State Key Laboratory of Biocontrol, Guangdong Provincial Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, China.
Provincial Key Laboratory of Agricultural & Rural Pollution Abatement and Environmental Safety, College of Natural Resources and Environment, South China Agricultural University, Guangzhou 510642, China.
Plant Cell. 2022 Feb 3;34(2):889-909. doi: 10.1093/plcell/koab289.
Phosphatidic acid (PA) is an important lipid essential for several aspects of plant development and biotic and abiotic stress responses. We previously suggested that submergence induces PA accumulation in Arabidopsis thaliana; however, the molecular mechanism underlying PA-mediated regulation of submergence-induced hypoxia signaling remains unknown. Here, we showed that in Arabidopsis, loss of the phospholipase D (PLD) proteins PLDα1 and PLDδ leads to hypersensitivity to hypoxia, but increased tolerance to submergence. This enhanced tolerance is likely due to improvement of PA-mediated membrane integrity. PA bound to the mitogen-activated protein kinase 3 (MPK3) and MPK6 in vitro and contributed to hypoxia-induced phosphorylation of MPK3 and MPK6 in vivo. Moreover, mpk3 and mpk6 mutants were more sensitive to hypoxia and submergence stress compared with wild type, and fully suppressed the submergence-tolerant phenotypes of pldα1 and pldδ mutants. MPK3 and MPK6 interacted with and phosphorylated RELATED TO AP2.12, a master transcription factor in the hypoxia signaling pathway, and modulated its activity. In addition, MPK3 and MPK6 formed a regulatory feedback loop with PLDα1 and/or PLDδ to regulate PLD stability and submergence-induced PA production. Thus, our findings demonstrate that PA modulates plant tolerance to submergence via both membrane integrity and MPK3/6-mediated hypoxia signaling in Arabidopsis.
磷脂酸（PA）是一种重要的脂质，对植物发育和生物及非生物胁迫反应的多个方面都至关重要。我们之前曾提出，淹水会诱导拟南芥中 PA 的积累；然而，PA 介导的调节淹水诱导缺氧信号的分子机制尚不清楚。在这里，我们表明在拟南芥中，磷脂酶 D（PLD）蛋白 PLDα1 和 PLDδ 的缺失导致对缺氧的敏感性增加，但对淹水的耐受性增强。这种增强的耐受性可能是由于改善了 PA 介导的膜完整性。PA 在体外与丝裂原活化蛋白激酶 3（MPK3）和 MPK6 结合，并有助于体内缺氧诱导的 MPK3 和 MPK6 的磷酸化。此外，与野生型相比，mpk3 和 mpk6 突变体对缺氧和淹水胁迫更敏感，并且完全抑制了 pldα1 和 pldδ 突变体的淹水耐受表型。MPK3 和 MPK6 与缺氧信号通路中的主转录因子 RELATED TO AP2.12 相互作用并磷酸化它，调节其活性。此外，MPK3 和 MPK6 与 PLDα1 和/或 PLDδ 形成一个调节反馈回路，以调节 PLD 的稳定性和淹水诱导的 PA 产生。因此，我们的研究结果表明，PA 通过膜完整性和 MPK3/6 介导的缺氧信号通路在拟南芥中调节植物对淹水的耐受性。
