Rapid acclimation of juvenile corals to CO2‐mediated acidification by upregulation of heat shock protein and Bcl‐2 genes
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Abstract:
Corals play a key role in ocean ecosystems and carbonate balance, but their molecular response to ocean acidification remains unclear. The only previous whole-transcriptome study (Moya et al. Molecular Ecology, 2012; 21, 2440) documented extensive disruption of gene expression, particularly of genes encoding skeletal organic matrix proteins, in juvenile corals (Acropora millepora) after short-term (3 d) exposure to elevated pCO2 . In this study, whole-transcriptome analysis was used to compare the effects of such 'acute' (3 d) exposure to elevated pCO2 with a longer ('prolonged'; 9 d) period of exposure beginning immediately post-fertilization. Far fewer genes were differentially expressed under the 9-d treatment, and although the transcriptome data implied wholesale disruption of metabolism and calcification genes in the acute treatment experiment, expression of most genes was at control levels after prolonged treatment. There was little overlap between the genes responding to the acute and prolonged treatments, but heat shock proteins (HSPs) and heat shock factors (HSFs) were over-represented amongst the genes responding to both treatments. Amongst these was an HSP70 gene previously shown to be involved in acclimation to thermal stress in a field population of another acroporid coral. The most obvious feature of the molecular response in the 9-d treatment experiment was the upregulation of five distinct Bcl-2 family members, the majority predicted to be anti-apoptotic. This suggests that an important component of the longer term response to elevated CO2 is suppression of apoptosis. It therefore appears that juvenile A. millepora have the capacity to rapidly acclimate to elevated pCO2 , a process mediated by upregulation of specific HSPs and a suite of Bcl-2 family members.Keywords:
Ocean Acidification
Ocean acidification, caused by the uptake of carbon dioxide (CO2) from the atmosphere, is impacting many marine organisms. This dissertation investigated the effects of direct exposure and parental acclimation to simulated ocean acidification on the larval stages of Atlantic cod (Gadus morhua, L.). For this, ocean acidification levels predicted for the year 2100 were applied on cod eggs from hatch to 36 days post hatch in in vivo laboratory experiments. The direct exposure experiment clearly showed that Atlantic cod larvae were severely affected by simulated ocean acidification on a phenotypic level (chapter 1). Changes in growth, bone and gill development as well as increased frequency of organ damages were observed under predicted ocean acidification levels compared to controls. Then, the underlying molecular phenotype was assessed, using whole transcriptome sequencing (RNA-Seq), to couple transcriptomic mechanisms to the observed phenotypes (chapter 2). Transcriptome analysis revealed 1413 differentially expressed genes in late larval stages, corresponding to the observed changes in growth and developmental patterns, leading to the conclusion that these changes represent an accelerated development under ocean acidification. Surprisingly, only few genes (3 and 16, respectively) were differentially expressed in the early larval stages. An experiment set to address the effects of long-term parental acclimation (5 month) was performed to assess whether or not this kind of acclimation can mediate the identified detrimental direct effects on the larvae (chapter 3). However, none of the previously observed phenotypes under ocean acidification were found in this experiment, making it impossible to draw any conclusion on the effectiveness of parental acclimation on larval susceptibility to simulated ocean acidification. A concluding meta-analysis between experiments shows that the larvae of Atlantic Cod are to be considered vulnerable to simulated ocean acidification.
Ocean Acidification
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