loading page

Phospholipase Dα1 mediates the high-Mg2+ stress response partially through regulation of K+ homeostasis
  • +4
  • Daniela Kocourková,
  • Zuzana Krčková,
  • Přemysl Pejchar,
  • Kristyna Kroumanova,
  • Tereza Podmanicka,
  • Michal Daněk,
  • Jan Martinec
Daniela Kocourková
The Czech Academy of Sciences
Author Profile
Zuzana Krčková
The Czech Academy of Sciences
Author Profile
Přemysl Pejchar
Czech Academy of Sciences
Author Profile
Kristyna Kroumanova
The Czech Academy of Sciences
Author Profile
Tereza Podmanicka
The Czech Academy of Sciences
Author Profile
Michal Daněk
The Czech Academy of Sciences
Author Profile
Jan Martinec
Author Profile

Peer review status:UNDER REVIEW

02 Jun 2020Submitted to Plant, Cell & Environment
02 Jun 2020Submission Checks Completed
02 Jun 2020Assigned to Editor
03 Jun 2020Reviewer(s) Assigned
10 Jun 2020Peer Review Completed
13 Jun 20201st Revision Received
13 Jun 2020Submission Checks Completed
13 Jun 2020Assigned to Editor
14 Jun 2020Peer Review Completed

Abstract

Intracellular levels of Mg2+ are tightly regulated, as Mg2+ deficiency or excess affects normal plant growth and development. In Arabidopsis, we determined that phospholipase Dα1 (PLDα1) is involved in the stress response to high-magnesium conditions. The T-DNA insertion mutant pldα1 is hypersensitive to increased concentrations of magnesium, exhibiting reduced primary root length and fresh weight. PLDα1 activity increases rapidly after high-Mg2+ treatment, and this increase was found to be dose-dependent. Two lines harboring mutations in the HKD motif, which is essential for PLDα1 activity, displayed the same high-Mg2+ hypersensitivity of pldα1 plants. Moreover, we show that high concentrations of Mg2+ disrupt K+ homeostasis, and that transcription of K+ homeostasis-related genes CIPK9 and HAK5 is impaired in pldα1. Additionally, we found that the akt1, hak5 double mutant is hypersensitive to high-Mg2+. We conclude that in Arabidopsis, the enzyme activity of PLDα1 is vital in the response to high-Mg2+ conditions, and that PLDα1 mediates this response partially through regulation of K+ homeostasis.