A NAC transcription factor NAC50 regulates Fe reutilization in Arabidopsis under Fe-deficient condition.

A lack of iron (Fe) inhibits the growth and development of plants, leading to reduced agricultural yields and quality. In the last ten years, numerous studies have focused on the induction of Fe uptake and translocation under Fe deficiency, but the regulatory mechanisms governing Fe reutilization within plants are still not well understood. Here, we demonstrated the involvement of the NAM/ATAF1/2/CUC2 (NAC) transcription factor NAC50 in response to Fe shortage. The content of soluble Fe was greatly reduced in nac50 mutants, leading to increased chlorosis in the newly emerging leaves under the Fe-deficient condition. Subsequent investigation revealed that the cell wall of the nac50 mutants' roots accumulated more Fe, along with an increment in hemicellulose content, indicating that a cell wall-associated Fe reutilization pathway was involved in the NAC50-regulated Fe insufficiency response. Interestingly, the expression of NINE-CIS-EPOXYCAROTENOID DIOXYGENASE 3 (NCED3), a key enzyme in the abscisic acid (ABA) biosynthetic pathway, was down-regulated in the Fe-deficient nac50 mutants, resulting in decreased endogenous ABA level and Fe-deficient sensitive phenotype. Since no direct relationship was observed between NAC50 and NCED3, this suggests a potential role of NAC50 in mediating the ABA accumulation. Moreover, exogenous ABA application in the nac50 mutant restored Fe deficiency resistance to the level observed in wild-type plants (WT), indicating that NAC50 induced the cell wall Fe reutilization potentially through the regulation of ABA accumulation.