Rapid acclimation of juvenile corals to CO2-mediated acidification by upregulation of heat shock protein and Bcl-2 genes

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 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.

Stable carbon and oxygen isotope ratios of planktonic and benthic foraminifera from ODP Site 162-982 in the North Atlantic

Changes in the intermediate water structure of the North Atlantic were reconstructed using benthic foraminiferal delta13C at Ocean Drilling Program (ODP) site 982 for the past 1.0 Myr. During most terminations of the late Pleistocene, melting of icebergs and low-salinity surface waters caused production of Glacial North Atlantic Intermediate Water to cease, resulting in decreased ventilation of the middepth North Atlantic. Poor ventilation of intermediate water masses lasted well into some interglacial stages until upper North Atlantic Deep Water (NADW) production resumed under full interglacial conditions. The magnitude of benthic delta13C minima and ice-rafted debris maxima at terminations at site 982 generally match the degree of glacial suppression of NADW inferred from site 607. These processes may be related and controlled by the spatial and seasonal extent of sea ice cover during glaciations in the Nordic Seas.