Biogenic habitat shifts under long-term ocean acidification show nonlinear community responses and unbalanced functions of associated invertebrates

Este artículo contiene 8 páginas, 4 figuras.
Experiments have shown that increasing dissolved CO2 concentrations (i.e. Ocean Acidification, OA) in marine ecosystems may act as nutrient for primary producers (e.g. fleshy algae) or a stressor for calcifying species (e.g., coralline algae, corals, molluscs). For the first time, rapid habitat dominance shifts and altered competitive replacement from a reef-forming to a non-reef-forming biogenic habitat were documented over one-year exposure to low pH/high CO2 through a transplant experiment off Vulcano Island CO2 seeps (NE Sicily, Italy). Ocean acidification decreased vermetid reefs complexity via a reduction in the reef-building species density, boosted canopy macroalgae and led to changes in composition, structure and functional diversity of the associated benthic assemblages. OA effects on invertebrate richness and abundance were nonlinear, being maximal at intermediate complexity levels of vermetid reefs and canopy forming algae. Abundance of higher order consumers (e.g. carnivores, suspension feeders) decreased under elevated CO2 levels. Herbivores were non-linearly related to OA conditions, with increasing competitive release only of minor intertidal grazers (e.g. amphipods) under elevated CO2 levels. Our results support the dual role of CO2 (as a stressor and as a resource) in disrupting the state of rocky shore communities, and raise specific concerns about the future of intertidal reef ecosystem under increasing CO2 emissions. We contribute to inform predictions of the complex and nonlinear community effects of OA on biogenic habitats, but at the sametime encourage the use ofmultiple natural CO2 gradients in providing quantitative data on changing community responses to long-term CO2 exposure.
This work contributes to the University of Palermo FFR-A project and the EU-FP7 MedSeA project (grant agreement no. 265103) to M.M.