Ferredoxin and flavodoxin as biochemical indicators of iron limitation during open-ocean iron enrichment
Limnol. Oceanogr., 44(7), 1999, 1609-1615 | DOI: 10.4319/lo.19188.8.131.529
ABSTRACT: Substitution of the noniron protein flavodoxin for the iron-sulfur protein ferredoxin is an iron-stress response employed by a variety of unicellular organisms, including many phytoplankton. The relative abundance of these two proteins has been shown to vary with the severity of growth limitation by iron in marine diatoms. During the IronEx II mesoscale iron-enrichment experiment, large volume (100-600 liters) phytoplankton samples were collected for analysis of community ferredoxin and flavodoxin abundance using a high-pressure liquid chromatography (HPLC) technique. In addition, three pennate diatom species isolated from the fertilization-induced phytoplankton bloom were used for follow-up laboratory experiments, which examined their iron physiology. Prior to iron enrichment, biomass levels were insufficient to obtain any ferredoxin or flavodoxin signals. Measurements were successful after iron enrichment, with unexpected results. The strength of the HPLC signal tracked the biomass levels of the IronEx II phytoplankton bloom. Chromatographic peaks were evident on the fifth day following enrichment and persisted throughout the experiment before they declined and eventually disappeared following the last iron infusion. The main chromatographic peak was identified as flavodoxin; there was no evidence of ferredoxin in any of the samples. Pennate diatom clones isolated from the fertilization-induced bloom and grown in the laboratory retain the ability to make ferredoxin when iron-replete and induce flavodoxin when iron-stressed. When iron-limited, they are able to completely repress flavodoxin expression in about 1 d in response to iron resupply. Thus, the unexpected absence of ferredoxin and the persistence of flavodoxin during IronEx II, despite the observed increases in biomass and photosynthetic efficiency, suggest that the iron additions were insufficient to completely relieve physiological iron limitation.