The transcription factor MYC1 interacts with FIT to negatively regulate iron homeostasis in Arabidopsis thaliana.

Abstract

Iron (Fe) is an indispensable trace mineral element for the normal growth of plants, and it is involved in different biological processes; Fe shortage in plants can induce chlorosis and yield loss. The objective of this research is to identify novel genes that participated in the regulation of Fe-deficiency stress in Arabidopsis thaliana. A basic helix-loop-helix (bHLH) transcription factor (MYC1) was identified to be interacting with the FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (FIT) using a yeast-two-hybrid assay. Transcript-level analysis showed that there was a decrease in MYC1 expression in Arabidopsis to cope with Fe-deficiency stress. Functional deficiency of MYC1 in Arabidopsis leads to an increase in Fe-deficiency tolerance and Fe-accumulation, whereas MYC1-overexpressing plants have an enhanced sensitivity to Fe-deficiency stress. Additionally, MYC1 inhibited the formation of FIT and bHLH38/39 heterodimers, which suppressed the expressed level for Fe acquisition genes FRO2 and IRT1 during Fe-deficiency stress. These results showed that MYC1 functions as a negative modulator of the Fe-deficiency stress response by inhibiting the formation of FIT and bHLH38/39 heterodimers, thereby suppressing the binding of FIT and bHLH38/39 heterodimers to the promoters of FRO2 and IRT1 to modulate Fe intake during Fe-deficiency stress. Overall, the findings of this study elucidated the role of MYC1 in coping with Fe-deficiency stress, and provided potential targets for the developing of crop varieties resistant to Fe-deficiency stress.