The endo-beta mannase MAN7 contributes to cadmium tolerance by modulating root cell wall binding capacity in Arabidopsis thaliana

The heavy metal cadmium(Cd) is detrimental to crop growth and threatens human health through the food chain. To cope with Cd toxicity,plants employ multiple strategies to decrease Cd uptake and its root-to-shoot translocation. However, genes that participate in the Cd-induced transcriptional regulatory network, including those encoding transcription factors, remain largely unidentified. In this study, we demonstrate that ENDO-BETA-MANNASE 7(MAN7) is necessary for the response of Arabidopsis thaliana to toxic Cd levels. We show that MAN7 is responsible for mannase activity and modulates mannose content in the cell wall, which plays a role in Cd compartmentalization in the cell wall under Cd toxicity conditions. Additionally,the repression of root growth by Cd was partially reversed via exogenous application of mannose,suggesting that MAN7-mediated cell wall Cd redistribution depends on the mannose pathway.Notably, we identified a basic leucine zipper(bZIP) transcription factor, bZIP44, that acts upstream of MAN7 in response to Cd toxicity.Transient dual-luciferase assays indicated that bZIP44 directly binds to the MAN7 promoter region and activates its transcription. Loss of bZIP44 function was associated with greater sensitivity to Cd treatment and higher accumulation of the heavy metal in roots and shoots.Moreover, MAN7 overexpression relieved the inhibition of root elongation seen in the bzip44mutant under Cd toxicity conditions. This study thus reveals a pathway showing that MAN7-associated Cd tolerance in Arabidopsis is controlled by bZIP44 upon Cd exposure.

AtHAP5A regulates iron translocation in iron-deficient Arabidopsis thaliana

Iron(Fe)deficient plants employ multiple strategies to increase root uptake and root-to-shoot translocation of Fe.The identification of genes that are responsible for these processes,and a comprehensive understanding of the regulatory effects of transcriptional networks on their expression,including transcription factors(TFs),is underway in Arabidopsis thaliana.Here,we show that a Histone-or heme-associated proteins(HAP)transcription factor(TF),HAP5A,is necessary for the response to Fe deficiency in Arabidopsis.Its ex-pression was induced under Fe deficiency,and the lack of HAP5A significantly decreased Fe translocation from the root to the shoot,resulting in substantial chlorosis of the newly expanded leaves,compared with the wild-type(WT,Col-0).Further analysis found that the expression of a gene encoding nicotianamine(NA)synthase(NAS1)was dramatically decreased in the hap5a mutant,regardless of the Fe status.Yeast-one-hybrid and ChIP analyses suggested that HAP5A directly binds to the promoter region of NAS1.Moreover,overexpression of NAS1 could rescue the chlorosis phenotype of hap5a in Fe deficient conditions.In summary,a novel pathway was elucidated,showing that NAS1-dependent translocation of Fe from the root to the shoot is controlled by HAP5A in Fe-deficient Arabidopsis thaliana.