With V, A. vinelandii levels increase up to a plateau in intermediate concentrations, but at higher concentrations the levels increase beyond the plateau. Similar with Fe, except Fe-only mutants might have a higher plateau than others. Which makes sense.
Metal Levels and Growth/Nitrogen Fixation
In wild-type A. vinelandii, when growing with V and limited amounts of Mo, the cells start by taking up Mo and growing constantly; when outside Mo runs out, they start taking up V. When that is depleted, the growth rate slows down.
Correspondingly, V-nitrogenase gene expression starts up when Mo runs out, though not all Mo-nitrogenase genes necessarily stop expression at that point.
And finally, overall nitrogenase protein levels stay fairly constant until both Mo and V run out, and then they rise a lot.
At lower metal concentrations, metallophores seem important in part because they allow the cells to capture metals and make them more available, but also because they make metal uptake easier to regulate so they don't become toxic. This isn't as easy at high levels, as shown by lower growth rates.
The molybdenum and vanadium toxicity could be due to inhibition of iron uptake, causing limitation; the observation that more iron helps alleviate toxicity supports this hypothesis. On the other hand, they didn't really see a drop in iron levels in lower-iron conditions.
They saw Mo storage, but strangely not Fe storage, despite A. vinelandii seeming to have iron-storing mechanisms. It could just be the growth conditions (exponential, nitrogen-fixing).
Overall, it's a lot of data about a pretty complex system. I liked this quote from the conclusions:
"Azotobacter vinelandii thus seems to be well adapted for diazotrophic growth in a soil environment where low availability, large spatiotemporal heterogeneity and strong competition may contribute to metal limitation."