Cytidinediphosphate diacylglycerol synthase-Mediated phosphatidic acid metabolism is crucial for early embryonic development of Arabidopsis.

Embryonic development is a key developmental event in plant sexual reproduction; however, regulatory networks of plant early embryonic development, particularly the effects and functional mechanisms of phospholipid molecules are still unknown due to the limitation of sample collection and analysis. We innovatively applied the microspore-derived in vitro embryogenesis of Brassica napus and revealed the dynamics of phospholipid molecules, especially phosphatidic acid (PA, an important second messenger that plays an important role in plant growth, development, and stress responses), at different embryonic developmental stages by using a lipidomics approach. Further analysis of Arabidopsis mutants deficiency of CDS1 and CDS2 (cytidinediphosphate diacylglycerol synthase, key protein in PA metabolism) revealed the delayed embryonic development from the proembryo stage, indicating the crucial effect of CDS and PA metabolism in early embryonic development. Decreased auxin level and disturbed polar localization of auxin efflux carrier PIN1 implicate that CDS-mediated PA metabolism may regulate early embryogenesis through modulating auxin transport and distribution. These results demonstrate the dynamics and importance of phospholipid molecules during embryo development, and provide informative clues to elucidate the regulatory network of embryogenesis.

A potassium-sensing niche in Arabidopsis roots orchestrates signaling and adaptation responses to maintain nutrient homeostasis.

Organismal homeostasis of the essential ion K+ requires sensing of its availability, efficient uptake, and defined distribution. Understanding plant K+ nutrition is essential to advance sustainable agriculture, but the mechanisms underlying K+ sensing and the orchestration of downstream responses have remained largely elusive. Here, we report where plants sense K+ deprivation and how this translates into spatially defined ROS signals to govern specific downstream responses. We define the organ-scale K+ pattern of roots and identify a postmeristematic K+-sensing niche (KSN) where rapid K+ decline and Ca2+ signals coincide. Moreover, we outline a bifurcating low-K+-signaling axis of CIF peptide-activated SGN3-LKS4/SGN1 receptor complexes that convey low-K+-triggered phosphorylation of the NADPH oxidases RBOHC, RBOHD, and RBOHF. The resulting ROS signals simultaneously convey HAK5 K+ uptake-transporter induction and accelerated Casparian strip maturation. Collectively, these mechanisms synchronize developmental differentiation and transcriptome reprogramming for maintaining K+ homeostasis and optimizing nutrient foraging by roots.

The Transcription Factor MYB59 Regulates K+/NO3 - Translocation in the Arabidopsis Response to Low K+ Stress.

Potassium and nitrogen are essential nutrients for plant growth and development. Plants can sense potassium nitrate (K+/NO3 -) levels in soils, and accordingly they adjust root-to-shoot K+/NO3 - transport to balance the distribution of these ions between roots and shoots. In this study, we show that the transcription factorMYB59 maintains this balance by regulating the transcription of the Arabidopsis (Arabidopsis thaliana) Nitrate Transporter1.5 (NRT1.5)/ Nitrate Transporter/Peptide Transporter Family7.3 (NPF7.3) in response to low K+ (LK) stress. The myb59 mutant showed a yellow-shoot sensitive phenotype when grown on LK medium. Both the transcript and protein levels of NPF7.3 were remarkably reduced in the myb59 mutant. LK stress repressed transcript levels of both MYB59 and NPF7.3 The npf7.3 and myb59 mutants, as well as the npf7.3 myb59 double mutant, showed similar LK-sensitive phenotypes. Ion content analyses indicated that root-to-shoot K+/NO3 - transport was significantly reduced in these mutants under LK conditions. Moreover, chromatin immunoprecipitation and electrophoresis mobility shift assay assays confirmed that MYB59 bound directly to the NPF7.3 promoter. Expression of NPF7.3 in root vasculature driven by the PHOSPHATE 1 promoter rescued the sensitive phenotype of both npf7.3 and myb59 mutants. Together, these data demonstrate that MYB59 responds to LK stress and directs root-to-shoot K+/NO3 - transport by regulating the expression of NPF7.3 in Arabidopsis roots.

NRT1.5/NPF7.3 Functions as a Proton-Coupled H+/K+ Antiporter for K+ Loading into the Xylem in Arabidopsis.

Potassium and nitrogen are essential macronutrients for plant growth and have a positive impact on crop yield. Previous studies have indicated that the absorption and translocation of K+ and NO3- are correlated with each other in plants; however, the molecular mechanism that coordinates K+ and NO3- transport remains unknown. In this study, using a forward genetic approach, we isolated a low-K+-sensitive Arabidopsis thaliana mutant, lks2, that showed a leaf chlorosis phenotype under low-K+ conditions. LKS2 encodes the transporter NRT1.5/NPF7.3, a member of the NRT1/PTR (Nitrate Transporter 1/Peptide Transporter) family. The lks2/nrt1.5 mutants exhibit a remarkable defect in both K+ and NO3- translocation from root to shoot, especially under low-K+ conditions. This study demonstrates that LKS2 (NRT1.5) functions as a proton-coupled H+/K+ antiporter. Proton gradient can promote NRT1.5-mediated K+ release out of root parenchyma cells and facilitate K+ loading into the xylem. This study reveals that NRT1.5 plays a crucial role in K+ translocation from root to shoot and is also involved in the coordination of K+/NO3- distribution in plants.