Consequences of the genotypic loss of mitochondrial Complex I in dinoflagellates and of phenotypic regulation of Complex I content in other photosynthetic organisms

The absence of mitochondrial Complex I in the dinoflagellates decreases ATP production per hexose catabolised by about 30%, with little evidence of compensation from other ATP-producing pathways. This decrease in ATP synthesis could account for the lower maximum specific growth rate of dinoflagellates when compared with some other higher taxa of algae, as well as the generally higher rate of respiration per unit of photosynthesis or growth. These effects might be smaller when nutrients are limiting. The iron requirement per cell for the synthesis of respiratory ATP at the observed rate in the absence of Complex I is predicted to be at least 85% of the iron content of cells containing Complex I. The limited data available show that the iron content per cell volume of iron-replete dinoflagellate cells is similar to that of other microalgae. Data also reveal that the minimum iron quota of a dinoflagellate is greater than that of three other microalgae. There is no effect of the absence of the Complex I-associated gamma-carbonic anhydrase protein, which has no detectable carbonic anhydrase activity but instead plays a role in the assembly of Complex I.