The type I H+-PPase AVP1 functions at the crossroads between auxin transport, low phosphate sensing and root architecture plasticity

Date of Completion

January 2006


Agriculture, Plant Culture|Biology, Plant Physiology




In addition to maintaining vacuolar pH, the H+-pyrophosphatase, AVP1, controls auxin transport and consequently auxin-dependent development. Furthermore, AVP1 functions in plant root architecture development responding to limiting phosphate (P). AVP1 overexpression results in increased cell division at the onset of organ formation, hyperplasia, and increased auxin transport. In contrast, avp1-1 null mutants have severely disrupted root and shoot development and reduced auxin transport. Changes in the expression of AVP1 affect the distribution and abundance of the plasmalemmal (PM) H +-ATPase and Pinformed 1 auxin efflux facilitator, two proteins implicated in auxin distribution. Thus, AVP1 facilitates the auxin fluxes that regulate organogenesis. Auxin plays an important role in root development. Overexpression of AVP1 in (AVP1OX) Arabidopsis, tomato and rice plants results in a significant increase in root proliferation. Plant roots undergo dramatic morphological and architectural changes in response to low Pi to increase the absorptive surface area. These adaptations have been associated with auxin transport. Our data support a pivotal role for AVP1 in the regulation of auxin-dependent root architectural responses to low Pi in Arabidopsis, tomato and rice plants. AVP1 abundance is regulated at both transcriptional and translational levels in plants treated with low Pi. Increase in H+-ATPase abundance induced by low Pifollows AVP1 induction. Acidification of the rhizosphere by the H+-ATPase is required for Pi scavenging. AVP1OX plants exhibit enhanced rhizosphere acidification and Pi uptake, but are not more sensitive than controls when challenged with aluminum phosphate (AlPO4). Furthermore, when AVP1 abundance is reduced by RNA interference, root proliferation is not enhanced in response to limiting Pi. Our data suggest that AVP1 functions at the intersection of auxin signaling and Pi sensing to mediate the plasticity of root architecture. We propose that a positive feedback loop enhances auxin-dependent root development under low Pi conditions: (1) low Pi enhances AVP1 expression; (2) increased AVP1 abundance facilitates P-ATPase trafficking to the PM; (3) increased P-ATPase at the PM results in apoplastic acidification and consequent increases in Pi uptake and auxin influx/polar efflux. We conclude that AVP1 overexpression is an effective strategy to improve the performance of crops under limiting Pi conditions.^