In Arabidopsis, root hair and non-hair cell fates are determined by a MYB-bHLH-WD40 transcriptional complex and are regulated by many internal and environmental cues. Brassinosteroids play important roles in regulating root hair specification by unknown mechanisms. Here, we systematically examined root hair phenotypes in brassinosteroid-related mutants, and found that brassinosteroid signaling inhibits root hair formation through GSK3-like kinases or upstream components. We found that with enhanced brassinosteroid signaling, GL2, a cell fate marker for non-hair cells, is ectopically expressed in hair cells, while its expression in non-hair cells is suppressed when brassinosteroid signaling is reduced. Genetic analysis demonstrated that brassinosteroid-regulated root epidermal cell patterning is dependent on the WER-GL3/EGL3-TTG1 transcriptional complex. One of the GSK3-like kinases, BIN2, interacted with and phosphorylated EGL3, and EGL3s mutated at phosphorylation sites were retained in hair cell nuclei. BIN2 phosphorylated TTG1 to inhibit the activity of the WER-GL3/EGL3-TTG1 complex. Thus, our study provides insights into the mechanism of brassinosteroid regulation of root hair patterning.
Roots anchor a plant into the ground, and allow the plant to absorb water and mineral nutrients from the soil. As roots grow and branch, they increase the surface area of root exposed to the soil—and many plant cells in the root's outer layer have a hair-like projection to further increase this surface area. Thus, root hairs are where most water and mineral nutrients are absorbed. Many factors affect whether, or not, a plant cell will develop into a root hair. These factors include both external cues (such as the mineral content of the soil) and signals from the plant itself (such as hormones).
Brassinosteroids are plant hormones that regulate the development of shoots and roots, as well as the timing of when flowers begin to develop. These hormones are detected on the outside of plant cells, and activate a signaling pathway within the cell that causes changes in gene expression. Brassinosteroids also control if a root cell will become a hair cell or not, although the mechanism behind this activity is unclear.
Here, Cheng et al. have looked at the root hairs of mutant Arabidopsis thaliana plants that have had individual genes involved in brassinosteroid signaling knocked-out. Plant biologists commonly study this plant species because it is small and grows quickly—and Arabidopsis has regular stripes of root hair cells and ‘non-hair cells’ in the outer layer of its roots. Cheng et al. reveal that brassinosteroids prevent the formation of root hairs via signaling pathways that involve proteins called GSK3-like kinases. These hormones ‘switch off’ these kinases’ activity, so knocking-out the genes that code for these kinases has the same effect as adding extra brassinosteroids to the plant roots: fewer root hair cells.
Cheng et al. show that one of the GSK3-like kinases binds and adds phosphate groups to protein complexes that control gene expression—and this causes these protein complexes to be less active. When GSK3-like kinase activity is switched off by brassinosteroids, these complexes instead become more active and trigger the expression of genes that direct a plant cell to become a non-hair cell.
The findings of Cheng et al. reveal the pathways that allow brassinosteroids to stop plant cells in roots from becoming hair cells, and that instead encourage these cells to become non-hair cells. However, further work is needed to uncover how the striped pattern of hair cells and non-hair cells on Arabidopsis roots is established, and how brassinosteroids work with other plant hormones to control this pattern.