摘要
Iron （Fe） homeostasis is integrated with the production of reactive oxygen species （ROS）, and distribution at the root tip participates in the control of root growth. Excess Fe increases ferritin abundance, enabling the storage of Fe, which contributes to protection of plants against Fe-induced oxidative stress. AtFerl and AtFer3 are the two ferritin genes expressed in the meristematic zone, pericycle and endodermis of theAra- bidopsis thaliana root, and it is in these regions that we observe Fe stained dots. This staining disappears in the triple ferl-3-4 ferritin mutant. Fe excess decreases primary root length in the same way in wild-type and in ferl-3-4 mutant. In contrast, the Fe-mediated decrease of lateral root （LR） length and density is enhanced in ferl-3-4 plants due to a defect in LR emergence. We observe that this interaction between excess Fe, ferritin, and root system architecture （RSA） is in part mediated by the H_2O_2/O2·^- balance between the root cell proliferation and differentiation zones regulated by the UPB1 transcription factor. Meristem size is also decreased in response to Fe excess in ferritin mutant plants, implicating cell cycle arrest mediated by the ROS-activated SMR5/SMR7 cyclin-dependent kinase inhibitors pathway in the interaction between Fe and RSA.
Iron （Fe） homeostasis is integrated with the production of reactive oxygen species （ROS）, and distribution at the root tip participates in the control of root growth. Excess Fe increases ferritin abundance, enabling the storage of Fe, which contributes to protection of plants against Fe-induced oxidative stress. AtFerl and AtFer3 are the two ferritin genes expressed in the meristematic zone, pericycle and endodermis of theAra- bidopsis thaliana root, and it is in these regions that we observe Fe stained dots. This staining disappears in the triple ferl-3-4 ferritin mutant. Fe excess decreases primary root length in the same way in wild-type and in ferl-3-4 mutant. In contrast, the Fe-mediated decrease of lateral root （LR） length and density is enhanced in ferl-3-4 plants due to a defect in LR emergence. We observe that this interaction between excess Fe, ferritin, and root system architecture （RSA） is in part mediated by the H_2O_2/O2·^- balance between the root cell proliferation and differentiation zones regulated by the UPB1 transcription factor. Meristem size is also decreased in response to Fe excess in ferritin mutant plants, implicating cell cycle arrest mediated by the ROS-activated SMR5/SMR7 cyclin-dependent kinase inhibitors pathway in the interaction between Fe and RSA.
