Loss-of-function mutations in the ERF96 gene enhance iron-deficient tolerance in Arabidopsis.

Iron is an essential micronutrient for plant growth and development. Here we provide evidence for a role of ERF96 in iron-deficiency response in Arabidopsis thaliana. The ERF96-loss-of-function mutants were found to be more tolerant to iron-deficiency stress than wild type (WT) and to have higher iron and chlorophyll content. Further studies showed that the transcriptional levels of iron-uptake related genes IRT1, FRO2, AHA2, FIT and bHLH38 in mutants were significantly higher than in WT under iron deficiency. Comparative transcriptome analysis suggested that the differentially expressed genes (DEGs) between ERF96-loss-of-function mutant and WT under iron deficiency were mainly enriched in iron uptake and chlorophyll degradation. According to the specific analysis of these two kinds of DEGs, the expression of iron uptake and transport related genes in ERF96-loss-of-function mutant was higher and the expression of chlorophyll degradation related genes was lower under iron deficiency. Furthermore, loss-of-function of ERF96 influenced the plant hormone, especially auxin and ethylene signal transduction. Altogether, our results demonstrate that loss-of-function of ERF96 increased Fe uptake and chlorophyll level through ethylene and auxin signal pathway in the regulation of iron-deficiency response in Arabidopsis.