Intracellular pH and its response to CO2-driven seawater acidification in symbiotic versus non-symbiotic coral cells.

Intracellular pH and its response to CO2-driven seawater acidification in symbiotic versus non-symbiotic coral cells.

Year: 

2014
Authors: 
Gibbin, E. M.Putnam, H. M.Davy, S. K.Gates, R. D.

Source: 

Journal of Experimental Biology

Abstract: 

Regulating intracellular pH (pH(i)) is critical for optimising the metabolic activity of corals, yet the mechanisms involved in pH regulation and the buffering capacity within coral cells are not well understood. Our study investigated how the presence of symbiotic dinoflagellates affects the response of pH(i) to P-CO2-driven seawater acidification in cells isolated from Pocillopora damicornis. Using the fluorescent dye BCECF-AM, in conjunction with confocal microscopy, we simultaneously characterised the pH(i) response in host coral cells and their dinoflagellate symbionts, in symbiotic and non-symbiotic states under saturating light, with and without the photosynthetic inhibitor DCMU. Each treatment was run under control (pH 7.8) and CO2-acidified seawater conditions (decreasing pH from 7.8 to 6.8). After 105 min of CO2 addition, by which time the external pH (pH(e)) had declined to 6.8, the dinoflagellate symbionts had increased their pH(i) by 0.5 pH units above control levels when in the absence of DCMU. In contrast, in both symbiotic and non-symbiotic host coral cells, 15 min of CO2 addition (0.2 pH unit drop in pH(e)) led to cytoplasmic acidosis equivalent to 0.3-0.4 pH units irrespective of whether DCMU was present. Despite further seawater acidification over the duration of the experiment, the pH(i) of non-symbiotic coral cells did not change, though in host cells containing a symbiont cell the pH(i) recovered to control levels when photsynthesis was not inhibited. This recovery was negated when cells were incubated with DCMU. Our results reveal that photosynthetic activity of the endosymbiont is tightly coupled with the ability of the host cell to recover from cellular acidosis after exposure to high CO2/low pH.

Volume: 

217

Issue: 

11

Pages: 

1963-1969

Publication Type: 

Journal Article

Research Areas: