Rodriguez Garcia, D. R. | Search bioRxiv

bioRxiv2021

Apoplastic class III peroxidases PRX62 and PRX69 regulate ROS-homeostasis and cell wall associated extensins linked to root hair growth at low-temperature in Arabidopsis thaliana

Root Hairs (RHs) growth is highly influenced by endogenous as well as by external environmental signals that coordinately regulate its final cell size. RHs actively expand the root surface responsible for nutrient uptake and water absorption. We have recently determined that RH growth was unexpectedly boosted when Arabidopsis thaliana seedlings are cultivated at low temperatures. It was proposed that RH growth plasticity in response to low temperature was linked to a reduced nutrient availability in the media. Here, we explored the molecular basis of this strong RH growth response by using the Genome Wide Association Studies (GWAS) approach on Arabidopsis thaliana natural accessions. We identified the poorly characterized PEROXIDASE 62 (PRX62) as a key protein triggering this conditional growth under a moderate low-temperature stress. In addition, we identified the related protein PRX69 as an important factor in this developmental process. The prx62 prx69 double mutant and the PRX62 and PRX69 over-expressing lines showed contrasting RH phenotypes, peroxidase activities and cyt/apoReactive Oxygen Species (ROS) levels. Strikingly, a cell wall protein extensin (EXT) reporter revealed the effect of peroxidase activity on the EXT cell wall association at 10{degrees}C in the RH apical zone. EXT cell wall insolubilization was enhanced at 10{degrees}C, which was completely abolished under the PRX inhibitor salicylhydroxamic acid (SHAM) treatment. Finally, we demonstrated that the Root Hair defective 6-like 4 (RSL4) bHLH family transcription factor directly controls the expression of PRX69. Collectively, our results indicate that both PRX62 and PRX69 are key apoplastic PRXs that modulate ROS-homeostasis and cell wall EXT-insolubilization linked to RH elongation at low-temperature.

plant biology↗

bioRxiv2019

A cell surface O-glycosylated peptide, AGP21, acts on the brassinosteroid pathway and modulates root hair cell fate

Root hairs (RHs) develop from specialized epidermal cells called trichoblasts, whereas epidermal cells that lack RHs are known as atrichoblasts. The mechanism controlling root epidermal cell fate is only partially understood. Root epidermis cell fate is regulated by a transcription factor complex that promotes the expression of the homeodomain protein GLABRA 2 (GL2), which blocks RH development by inhibiting ROOT HAIR DEFECTIVE 6 (RHD6). Suppression of GL2 expression activates RHD6, a series of downstream TFs including ROOT HAIR DEFECTIVE 6 LIKE-4 (RSL4 [Yi et al. 2010]) and their target genes, and causes epidermal cells to develop into RHs. Brassinosteroids (BRs) influence root epidermis cell fate. In the absence of BRs, phosphorylated BIN2 (a Type-II GSK3-like kinase) inhibits a protein complex that directly downregulates GL2 [Chen et al. 2014]. Here, we show that the genetic and pharmacological perturbation of the arabinogalactan peptide (AG) AGP21 in Arabidopsis thaliana, triggers aberrant RH development, similar to that observed in plants with defective BR signaling. We reveal that an O-glycosylated AGP21 peptide, which is positively regulated by BZR1, a transcription factor activated by BR signaling, affects RH cell fate by altering GL2 expression in a BIN2-dependent manner. These results suggest that perturbation of a cell surface AGP disrupts BR responses and inhibits the downstream effect of BIN2 on the RH repressor GL2 in root epidermal cells. In addition, AGP21 also acts in a BR-independent, AGP-dependent mode that together with BIN2 signalling cascade controls RH cell fate. SignificanceIn the plant Arabidopsis thaliana, the root epidermis forms in an alternating pattern atrichoblasts with trichoblast cells that end up developing root hairs (RHs). Atrichoblast cell fate is directly promoted by the transcription factor GLABRA2 (GL2) while the lack of GL2 allows RH formation. The loss of AGP21 peptide triggers an abnormal RH cell fate in two contiguous cells in a similar manner as brassinosteroid (BRs) mutants. In the absence of BR signaling, BIN2 (a GSK3 like-kinase) in a phosphorylated state, downregulate GL2 expression to trigger RH cell fate. The absence of AGP21 is able to repress GL2 expression and activates the expression of RSL4 and EXP7 root hair proteins.

plant biology↗