Abstract
Root hair morphogenesis is driven by an amalgam of interacting processes controlled by complex signaling events. Redox processes and transcriptional control are critical for root hair development. However, the molecular mechanisms that integrate redox state and transcription are largely unknown. To elucidate a possible role of transcriptional Mediators in root hair formation, we analyzed the Arabidopsis root hair phenotype of T-DNA insertion lines that harbor homozygous mutations in genes encoding Mediator subunits. Genetic evidence indicates that the Mediator subunits PFT1/MED25 and MED8 are critical for root hair differentiation, but act via separate mechanisms. Transcriptional profiling of pft1 roots revealed that PFT1 activates a subset of hydrogen peroxide (H(2)O(2))-producing class III peroxidases. pft1 mutants showed perturbed H(2)O(2) and superoxide (O(2)(·-)) distribution, suggesting that PFT1 is essential to maintain redox homeostasis in the root. Chemical treatments rescued the pft1 mutant phenotype, indicating that correct reactive oxygen species (ROS) distribution is an essential prerequisite for root hair differentiation. In addition, PFT1 positively regulates cell wall remodeling genes that are essential for root hair formation. Our results demonstrate that PFT1 maintains ROS distribution which, in turn, controls root hair differentiation. Thus, our findings reveal a novel mechanism in which the Mediator controls ROS homeostasis by regulating the transcriptional machinery.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.