4.7 Article

Effects of elevated pCO2 and temperature on the calcification rate, survival, extrapallial fluid chemistry, and respiration of the Atlantic Sea scallop Placopecten magellanicus

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LIMNOLOGY AND OCEANOGRAPHY
卷 67, 期 8, 页码 1670-1686

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WILEY
DOI: 10.1002/lno.12153

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  1. NOAA [NA14NMF4540072]
  2. NOAA/MIT SeaGrant [NA14OAR41705710004054, NA18OAR4170105]
  3. NSF-BIO-OCE [1437371]

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Anthropogenic CO2 emissions contribute to ocean warming and acidification. A study on Atlantic sea scallops revealed that elevated pCO(2) inhibits calcification and respiration rates, leading to mortality under high-temperature stress. The examination of extrapallial fluid (EPF) chemistry showed that scallops regulate pH to support calcification, but the regulation efforts are insufficient to offset the negative impacts of elevated pCO(2).
Anthropogenic CO2-emission is causing ocean warming and acidification. Understanding how basic physiological processes of marine organisms respond to these stressors is important for predicting their responses to future global change. We examined the effects of elevated pCO(2) and temperature (pCO(2) = 344-2199 ppm; temperature = 6 degrees C, 9 degrees C, and 12 degrees C) on the calcification rate, extrapallial fluid (EPF) carbonate chemistry, respiration, and survivorship of Atlantic sea scallops (Placopecten magellanicus) in a fully crossed 143-d experiment. Rates of calcification and respiration were inhibited by elevated pCO(2), and mortality occurred when elevated pCO(2) was accompanied by high-temperature stress. Declines in growth and survivorship were likely caused by external shell dissolution, thermal stress, and hypercapnic reduction of metabolism under elevated pCO(2). Concentrations of dissolved inorganic carbon (DIC) and total alkalinity in the EPF increased above seawater concentrations in response to elevated pCO(2). EPF pH declined, but did not decline as much as seawater pH, indicating that scallops regulate EPF pH to support calcification. The combination of EPF pH regulation and DIC elevation yielded an increase in EPF [CO32-$$ {\mathrm{CO}}_3<^>{2-} $$] under elevated pCO(2) treatments. The combination of low respiration rates, high EPF [CO32-$$ {\mathrm{CO}}_3<^>{2-} $$], and low calcification rates under elevated pCO(2) suggests that the impaired calcification arises more from hypercapnic inhibition of metabolic activity and external shell dissolution than from chemically unfavorable conditions in the EPF. These results demonstrate the importance of EPF chemistry for bivalve biomineralization, but show that regulation efforts are insufficient to fully offset the deleterious effects of elevated pCO(2) on scallop performance.

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