Figure 4. Summary of causes of vital effects.

Summary of causes of carbon isotope vital effects in coccolith calcite. (a) Coccolithophore cell with isotopically depleted POC produced in the chloroplast and isotopically enriched PIC produced in the coccolith vesicle. (b) Schematic representation of the effect of three dominant processes affecting the isotopic composition of calcite (δ¹³C_calcite). (c) Net result of carbon isotopic vital effects in coccolith calcite. At low τ (that is, high CO₂, low cell size or low growth rate), the flux of carbon into the cell far exceeds intracellular processes, and all species plateau at the same value (I). The value of this plateau is heavier than that of the carbon entering the cell due to intracellular interconversion of carbon species and preferential loss of light carbon dioxide. Low PIC:POC: for a cell of low PIC:POC, as τ increases (I–II), the flux of isotopically heavy carbon leaving the chloroplast (depleted in light carbon by carbon fixation catalysed by RuBisCO) influences the isotopic composition of the coccolith vesicle. As τ increases further (II–III), the flux of carbon from the chloroplast, although isotopically increasingly heavy, tends towards zero, and Rayleigh-type fractionation within the coccolith vesicle itself (which removes isotopically heavy carbon) takes over, driving the pool to light values. High PIC:POC: For a cell of high PIC:POC, as τ increases (I–IV) the Rayleigh-type fractionation due to calcite precipitation drives the isotopic composition of the coccolith vesicle to light values. The effect of heavy carbon leaking from the chloroplast is obscured. Across all cells of all PIC:POC values, the trends in vital effects are moderated by the biological up-regulation of HCO₃⁻ transport proteins, which increases overall permeability to carbon and increases the and isotopic composition of carbon entering the cell with increasing τ, and which dampens the Rayleigh fractionation-type effects when τ is high.