Genetius

The study examined the roles of AtKUP2, AtKUP6, AtKUP8, and GORK potassium transport proteins in guard cell function by performing gas-exchange measurements on mature Arabidopsis leaves. Loss of KUP2/6/8 reduced stomatal conductance, whereas a GORK loss‑of‑function mutant showed increased conductance, yet the magnitude of light‑ and ABA‑induced transpiration changes remained similar across genotypes, suggesting a limited dynamic range for rapid stomatal movements that relies on small ionic osmolytes.

The study shows that Arabidopsis root tips adapt to hypoxia by increasing H3K4me3 levels, linked to the inhibition of group 7 demethylases (KDM7s). Genetic loss of KDM7s mimics hypoxic conditions, activating genes that sustain meristem survival, suggesting KDM7s act as root‑specific oxygen sensors that prime epigenetic tolerance mechanisms.

The study surveyed Cys/Arg N‑degron pathway components across 55 angiosperm genomes and performed hypoxia profiling, revealing habitat‑driven diversification of Plant Cysteine Oxidases and ERFVIIs, especially in aquatic monocots. Despite this variation, a conserved transcriptional core including MYB and LBD factors persists, and functional assays in Arabidopsis confirm their role in hypoxia tolerance.

The study demonstrates that UDP‑glucose directly binds Arabidopsis RGS1 with micromolar affinity, rapidly inducing its phosphorylation, endocytosis, and G‑protein activation. SUS1 and SUS4 supply UDP‑glucose, linking metabolism to signaling, and this activation reshapes transcription of defense‑related genes.

The authors created a high‑throughput yeast two‑hybrid platform using F‑box and U‑box E3 decoys to map ubiquitination interactions, screening 283 Arabidopsis E3s against 21 core circadian regulators and uncovering 77 candidate pairs. They validated PUB18 as a physical interactor and ubiquitin ligase for LHY and JMJD5, showing that PUB18 and its homolog PUB19 redundantly influence clock function, demonstrating the platform’s utility for dissecting ubiquitination networks.

The authors developed a method to isolate autophagic membranes from Arabidopsis using cell fractionation and immuno‑isolation, and performed proteomic and lipidomic analyses to define the protein and lipid composition of the phagophore. They identified candidate proteins involved in membrane remodeling, trafficking and lipid metabolism, and showed that the isolated membranes are enriched in glycerophospholipids, especially phosphatidylcholine and phosphatidylglycerol. This work provides a molecular blueprint of the plant phagophore for future functional studies.

The study demonstrates that non‑symbiotic NIN orthologs can drive intracellular infection and nodule initiation, indicating these functions existed before nodulation evolved. Symbiotic NIN proteins later acquired nitrate‑independent activity such as constitutive nuclear localization, and a single amino‑acid change in Arabidopsis AtNLP2 mimics this trait, highlighting the pre‑adaptation of NIN for symbiosis.

The study demonstrates that the ethylene‑responsive transcription factor EIN3 is directly degraded via ATG8‑mediated autophagy, linking autophagy to ethylene signaling. Autophagy‑deficient Arabidopsis plants show defective EIN3‑dependent hypocotyl elongation, premature senescence, and impaired transcriptional reprogramming during submergence, highlighting autophagy’s role in modulating EIN3 stability and stress adaptation.

The study reveals that the transcription factor WIND1 drives somatic embryogenesis by simultaneously repressing existing shoot identity genes and activating embryogenic regulators through coordinated histone acetylation and deacetylation. WIND1 physically interacts with the histone deacetylase HDA9 and the acetyltransferase complex component ADA2a, enabling locus-specific H3K27 deacetylation and acetylation to remodel chromatin during regeneration.

The study identifies two Arabidopsis phospholipases, LCAT3 and LCAT4, as essential components that hydrolyze autophagic bodies within the vacuole, a step required for autophagy completion. Genetic double knockouts accumulate autophagic bodies and diminish autophagy, while in vivo reconstitution shows LCAT3 initiates membrane hydrolysis enabling LCAT4 activity.