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ARS Home » Northeast Area » Ithaca, New York » Robert W. Holley Center for Agriculture & Health » Plant, Soil and Nutrition Research » Research » Publications at this Location » Publication #334364
Title: An Arabidopsis ABC transporter mediates phosphate deficiency-induced remodeling of root architecture by modulating iron homeostasis in roots

Author
item DONG, JINSONG - Tsinghua University
item Pineros, Miguel
item LI, XIAOXUAN - Tsinghua University
item YANG, HAIBING - Purdue University
item LIU, YU - Zhejiang University
item MURPHY, ANGUS - University Of Maryland
item Kochian, Leon
item LIU, DONG - Tsinghua University

Submitted to: Molecular Plant
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/21/2016
Publication Date: 2/13/2017
Citation: Dong, J., Pineros, M., Li, X., Yang, H., Liu, Y., Murphy, A., Kochian, L.V., Liu, D. 2017. An Arabidopsis ABC transporter mediates phosphate deficiency-induced remodeling of root architecture by modulating iron homeostasis in roots. Molecular Plant. 10(2):244-259. https://doi.org/10.1016/j.molp.2016.11.001.
DOI: https://doi.org/10.1016/j.molp.2016.11.001

Interpretive Summary: Abiotic stress and mineral nutrition are major limiting factors for the world wide agronomical productivity. The understanding of the physiological mechanisms and underlying genes determining advantageous and efficient root architectures is essential for guide and accelerate breeding programs aimed at increasing plant yield and optimize agriculture in marginal soils. A novel molecular control mechanism modulating to root’s iron status has been identified as a key component of the signaling pathway involve in remodeling root architecture in response to phosphate deficiency, thereby enhancing the plant’s ability to forage for nutrients in topsoil.

Technical Abstract: Remodeling of root architecture is a major developmental response of plants to phosphate (Pi) deficiency, thought to enhance the plant’s ability to forage for nutrients in topsoil. The underlying mechanism controlling this response, however, is poorly understood. In this work, we identified an Arabidopsis mutant, hps10 (hypersensitive to Pi starvation 10), that is morphologically normal under Pi sufficiency, but under Pi deficiency shows increased inhibition of primary root growth and enhanced production of lateral roots. hps10 was found to be the previously identified allele (als3-3) of the ALUMINUM SENSITIVE3 (ALS3) gene. Our results show that ALS3 and its interacting protein AtSTAR1 form an ABC transporter protein complex located in tonoplasts. The protein complex mediates a highly electrogenic transport in Xenopus oocytes. Exogenously applied UDP-glucose or UDP-glucuronic acid rescues the als3 mutant phenotypes. Under Pi deficiency, als3 accumulates higher levels of Fe3+ in its root than wild type plants. When Fe is omitted in Pi-deficient medium, the root growth of als3-3 is similar to that of the WT. In Arabidopsis, LPR1 (LOW PHOSPHATE ROOT1) and LPR2 encode ferroxidase, which when mutated reduces Fe3+ accumulation in roots and causes root growth to be insensitive to Pi deficiency. The root growth phenotype of als3-3lpr1lpr2 resembles that of lpr1lpr2. Under Pi deficiency, the over-accumulation of Fe3+ is diminished in UDP-glucose-treated als3-3, als3-3lpr1lpr2, and a genetic suppressor of als3-3, which contains a mutation in LPR1. We therefore conclude that ALS3 and LPR1/2 act in the same pathway to regulate Pi deficiency-induced remodeling of root architecture by modulating Fe homeostasis in roots.