In Arabidopsis, low external Pi availability is locally sensed by the growing root tip, which causes reduction of cell elongation and meristematic activity at the site of Pi depletion. ĭynamic redesign of the root system architecture (RSA) provides another strategy to maintain cellular Pi supply. Most of the Pi starvation response ( PSR) genes involved in these systemic adjustments are regulated by the myb transcription factor PHR1 (PHOSPHATE STARVATION RESPONSE1). Previous efforts elucidated some of these adaptive responses, including the identification of high-affinity Pi transport systems, the characterization of diverse metabolic bypass reactions, the reutilization of Pi from phospholipids, and many more. Thus, plants evolved strategies to enhance Pi acquisition and to conserve or remobilize Pi from internal sources to adapt to Pi limiting conditions. Despite its high abundance in the rhizosphere, bioavailability of Pi is typically limited because its majority is bound in organic compounds or complexed with metal ions such as Ca (alkaline soils), Fe or Al (acidic soils). Inorganic phosphate (Pi) is an essential macronutrient for plant growth and development. We further demonstrate that root growth modulation correlates with an altered expression of cell wall modifying enzymes and changes in the pectin network of the phosphate-deprived root tip, supporting the hypothesis that pectins are involved in iron binding and/or phosphate mobilization. The results emphasize the importance of apoplastic iron redistribution to mediate phosphate-dependent root growth adjustment and suggest an important role for citrate in phosphate-dependent apoplastic iron transport. Our study reveals new aspects of the elaborate interplay between phosphate starvation responses and changes in iron homeostasis. We further highlight expressional changes of several cell wall-modifying enzymes and provide evidence for adjustment of the pectin network at sites of iron accumulation in the root. Our experiments reveal that FERRIC REDUCTASE DEFECTIVE 3 mediated, apoplastic iron redistribution, but not intracellular iron uptake and iron storage, triggers phosphate-dependent root growth modulation. We observed an overrepresentation of genes and proteins that are involved in the regulation of iron homeostasis, cell wall remodeling and reactive oxygen species formation, and we highlight a number of candidate genes with a potential function in root adaptation to limited phosphate availability. We took advantage of the opposite phosphate-conditional root phenotype of the phosphate deficiency response 2 mutant (hypersensitive) and low phosphate response 1 and 2 double mutant (insensitive) to investigate the phosphate dependent regulation of gene and protein expression in roots using genome-wide transcriptome and proteome analysis. Iron deposition coincides with sites of reactive oxygen species generation and triggers cell wall thickening and callose accumulation, which interfere with cell-to-cell communication and inhibit root growth.
We recently demonstrated that the LOW PHOSPHATE RESPONSE 1 - PHOSPHATE DEFICIENCY RESPONSE 2 (LPR1-PDR2) module mediates apoplastic deposition of ferric iron (Fe 3+) in the growing root tip during phosphate limitation. The functionally interacting Arabidopsis genes, LOW PHOSPHATE RESPONSE 1 and 2 ( LPR1/LPR2) and PHOSPHATE DEFICIENCY RESPONSE 2 ( PDR2), are key components of root phosphate sensing. Changes in external phosphate availability are locally sensed at root tips and adjust root growth by modulating cell expansion and cell division. Vigorous restructuring of root system architecture provides a developmental strategy for topsoil exploration and phosphate scavenging.
Plant adaptation to limited phosphate availability comprises a wide range of responses to conserve and remobilize internal phosphate sources and to enhance phosphate acquisition.
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