Phosphate Availability Alters Lateral Root Development inArabidopsisby Modulating Auxin Sensitivity via a Mechanism Involving the TIR1 Auxin Receptor

Abstract

The survival of plants, as sessile organisms, depends on a series of postembryonic developmental events that determine the final architecture of plants and allow them to contend with a continuously changing environment. Modulation of cell differentiation and organ formation by environmental signals has not been studied in detail. Here, we report that alterations in the pattern of lateral root (LR) formation and emergence in response to phosphate (Pi) availability is mediated by changes in auxin sensitivity in Arabidopsis thaliana roots. These changes alter the expression of auxin-responsive genes and stimulate pericycle cells to proliferate. Modulation of auxin sensitivity by Pi was found to depend on the auxin receptor TRANSPORT INHIBITOR RESPONSE1 (TIR1) and the transcription factor AUXIN RESPONSE FACTOR19 (ARF19). We determined that Pi deprivation increases the expression of TIR1 in Arabidopsis seedlings and causes AUXIN/INDOLE-3-ACETIC ACID (AUX/IAA) auxin response repressors to be degraded. Based on our results, we propose a model in which auxin sensitivity is enhanced in Pi-deprived plants by an increased expression of TIR1, which accelerates the degradation of AUX/IAA proteins, thereby unshackling ARF transcription factors that activate/repress genes involved in LR formation and emergence.

Plasticity of the Arabidopsis Root System under Nutrient Deficiencies

“…This method allows a more accurate description of the effects that treatments have on the emergence of LRs. It has been reported previously that the induction of root branching under low P supply occurs before any change in PR elongation is detected (Pérez-Torres et al, 2008). Thus, these results strongly indicate that the processes underlying the induction of root branching can also be uncoupled from the elongation of the parental root.…”

“…1A). Such an effect of low P on RSA has already been reported (Williamson et al, 2001;López-Bucio et al, 2002Pérez-Torres et al, 2008). However, our detailed RSA analysis also revealed that low P supply not only inhibited PR length but also decreased the length of the LR formation zone in the PR (LR FZ PR ) relative to the length of the whole PR (Fig.…”

“…1D), P deficiency induces the production of LRs (Williamson et al, 2001;López-Bucio et al, 2002Sanchez-Calderon et al, 2005). This induction has been shown to be associated with a P deficiency-induced expression of the auxin receptor TRANSPORT INHIBITOR RESPONSE1 (TIR1) in pericycle cells that results in increased sensitivity of roots to auxin (Pérez-Torres et al, 2008). As a consequence, the initiation and emergence of LRs is significantly enhanced in P-deficient roots.…”

Strigolactones fine-tune the root system

“…This is evidenced in auxin receptor mutants (tir1afb2afb3) that show a drastic reduction in lateral root formation (Dharmasiri et al 2005;Pérez-Torres et al 2008) and in several mutants perturbed in AUX/IAAand ARF-mediated signaling that display severe defects in lateral root organogenesis, or block it completely [in the case of stabilized SOLITARY ROOT(SLR)/IAA14 or loss of ARF7 and ARF19 (Vanneste et al 2005)]. Local accumulation of auxin in root pericycle cells is ensured by PINdependent auxin recirculation inside the root tip (Casimiro et al 2001), a process that is very well described elsewhere and falls beyond the scope of this review.…”

Strigolactones as mediators of plant growth responses to environmental conditions

“…For example, under low Pi conditions, the changes in root-system architecture and roothair formation in Arabidopsis were suggested to be a result of increased auxin sensitivity. 65 Nitrate application was also shown to increase cytokinin biosynthesis and expression of its signaling components, leading to morphological effects on both roots and shoots (reviewed in ref. 24), whereas the reduction in shoot apical dominance in pea was suggested to be a result of reduced auxin transport out of the apex under conditions of B deficiency.…”