Ocean Acidification

Reef dwelling algae employ a variety of physical and chemical defenses against herbivory, and the response to wounding is extremely important in algal communities. Wound healing mechanisms in crustose coralline algae (CCA) are related to skeletal growth and net calcification rate. Ocean acidification (OA) is known to affect rates of net calcification in a number of calcifying organisms, including CCA. Reduced rates of net calcification in CCA are likely to alter wound healing, and thus affect the consequences of herbivore-CCA interactions on coral reefs. The response of the tropical CCA Porolithon onkodes to OA and artificial wounding was quantified in a 51-day laboratory experiment. Eight artificially wounded (cut to a mean depth of 182 μm) and eight non-wounded samples of P. onkodes were randomly placed into each of four treatments (n = 64 samples total). Each treatment was maintained at a different pCO₂ level representative of either ambient conditions or end-of-the-century, predicted conditions (IPCC, 2014); 429.31 ± 20.84 (ambient), 636.54 ± 27.29 (RCP4.5), 827.33 ± 38.51 (RCP6.0), and 1179.39 ± 88.85 μatm (RCP8.5; mean ± standard error). Elevated pCO₂ significantly reduced rates of net calcification in both wounded and non-wounded samples of P. onkodes (slopes = −6.4 × 10⁻⁴ and −5.5 × 10⁻⁴ mg cm⁻² d⁻¹ per μatm pCO₂, respectively over 51 days). There also was a significant reduction in the rate of vertical regeneration of thallus tissue within the wounds as pCO₂ increased (slope = −1.5 × 10⁻³ μm d⁻¹ per μatm pCO₂ over 51 days). This study provides evidence that elevated pCO₂ could reduce the ability of this important alga to recover from wounding. Because wounding by herbivores plays an important role in determining CCA community structure, we propose reduced wound healing as a mechanism by which OA might affect the structure and functional roles of CCA communities on coral reefs.