Fig. 4.

A working model to explain the control of the AtFer1 gene expression in response to iron. (A) Under low-iron conditions, a repressor not directly bound to the AtFer1 promoter would interact with the transcription factor which recognizes the iron-dependent regulatory sequence (IDRS), leading to the repression of AtFer1 gene expression. (B) Under high-iron conditions, an enzymatically produced nitric oxide (NO) burst occurs within the plastids, preceding ubiquitination and proteasome-dependent degradation of the repressor. De-phosphorylation events depending upon a PP2A phosphatase activity would also occur. These events lead to a de-repression of the AtFer1 gene expression (Arnaud et al., 2006). The corresponding ferritin transcript is then translated to give the ferritin precursor polypeptide which is transported to plastids where it is assembled in the 24-mers ferritin protein.