scholarly journals A cell surface arabinogalactan‐peptide influences root hair cell fate

2020 ◽  
Vol 227 (3) ◽  
pp. 732-743 ◽  
Author(s):  
Cecilia Borassi ◽  
Javier Gloazzo Dorosz ◽  
Martiniano M. Ricardi ◽  
Mariana Carignani Sardoy ◽  
Laercio Pol Fachin ◽  
...  
2018 ◽  
Vol 35 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Naoto Hayashi ◽  
Takuya Tetsumura ◽  
Shinichiro Sawa ◽  
Takuji Wada ◽  
Rumi Tominaga-Wada

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Yinwei Cheng ◽  
Wenjiao Zhu ◽  
Yuxiao Chen ◽  
Shinsaku Ito ◽  
Tadao Asami ◽  
...  

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.


2017 ◽  
Vol 41 (2) ◽  
pp. 204-220.e5 ◽  
Author(s):  
Shawn W. Foley ◽  
Sager J. Gosai ◽  
Dongxue Wang ◽  
Nur Selamoglu ◽  
Amelia C. Sollitti ◽  
...  

2019 ◽  
Author(s):  
Cecilia Borassi ◽  
Javier Gloazzo Dorosz ◽  
Martiniano M. Ricardi ◽  
Laercio Pol Fachin ◽  
Mariana Carignani Sardoy ◽  
...  

SummaryRoot 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.


BIO-PROTOCOL ◽  
2015 ◽  
Vol 5 (7) ◽  
Author(s):  
Ling Bai ◽  
Yun Zhou ◽  
Pengtao Wang ◽  
Chun-Peng Song

Plants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 150 ◽  
Author(s):  
Katarzyna Retzer ◽  
Wolfram Weckwerth

Plant growth and productivity are orchestrated by a network of signaling cascades involved in balancing responses to perceived environmental changes with resource availability. Vascular plants are divided into the shoot, an aboveground organ where sugar is synthesized, and the underground located root. Continuous growth requires the generation of energy in the form of carbohydrates in the leaves upon photosynthesis and uptake of nutrients and water through root hairs. Root hair outgrowth depends on the overall condition of the plant and its energy level must be high enough to maintain root growth. TARGET OF RAPAMYCIN (TOR)-mediated signaling cascades serve as a hub to evaluate which resources are needed to respond to external stimuli and which are available to maintain proper plant adaptation. Root hair growth further requires appropriate distribution of the phytohormone auxin, which primes root hair cell fate and triggers root hair elongation. Auxin is transported in an active, directed manner by a plasma membrane located carrier. The auxin efflux carrier PIN-FORMED 2 is necessary to transport auxin to root hair cells, followed by subcellular rearrangements involved in root hair outgrowth. This review presents an overview of events upstream and downstream of PIN2 action, which are involved in root hair growth control.


Planta ◽  
2015 ◽  
Vol 242 (5) ◽  
pp. 1123-1138 ◽  
Author(s):  
Artur Muszyński ◽  
Malcolm A. O’Neill ◽  
Easwaran Ramasamy ◽  
Sivakumar Pattathil ◽  
Utku Avci ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document