Phosphorus (Pi) is an essential macronutrient for numerous metabolic and developmental processes in plants. In most natural soils, Pi is often limited due to its strong affinity for cations such as Ca, Mg and Fe, and because its rapid conversion to organic forms that are not readily available for plant uptake.1
Pi deprivation results in adaptive morphological modifications such as altered root architecture that helps the plant to explore greater soil volumes for Pi acquisition.2
Important factors in root system remodeling under low Pi conditions include increased lateral root formation and root hair proliferation, which are related to the entrance of the primary root into a determinate program of growth, in which cell division is arrested and cell differentiation promoted at the root tip.3
This particular developmental program enhances the expression of genes involved in the low-Pi rescue response in the differentiating root regions as revealed by the transcriptional activation of Pi-responsive genes such as those encoding high affinity Pi transporters and phosphatases, which directly participates in Pi uptake from the soil.3
Auxin plays an important role in modulating root system architecture. Many previous studies have shown that application of exogenous auxin (IAA) increases the number of LRs.4,5
In contrast, treatment with auxin transport inhibitors such as NPA (N
-1-naphthylphthalamic acid) decreases the number of LRs.6,7
Recent molecular genetic studies using Arabidopsis mutants have provided considerable information on the role of auxin biosynthesis, homeostasis, transport and signaling regulating root morphogenetic processes.8–10
It has been found that LR initiation and subsequent LR primordium development require both auxin transport and signaling. At low concentrations of auxin, AUX/IAA repressors inhibit the activity of AUXIN RESPONSE FACTORS (ARFs) transcription factors. When auxin concentrations exceed a certain threshold, the interaction between AUX/IAA proteins and the SCFTIR1/AFB1–3
ubiquitine ligase is promoted, thus triggering the destruction of AUX/IAA proteins by the proteosome. ARFs are then free to regulate the expression of auxin-responsive genes, such as those involved in LR formation.11
In a recent work, we investigated the role of various components of the auxin signaling pathway in root system architecture adjustment during Pi-deprivation in Arabidopsis. It was found that roots of Pi-deprived seedlings were resistant to the inhibitory effects of the auxin transport inhibitor NPA on LR formation. In addition, seedlings grown under low Pi conditions that were transferred to medium containing NPA and auxin produced more LR primordia and LRs than seedlings grown under sufficient Pi conditions transferred to media with the same concentration of NPA and auxin. These results showed that low Pi signaling makes the pericycle cells more sensitive to auxin, thus resulting in an increased LR proliferation and the formation of more branched root systems.
Since the TIR1 auxin receptor is a central player in auxin perception, it was investigated whether TIR1 was responsible for the increased auxin sensitivity of Pi-deprived seedlings. Kinetic studies of TIR1:uidA expression and qRT-PCR analysis showed that TIR1 is specifically induced in response to Pi-deprivation. By examining the root growth responses of mutants defective on the TIR1/AFB1–3 family of auxin receptors under contrasting Pi availability, it was found that these genes play partially redundant roles in LR formation in response to Pi-deprivation. Interestingly, transgenic plants that overexpress TIR1 grown under Pi-sufficient conditions have a phenotype similar to that observed in Pi-deprived WT seedlings, confirming that TIR1 is indeed a limiting factor in determining auxin sensitivity and LR formation, and that small changes in its transcription level can have profound effects on root system architecture. Based on this information, it was proposed that auxin sensitivity in pericycle cells is enhanced in Pi-deprived seedlings due to the increased expression of TIR1. This in turn causes the degradation of AUX/IAA proteins, which liberates ARF transcription factors to activate the expression of genes involved in LR formation.