Iron(Fe)deficiency is common in agricultural crops and affects millions of people worldwide.Translocation of Fe in the xylem is a key step for Fe distribution in plants.The mechanism controlling this process remains l...Iron(Fe)deficiency is common in agricultural crops and affects millions of people worldwide.Translocation of Fe in the xylem is a key step for Fe distribution in plants.The mechanism controlling this process remains largely unknown.Here,we report that two Arabidopsis ferroxidases,LPR1 and LPR2,play a crucial and redundant role in controlling Fe translocation in the xylem.LPR1 and LPR2 are mainly localized in the cell walls of xylem vessels and the surrounding cells in roots,leaves,and stems.Knockout of both LPR1 and LPR2 increased the proportion of Fe(II)in the xylem sap,and caused Fe deposition along the vascular bundles especially in the petioles and main veins of leaves,which was alleviated by blocking blue light.The lpr1 lpr2 double mutant displayed constitutive expression of Fe deficiency response genes and overaccumulation of Fe in the roots and mature leaves under Fe-sufficient supply,but Fe deficiency chlorosis in the new leaves and inflorescences under low Fe supply.Moreover,the lpr1 lpr2 double mutant showed lower Fe concentrations in the xylem and phloem saps,and impaired 57Fe translocation along the xylem.In vitro assays showed that Fe(III)-citrate,the main form of Fe in xylem sap,is easily photoreduced to Fe(II)-citrate,which is unstable and prone to adsorption by cell walls.Taken together,these results indicate that LPR1 and LPR2 are required to oxidize Fe(II)and maintain Fe(III)-citrate stability and mobility during xylem translocation against photoreduction.Our study not only uncovers an essential physiological role of LPR1 and LPR2 but also reveals a new mechanism by which plants maintain Fe mobility during long-distance translocation in the xylem.展开更多
Although roots are mainly embedded in the soil, recent studies revealed that light regulates mineral nutrient uptake by roots. However, it remains unclear whether the change in root system architecture in response to ...Although roots are mainly embedded in the soil, recent studies revealed that light regulates mineral nutrient uptake by roots. However, it remains unclear whether the change in root system architecture in response to different rhizosphere nutrient statuses involves light signaling. Here, we report that blue light regulates primary root growth inhibition under phosphate-deficient conditions through the cryptochromes and their downstream signaling factors. We showed that the inhibition of root elongation by low phosphate requires blue light signal perception at the shoot and transduction to the root. In this process, SPA1 and COP1 play a negative role while HY5 plays a positive role. Further experiments revealed that HY5 is able to migrate from the shoot to root and that the shoot-derived HY5 autoactivates root HY5 and regulates primary root growth by directly activating the expression of LPR1, a suppressor of root growth under phosphate starvation. Taken together, our study reveals a regulatory mechanism by which blue light signaling regulates phosphate deficiency-induced primary root growth inhibition, providing new insights into the crosstalk between light and nutrient signaling.展开更多
基金This work was supported by the Natural Science Foundation of Jiangsu Province(grant no.BK20190544)the Natural Science Foundation of China(grant no.41977375)+1 种基金the Fundamental Research Funds for the Central Universities(grant no.KYT201802KYCXJC2022002).
文摘Iron(Fe)deficiency is common in agricultural crops and affects millions of people worldwide.Translocation of Fe in the xylem is a key step for Fe distribution in plants.The mechanism controlling this process remains largely unknown.Here,we report that two Arabidopsis ferroxidases,LPR1 and LPR2,play a crucial and redundant role in controlling Fe translocation in the xylem.LPR1 and LPR2 are mainly localized in the cell walls of xylem vessels and the surrounding cells in roots,leaves,and stems.Knockout of both LPR1 and LPR2 increased the proportion of Fe(II)in the xylem sap,and caused Fe deposition along the vascular bundles especially in the petioles and main veins of leaves,which was alleviated by blocking blue light.The lpr1 lpr2 double mutant displayed constitutive expression of Fe deficiency response genes and overaccumulation of Fe in the roots and mature leaves under Fe-sufficient supply,but Fe deficiency chlorosis in the new leaves and inflorescences under low Fe supply.Moreover,the lpr1 lpr2 double mutant showed lower Fe concentrations in the xylem and phloem saps,and impaired 57Fe translocation along the xylem.In vitro assays showed that Fe(III)-citrate,the main form of Fe in xylem sap,is easily photoreduced to Fe(II)-citrate,which is unstable and prone to adsorption by cell walls.Taken together,these results indicate that LPR1 and LPR2 are required to oxidize Fe(II)and maintain Fe(III)-citrate stability and mobility during xylem translocation against photoreduction.Our study not only uncovers an essential physiological role of LPR1 and LPR2 but also reveals a new mechanism by which plants maintain Fe mobility during long-distance translocation in the xylem.
基金This study was funded by Chinese Academy of Sciences(XDB27010103 to D.-Y.C.)the Natural Science Foundation of China(31930024 to D.-Y.C.)the China Postdoctoral Science Foundation(BX20180334 and 2018M642101 to Y.-Q.G.).
文摘Although roots are mainly embedded in the soil, recent studies revealed that light regulates mineral nutrient uptake by roots. However, it remains unclear whether the change in root system architecture in response to different rhizosphere nutrient statuses involves light signaling. Here, we report that blue light regulates primary root growth inhibition under phosphate-deficient conditions through the cryptochromes and their downstream signaling factors. We showed that the inhibition of root elongation by low phosphate requires blue light signal perception at the shoot and transduction to the root. In this process, SPA1 and COP1 play a negative role while HY5 plays a positive role. Further experiments revealed that HY5 is able to migrate from the shoot to root and that the shoot-derived HY5 autoactivates root HY5 and regulates primary root growth by directly activating the expression of LPR1, a suppressor of root growth under phosphate starvation. Taken together, our study reveals a regulatory mechanism by which blue light signaling regulates phosphate deficiency-induced primary root growth inhibition, providing new insights into the crosstalk between light and nutrient signaling.
