LPCAT1 controls phosphate homeostasis in a zinc-dependent manner
Abstract
All living organisms require a variety of essential elements for their basic biological functions. While the homeostasis of nutrients is highly intertwined, the molecular and genetic mechanisms of these dependencies remains poorly understood. Here, we report a discovery of a molecular pathway that control phosphate (Pi) accumulation plants in Zn deficiency. Using genome-wide association studies we first identified allelic variation of the Lyso-PhosphatidylCholine (PC) AcylTransferase 1 (LPCAT1) gene as the key determinant of shoot Pi accumulation under Zn deficiency. We then show that regulatory variation at the LPCAT1 locus contributes significantly to this natural variation and we further demonstrate that the regulation of LPCAT1 expression involves bZIP23 TF, for which we identified a new binding site sequence. Finally, we show that in Zn deficient conditions loss of function of LPCAT1 increases the phospholipid Lyso-PhosphatidylCholine/PhosphatidylCholine ratio, the expression of the Pi transporter PHT1;1, and that this leads to shoot Pi accumulation.
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Author details
Funding
Institut National de la Recherche Agronomique
- Hatem Rouached
The Austrian Academy of Sciences through Gregor Mendel Institute
- Wolfgang Busch
The Netherland Genome Initiative ZonMW Horizon program Zenith (no. 40-41009-98-11084)
- Mark GM Aarts
Iraq Government Doctoral Fellowship
- Mushtak Kisko
Région Languedoc-Roussillon: Chercheurd'Avenir/Projet Cofinancé par le Fonds Européen de Développement Regional
- Hatem Rouached
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2018, Kisko et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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