and the Notch and Wnt signaling pathways. Genes encoding redox regulation proteins and molecular chaperones may be considered accurate “early warning genes”, while genes related to sensing and repairing DNA damage are severe heat-related genes. Here, we suggest that during short-term heat stress, S. pistillata might divert cellular energy into mechanisms such as UPR and ERAD at the expense of growth and biomineralization processes in an effort to recover from the stress.
Project description:The declining health of coral reefs worldwide is likely to intensify in response to continued anthropogenic disturbance from coastal development, pollution, and climate change. In response to these stresses, reef-building corals may exhibit bleaching, which marks the breakdown in symbiosis between coral and zooxanthellae. Mass coral bleaching due to elevated water temperature can devastate coral reefs on a large geographic scale. In order to understand the molecular and cellular basis of bleaching in corals, we have measured gene expression changes associated with thermal stress and bleaching using a cDNA microarray containing 1,310 genes of the Caribbean coral Montastraea faveolata. In a first experiment, we identified differentially expressed genes by comparing experimentally bleached M. faveolata fragments to control non-heat-stressed fragments. We also identified differentially expressed genes during a time course experiment with four time points across nine days. Results suggest that thermal stress and bleaching in M. faveolata affect the following processes: oxidative stress, Ca2+ homeostasis, cytoskeletal organization, cell death, calcification, metabolism, protein synthesis, heat shock protein activity, and transposon activity. These results represent the first large-scale transcriptomic study focused on revealing the cellular foundation of thermal stress-induced coral bleaching. We postulate that oxidative stress in thermal-stressed corals causes a disruption of Ca2+ homeostasis, which in turn leads to cytoskeletal and cell adhesion changes, decreased calcification, and the initiation of cell death via apoptosis and necrosis. Keywords: thermal stress response, time course, coral bleaching
Project description:The declining health of coral reefs worldwide is likely to intensify in response to continued anthropogenic disturbance from coastal development, pollution, and climate change. In response to these stresses, reef-building corals may exhibit bleaching, which marks the breakdown in symbiosis between coral and zooxanthellae. Mass coral bleaching due to elevated water temperature can devastate coral reefs on a large geographic scale. In order to understand the molecular and cellular basis of bleaching in corals, we have measured gene expression changes associated with thermal stress and bleaching using a cDNA microarray containing 1,310 genes of the Caribbean coral Montastraea faveolata. In a first experiment, we identified differentially expressed genes by comparing experimentally bleached M. faveolata fragments to control non-heat-stressed fragments. We also identified differentially expressed genes during a time course experiment with four time points across nine days. Results suggest that thermal stress and bleaching in M. faveolata affect the following processes: oxidative stress, Ca2+ homeostasis, cytoskeletal organization, cell death, calcification, metabolism, protein synthesis, heat shock protein activity, and transposon activity. These results represent the first large-scale transcriptomic study focused on revealing the cellular foundation of thermal stress-induced coral bleaching. We postulate that oxidative stress in thermal-stressed corals causes a disruption of Ca2+ homeostasis, which in turn leads to cytoskeletal and cell adhesion changes, decreased calcification, and the initiation of cell death via apoptosis and necrosis. Keywords: thermal stress response; coral bleaching
Project description:The declining health of coral reefs worldwide is likely to intensify in response to continued anthropogenic disturbance from coastal development, pollution, and climate change. In response to these stresses, reef-building corals may exhibit bleaching, which marks the breakdown in symbiosis between coral and zooxanthellae. Mass coral bleaching due to elevated water temperature can devastate coral reefs on a large geographic scale. In order to understand the molecular and cellular basis of bleaching in corals, we have measured gene expression changes associated with thermal stress and bleaching using a cDNA microarray containing 1,310 genes of the Caribbean coral Montastraea faveolata. In a first experiment, we identified differentially expressed genes by comparing experimentally bleached M. faveolata fragments to control non-heat-stressed fragments. We also identified differentially expressed genes during a time course experiment with four time points across nine days. Results suggest that thermal stress and bleaching in M. faveolata affect the following processes: oxidative stress, Ca2+ homeostasis, cytoskeletal organization, cell death, calcification, metabolism, protein synthesis, heat shock protein activity, and transposon activity. These results represent the first large-scale transcriptomic study focused on revealing the cellular foundation of thermal stress-induced coral bleaching. We postulate that oxidative stress in thermal-stressed corals causes a disruption of Ca2+ homeostasis, which in turn leads to cytoskeletal and cell adhesion changes, decreased calcification, and the initiation of cell death via apoptosis and necrosis. Keywords: thermal stress response; coral bleaching 5 control and 5 heat-stressed RNA samples were hybridized in a 5-replicate dye-swap design (10 total hyb's).
Project description:The declining health of coral reefs worldwide is likely to intensify in response to continued anthropogenic disturbance from coastal development, pollution, and climate change. In response to these stresses, reef-building corals may exhibit bleaching, which marks the breakdown in symbiosis between coral and zooxanthellae. Mass coral bleaching due to elevated water temperature can devastate coral reefs on a large geographic scale. In order to understand the molecular and cellular basis of bleaching in corals, we have measured gene expression changes associated with thermal stress and bleaching using a cDNA microarray containing 1,310 genes of the Caribbean coral Montastraea faveolata. In a first experiment, we identified differentially expressed genes by comparing experimentally bleached M. faveolata fragments to control non-heat-stressed fragments. We also identified differentially expressed genes during a time course experiment with four time points across nine days. Results suggest that thermal stress and bleaching in M. faveolata affect the following processes: oxidative stress, Ca2+ homeostasis, cytoskeletal organization, cell death, calcification, metabolism, protein synthesis, heat shock protein activity, and transposon activity. These results represent the first large-scale transcriptomic study focused on revealing the cellular foundation of thermal stress-induced coral bleaching. We postulate that oxidative stress in thermal-stressed corals causes a disruption of Ca2+ homeostasis, which in turn leads to cytoskeletal and cell adhesion changes, decreased calcification, and the initiation of cell death via apoptosis and necrosis. Keywords: thermal stress response, time course, coral bleaching Time course with 4 time points and 4 biological replicates per time point. Each biological replicate at each time point was hybridized to a pooled reference control sample containing RNA from all control non-heat-stressed coral fragments.
Project description:Aging is a multifactorial process that results in progressive loss of regenerative capacity and tissue function while simultaneously favoring the development of a large array of age-related diseases. Evidence suggests that the accumulation of senescent cells in tissue promotes both normal and pathological aging. Oxic stress is a key driver of cellular senescence. Because symbiotic long-lived reef corals experience daily hyperoxic and hypoxic transitions, we hypothesized that these long-lived animals have developed specific longevity strategies in response to light. We analyzed transcriptome variation in the reef coral Stylophora pistillata during the day–night cycle and revealed a signature of the FoxO longevity pathway. We confirmed this pathway by immunofluorescence using antibodies against coral FoxO to demonstrate its nuclear translocation. Among genes that were specifically up- or downregulated on exposure to light, human orthologs of two “light-up” genes (HEY1 and LONF3) exhibited anti-senescence properties in primary human fibroblasts. Therefore, these genes are interesting candidates for counteracting skin aging. We propose a large screen for other light-up genes and an investigation of the biological response of reef corals to light (e.g., metabolic switching) to elucidate these processes and identify effective interventions for promoting healthy aging in humans.