AI Article Synopsis
- Iron (Fe) homeostasis plays a crucial role in root growth by influencing the production of reactive oxygen species (ROS) and their distribution at root tips.
- The presence of excess Fe triggers an increase in ferritin, which helps to store Fe and protects plants from oxidative stress, particularly in the root's meristematic zone where ferritin genes AtFer1 and AtFer3 are expressed.
- In mutants lacking ferritin, excess Fe negatively affects lateral root length and density more severely, suggesting that the balance of ROS and regulation by the UPB1 transcription factor is key to understanding how Fe impacts root system architecture.
Article Abstract
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. AtFer1 and AtFer3 are the two ferritin genes expressed in the meristematic zone, pericycle and endodermis of the Arabidopsis thaliana root, and it is in these regions that we observe Fe stained dots. This staining disappears in the triple fer1-3-4 ferritin mutant. Fe excess decreases primary root length in the same way in wild-type and in fer1-3-4 mutant. In contrast, the Fe-mediated decrease of lateral root (LR) length and density is enhanced in fer1-3-4 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 H2O2/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.
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| http://dx.doi.org/10.1016/j.molp.2014.11.014 | DOI Listing |
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