LPCAT1 controls phosphate homeostasis in a zinc-dependent manner

eLife

Hatem Rouached¹  Mushtak Kisko²  Nadia Bouain²  Gabriel Krouk²  David Secco²  Alaeddine Safi²  Anna Medici²  Wolfgang Busch³  Mark GM Aarts⁴  Robert C Akkers⁴  Gilles Fouret⁵ 

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

关键词: natural variation;    phosphate homeostasis;    zinc deficiency;   

DOI  :  10.7554/eLife.32077

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown