Experimental study reveals that MNB1 gene repression improves iron accumulation in Arabidopsis thaliana, indicating a key regulatory link between reactive oxygen species and iron uptake.
Background Iron (Fe) is an essential mineral element that involves in many biological processes important for most plants growth and development. Fe-deficiency induces a complex series of responses in plants, involving physiological and developmental changes, to increase Fe uptake from soil. However, the molecular mechanism involved in plant Fe-deficiency is not well understood. Results Here, we found that the MNB1 (mannose-binding-lectin 1) gene is involved in the regulation of Fe-deficiency stress response in Arabidopsis thaliana. The expression abundance of MNB1 was inhibited by Fe-deficiency stress. Knockout of MNB1 led to enhanced Fe accumulation and tolerance, whereas the MNB1-overexpressing plants were sensitive to Fe-deficiency stress. Under conditions of normal and Fe-deficiency, lower H2O2 concentrations were detected in mnb1 mutant plants compared to wild type. On the contrary, higher H2O2 concentrations were found in MNB1-overexpressing plants, which was negatively correlated with malondialdehyde (MDA) levels. Furthermore, in mnb1 mutants, the transcription level of the Fe uptake- and translocation-related genes, FIT, IRT1, FRO2, ZIF, FRD3, NAS4, PYE and MYB72, were considerably elevated during Fe-deficiency stress, resulting in enhanced Fe uptake and translocation, thereby increasing Fe accumulation. Conclusions Together, our findings show that the MNB1 gene negatively controls the Fe-deficiency response in Arabidopsis via modulating reactive oxygen species (ROS) levels and the ROS-mediated signaling pathway, thereby affecting the expression of Fe uptake- and translocation-related genes.
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