Figure 3.

Biochemical machinery during compensated/ early onset iron deficiency. As the cytosolic levels of ferrous iron decline, the differential activity profile of 2OG-dependent enzymes influences the cellular response. These are depicted in reference to the non-linear regression model of predicted iron affinity data (NLR_Km_Fe). Key players include prolyl 4-hydroxylase, despite being almost entirely organellar; secondary metabolites (GAs, bioflavonoids, alkaloids) and monotonic incremental- and decremental-responders; and dual-origin ethylene formation (enzymatic and FETs). Much of this cellular biochemistry is directed toward diminishing the resistance of the cell wall in preparation for growth, development, and the release of rhizosphere influencing metabolites.