Abstract

Abstract. The ongoing rise in atmospheric pCO2 and consequent increase in ocean acidification have direct effects on marine calcifying phytoplankton, which potentially alters carbon export. To date it remains unclear, firstly, how nutrient regime, in particular by coccolithophores preferred phosphate limitation, interacts with pCO2 on particulate carbon accumulation; secondly, how direct physiological responses on the cellular level translate into total population response. In this study, cultures of Emiliania huxleyi were full-factorially exposed to two different N:P regimes and three different pCO2 levels. Cellular biovolume and PIC and POC content significantly declined in response to pCO2 in both nutrient regimes. Cellular PON content significantly increased in the Redfield treatment and decreased in the high N:P regime. Cell abundance significantly declined in the Redfield and remained constant in the high N:P regime. We hypothesise that in the high N:P regime severe phosphorous limitation could be compensated either by reduced inorganic phosphorous demand and/or by enzymatic uptake of organic phosphorous. In the Redfield regime we suggest that enzymatic phosphorous uptake to supplement enhanced phosphorous demand with pCO2 was not possible and thus cell abundance declined. These hypothesised different physiological responses of E. huxleyi among the nutrient regimes significantly altered population carrying capacities along the pCO2 gradient. This ultimately led to the attenuated total population response in POC and PIC content and biovolume to increased pCO2 in the high N:P regime. Our results point to the fact that the physiological (i.e. cellular) PIC and POC response to ocean acidification cannot be linearly extrapolated to total population response and thus carbon export. It is therefore necessary to consider both effects of nutrient limitation on cell physiology and their consequences for population size when predicting the influence of coccolithophores on atmospheric pCO2 feedback and their function in carbon export mechanisms.

Highlights

  • At present, earth faces an atmospheric CO2 partial pressure of 398 μatm, which is approximately 100 μatm higher than pre-industrial conditions

  • The ongoing rise in atmospheric pCO2 and consequent increase in ocean acidification have direct effects on marine calcifying phytoplankton, which potentially alters carbon export. To date it remains unclear, firstly, how nutrient regime, in particular by coccolithophores preferred phosphate limitation, interacts with pCO2 on particulate carbon accumulation; secondly, how direct physiological responses on the cellular level translate into total population response

  • Since about half of the pelagic calcification is accomplished by coccolithophores (Broecker and Clark, 2009) and the sinking of their calcareous coccoliths might play a crucial role in carbon export mechanisms (Klaas and Archer, 2002), the physiological response of coccolithophores to ocean acidification is of special interest

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Summary

Introduction

Earth faces an atmospheric CO2 partial pressure of 398 μatm, which is approximately 100 μatm higher than pre-industrial conditions This fraction, would be considerably larger if the surface oceans had not absorbed approximately 50 % of previous fossil fuel emissions (Sabine et al, 2004). The ongoing increase in atmospheric pCO2 results in decreasing surface ocean pH and CO23− concentration and increasing HCO−3 – and CO2-concentrations These variations in ocean carbonate chemistry have direct implications on physiological processes, such as photosynthesis and calcification of many organisms (Turley et al, 2010). Coccolithophores are among the best examined organisms with respect to their response to ocean acidification These mainly negative responses in calcification and photosynthesis of various coccolithophore species and species strains were usually measured per unit cell in the exponential growth phase These mainly negative responses in calcification and photosynthesis of various coccolithophore species and species strains were usually measured per unit cell in the exponential growth phase (e.g. Riebesell et al, 2000; Zondervan et al, 2001, 2002; Langer et al, 2006, 2009; Shi et al, 2009; Krug et al, 2011)

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