Comparative expression profiling reveals a role of the root apoplast in local phosphate response. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Hoehenwarter, Wolfgang; Mönchgesang, Susann; Neumann, Steffen; Majovsky, Petra; Abel, Steffen; Müller, Jens
• Is Part Of: BMC plant biology. Volume 16:Issue 1(2016)
• Page Start: 1
• Page End: 21
• Publication Date: 2016-12
• Subjects: Arabidopsis thaliana -- Phosphate deficiency -- Root growth -- Proteomics -- Transcriptomics -- Iron transport -- Cell wall -- Pectin; Plant molecular biology -- Periodicals; Botany -- Periodicals; 580.5
• DOI: 10.1186/s12870-016-0790-8
• Languages: English
• ISSNs: 1471-2229

Abstract

Abstract Background Plant adaptation to limited phosphate availability comprises a wide range of responses to conserve and remobilize internal phosphate sources and to enhance phosphate acquisition. Vigorous restructuring of root system architecture provides a developmental strategy for topsoil exploration and phosphate scavenging. Changes in external phosphate availability are locally sensed at root tips and adjust root growth by modulating cell expansion and cell division. The functionally interactingArabidopsis genes, LOW PHOSPHATE RESPONSE 1 and2 (LPR1/LPR2 ) andPHOSPHATE DEFICIENCY RESPONSE 2 (PDR2 ), are key components of root phosphate sensing. We recently demonstrated that theLOW PHOSPHATE RESPONSE 1 - PHOSPHATE DEFICIENCY RESPONSE 2 (LPR1-PDR2) module mediates apoplastic deposition of ferric iron (Fe3+ ) in the growing root tip during phosphate limitation. 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. Results We took advantage of the opposite phosphate-conditional root phenotype of thephosphate deficiency response 2 mutant (hypersensitive) andlow phosphate response 1 and2 double mutant (insensitive) to investigate the phosphate dependent regulation of gene and protein expression in roots using genome-wide transcriptome and proteome analysis. 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. Our experiments reveal thatFERRIC REDUCTASE DEFECTIVE 3 mediated, apoplastic iron redistribution, but not intracellular iron uptake and iron storage, triggers phosphate-dependent root growth modulation. 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. Conclusion Our study reveals new aspects of the elaborate interplay between phosphate starvation responses and changes in iron homeostasis. 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. 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.