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Phosphorus concentration coordinates a respiratory bypass, synthesis and exudation of citrate, and the expression of high‐affinity phosphorus transporters in Solanum lycopersicum
Author(s) -
DelSaz Néstor Fernández,
RomeroMunar Antonia,
Cawthray Gregory R.,
Palma Francisco,
Aroca Ricardo,
Baraza Elena,
FlorezSarasa Igor,
Lambers Hans,
RibasCarbó Miquel
Publication year - 2018
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1111/pce.13155
Subject(s) - alternative oxidase , phosphorus , solanum , biology , efflux , biochemistry , transporter , oxidase test , chemistry , botany , gene , enzyme , organic chemistry
Plants exhibit respiratory bypasses (e.g., the alternative oxidase [AOX]) and increase the synthesis of carboxylates in their organs (leaves and roots) in response to phosphorus (P) deficiency, which increases P uptake capacity. They also show differential expression of high‐affinity inorganic phosphorus (Pi) transporters, thus avoiding P toxicity at a high P availability. The association between AOX and carboxylate synthesis was tested in Solanum lycopersicum plants grown at different soil P availability, by using plants grown under P‐sufficient and P‐limiting conditions and by applying a short‐term (24 hr) P‐sufficient pulse to plants grown under P limitation. Tests were also performed with plants colonized with arbuscular mycorrhizal fungi, which increased plant P concentration under reduced P availability. The in vivo activities of AOX and cytochrome oxidase were measured together with the concentration of carboxylates and the P concentration in plant organs. Gene transcription of Pi transporters ( LePT1 and LePT2 ) was also studied. A coordinated response between plant P concentration with these traits was observed, indicating that a sufficient P availability in soil led to a suppression of both AOX activity and synthesis of citrate and a downregulation of the transcription of genes encoding high‐affinity Pi transporters, presumably to avoid P toxicity.

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