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Elife. 2018 Feb 17;7. pii: e32077. doi: 10.7554/eLife.32077.

LPCAT1 controls phosphate homeostasis in a zinc-dependent manner.

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BPMP, Univ Montpellier, CNRS, INRA, SupAgro, Montpellier, France.
Laboratory of Genetics, Wageningen University, Wageningen, Netherlands.
Unité Mixte de Recherche, Montpellier, France.
Gregor Mendel Institute, Austrian Academy of Sciences, Vienna Biocenter, Vienna, Austria.
Plant Molecular and Cellular Biology Laboratory, Salk Institute for Biological Studies, La Jolla, United States.


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 remain poorly understood. Here, we report a discovery of a molecular pathway that controls phosphate (Pi) accumulation in plants under 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.


A. thaliana; natural variation; phosphate homeostasis; plant biology; zinc deficiency

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