Pseudomonas putida configures Arabidopsis root architecture through modulating the sensing systems for phosphate and iron acquisition.

Iron (Fe) and phosphate (Pi) are two essential nutrients that are poorly available in the soil and should be supplemented either as fertilizers or organic amendments to sustain crop production. Currently, determining how rhizosphere bacteria contribute to plant mineral nutrient acquisition is an area of growing interest regarding its potential application in agriculture. The aim of this study was to investigate the influence of root colonization by Pseudomonas putida for Arabidopsis growth through Fe and Pi nutritional signaling. We found that root colonization by the bacterium inhibits primary root elongation and promotes the formation of lateral roots. These effects could be related to higher expression of two Pi starvation-induced genes and AtPT1, the major Pi transporter in root tips. In addition, P. putida influenced the accumulation of Fe in the root and the expression of different elements of the Fe uptake pathway. The loss of function of the protein ligase BRUTUS (BTS), and the bHLH transcription factors POPEYE (PYE) and IAA-LEUCINE RESISTANT3 (ILR3) compromised the root branching stimulation triggered by bacterial inoculation while the leaf chlorosis in the fit1 and irt1-1 mutant plants grown under standard conditions could be bypassed by P. putida inoculation. The WT and both mutant lines showed similar Fe accumulation in roots. P. putida repressed the expression of the IRON-REGULATED TRANSPORTER 1 (IRT1) gene suggesting that the bacterium promotes an alternative Fe uptake mechanism. These results open the door for the use of P. putida to enhance nutrient uptake and optimize fertilizer usage by plants.

The growth of Arabidopsis primary root is repressed by several and diverse amino acids through auxin-dependent and independent mechanisms and MPK6 kinase activity.

Amino acids serve as structural monomers for protein synthesis and are considered important biostimulants for plants. In this report, the effects of all 20-L amino acids in Arabidopsis primary root growth were evaluated. 15 amino acids inhibited growth, being l-leucine (l-Leu), l-lysine (l-Lys), l-tryptophan (l-Trp), and l-glutamate (l-Glu) the most active, which repressed both cell division and elongation in primary roots. Comparisons of DR5:GFP expression and growth of WT Arabidopsis seedlings and several auxin response mutants including slr, axr1 and axr2 single mutants, arf7/arf19 double mutant and tir1/afb2/afb3 triple mutant, treated with inhibitory concentrations of l-Glu, l-Leu, l-Lys and l-Trp revealed gene-dependent, specific changes in auxin response. In addition, l- isomers of Glu, Leu and Lys, but not l-Trp diminished the GFP fluorescence of pPIN1::PIN1:GFP, pPIN2::PIN2:GFP, pPIN3::PIN3:GFP and pPIN7::PIN7:GFP constructs in root tips. MPK6 activity in roots was enhanced by amino acid treatment, being greater in response to l-Trp while mpk6 mutants supported cell division and elongation at high doses of l-Glu, l-Leu, l-Lys and l-Trp. We conclude that independently of their auxin modulating properties, amino acids signals converge in MPK6 to alter the Arabidopsis primary root growth.

Folic acid orchestrates root development linking cell elongation with auxin response and acts independently of the TARGET OF RAPAMYCIN signaling in Arabidopsis thaliana.

Folic acid is a precursor of tetrahydrofolate (vitamin B9), which is an essential cofactor in most organisms, acting as a carrier for one-carbon units in enzymatic reactions. In this work, we employed pharmacological, genetic and confocal imaging strategies to unravel the signaling mechanism by which folic acid modulates root growth and development. Folic acid supplementation inhibits primary root elongation and induces lateral root formation in a concentration-dependent manner. An analysis of the expression of cell cycle genes pCycD6;1:GFP and CycB1:uidA, and cell expansion Exp7:uidA showed that folic acid promotes cell division but prevented cell elongation, and this correlated with altered expression of auxin-responsive DR5:GFP gene, and PIN1:PIN1:GFP, PIN3:PIN3:GFP, and PIN7:PIN7:GFP auxin transporters at the columella and vasculature of primary roots, whereas mutants defective in auxin signaling (tir1/afb1/afb2 [receptors], slr1 [repressor] and arf7/arf19 [transcription factors]) were less sensitive to folic acid induced primary root shortening and lateral root proliferation. Comparison of growth of WT and TARGET OF RAPAMYCIN (TOR) antisense lines indicates that folic acid acts by an alternative mechanism to this central regulator. Thus, folic acid modulation of root architecture involves auxin and acts independently of the TOR kinase to influence basic cellular programs.