Camacho-Cristóbal Juan José, Rexach Jesús, Conéjéro Geneviève, Al-Ghazi Yves, Nacry Philippe, Doumas Patrick
Departamento de Fisiología, Anatomía y Biología Celular, Facultad de Ciencias Experimentales, Universidad Pablo de Olavide, 41013, Sevilla, Spain.
Planta. 2008 Aug;228(3):511-22. doi: 10.1007/s00425-008-0754-9. Epub 2008 May 28.
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.
根系结构的变化是植物用于补偿土壤中局部磷（Pi）缺乏的适应性策略之一。在拟南芥（Arabidopsis thaliana）中，由磷有效性引发的根系结构变量已有充分记录，但这些适应性反应背后的分子机制仍有待阐明。通过转录组学和定量逆转录-聚合酶链反应分析，我们观察到一个类AINTEGUMENTA基因，命名为PRD（Phosphate Root Development，磷根系发育），在低磷条件下在根中迅速受到抑制。通过无效等位基因突变体prd分析了PRD基因的生理功能，该突变体在磷饥饿条件下主根和侧根的发育比野生型植物少。用野生型基因对prd突变体进行互补，导致其对磷饥饿的反应与野生型植物相似，表明突变体表型得到了完全拯救。这些结果表明，PRD基因通过控制主根和侧根的伸长参与了对磷饥饿的根系结构反应的调控。该模型与PRD基因表达的组织特异性模式一致，观察到该模式在主根和侧根的根尖中特异性发生。然而，在野生型和prd植物中，响应磷饥饿时的磷流入、阴离子谱以及通常由磷饥饿诱导的基因的根表达，如高亲和力磷转运体（PHT1;1和PHT1;4）和酸性磷酸酶（AtACP5），是相似的。这些结果支持了这样的假设，即PRD基因不是磷饥饿反应的检查点，而是专门作为对磷饥饿的根系结构反应的调节因子起作用。
