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.