Abstract

Here we report the function of a general regulatory factor, GENERAL REGULATORY FACTOR11 (GRF11), in terms of the iron (Fe) deficiency response. Physiological and molecular responses of the loss-of-function Arabidopsis thaliana grf11 mutant to Fe supply were investigated. Genes involved in posttranscriptional regulation of FER-LIKE FE DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (FIT) were also analyzed. In addition, the molecular link between the signaling molecule nitric oxide (NO) and Fe deficiency responses was further dissected. Our results suggest that GRF11 is necessary for induction of Fe-deficiency-tolerance mechanisms. The FIT protein can bind to the promoter of GRF11, which contains an E-box motif. GRF11 also positively affects FIT transcription but has no influence on the genes involved in posttranscriptional regulation of FIT. Furthermore, NO positively regulates GRF11 induction upon the onset of Fe deficiency. We propose that, upon the onset of Fe deficiency, induction of FIT expression is dependent on GRF11, which acts downstream of NO to mediate Fe deficiency responses.

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