Résumé
Changes in root architecture are one of the adaptive strategies used by plants to compensate for local phosphate (Pi) deficiency in soils. Root architecture variables triggered by Pi availability are well documented in Arabidopsis (Arabidopsis thaliana), but the molecular mechanisms behind these adaptive responses remain to be elucidated. By the use of transcriptomic and quantitative RT-PCR analysis, we observed that an AINTEGUMENTA-like gene, named PRD for Phosphate Root Development, was rapidly repressed in roots under low Pi conditions. The physiological function of the PRD gene was analyzed through the null allele mutant prd, which displayed less development of primary and lateral roots under Pi-starvation conditions than wild-type plants. Complementation of the prd mutant with the wild-type gene led to a similar response to Pi starvation as wild-type plants, indicating the complete rescue of the mutant phenotype. These results suggest that PRD gene is involved in the regulation of root architectural responses to Pi starvation by controlling primary and lateral root elongation. This model is in agreement with the tissue-specific pattern of PRD gene expression, which was observed to occur specifically in the apex in both the primary and lateral roots. However, Pi influx, anionic profiles and root expression of genes typically induced by Pi starvation, such as high affinity Pi transporters (PHT1;1 and PHT1;4) and an acid phosphatase (AtACP5), were similar in wild type and prd plants in response to Pi starvation. These results support the hypothesis that the PRD gene is not a checkpoint for Pi-starvation responses, but acts specifically as a regulator of root architectural responses to Pi starvation.