Botrytis cinerea mutants engineered to constitutively express the salicylate‑hydroxylase NahG grew better on salicylic‑acid media and showed heightened virulence on Arabidopsis thaliana and Phaseolus vulgaris, an effect that required host SA biosynthesis. Genomic analysis identified four fungal salicylate‑hydroxylase‑like genes whose expression varied during infection, suggesting B. cinerea can degrade host SA to promote colonization.

The study reveals that the Kelch phosphatase BSU1, previously thought to act as a tyrosine phosphatase in brassinosteroid signaling, actually functions as a PP1-like serine/threonine phosphatase whose activity is inhibited by CDK-mediated phosphorylation of its C‑terminal tail. Structural analysis, mutagenesis, and genetic experiments in Arabidopsis and Marchantia demonstrate that this regulatory mechanism links BSU1 to cell‑cycle control, affecting stomatal patterning, fertility, and undifferentiated cell mass formation.

The study characterizes the chloroplast‑localized protein AT4G33780 in Arabidopsis thaliana using CRISPR/Cas9 knockout and overexpression lines, revealing tissue‑specific expression and context‑dependent effects on seed germination, seedling growth, vegetative development, and root responses to nickel stress. Integrated transcriptomic (RNA‑seq) and untargeted metabolomic analyses show extensive transcriptional reprogramming—especially of cell‑wall genes—and altered central energy metabolism, indicating AT4G33780 coordinates metabolic state with developmental regulation rather than controlling single pathways.

The study re-analyzed AtGenExpress microarray data to profile expression of Arabidopsis papain-like cysteine proteases (PLCPs) and cystatins under bacterial infection, wounding, and drought, and performed in vitro assays to determine cystatin inhibition specificity for abundant PLCPs. Integrating co‑expression and inhibition data with support vector machine modeling revealed distinct PLCP‑cystatin modules for virulent versus avirulent bacterial infections and overlapping modules between drought and basal defense, indicating shared regulatory programs across stress types.

The study shows that maize plants carrying autophagy-defective atg10 mutations exhibit delayed flowering and significant reductions in kernel size, weight, and number, culminating in lower grain yield. Reciprocal crossing experiments reveal that the maternal genotype, rather than the seed genotype, primarily drives the observed kernel defects, suggesting impaired nutrient remobilization from maternal tissues during seed development.

The study investigated the role of the ABA transporter NPF4.6 in Arabidopsis thaliana by analyzing loss-of-function mutants under steady and fluctuating light. Mutants displayed faster stomatal opening, higher CO2 assimilation, and increased shoot biomass under well‑watered, dynamic‑light conditions, while showing no advantage under drought stress, indicating NPF4.6 fine‑tunes stomatal kinetics in variable light environments.

The study investigates the role of the SNF1-related kinase 1 (SnRK1) in conferring quantitative resistance to clubroot disease caused by Plasmodiophora brassicae in Arabidopsis thaliana. Increased nuclear SnRK1 activity suppresses disease development by down‑regulating sucrose transporter and cell wall invertase expression and activity, thereby reducing sink strength, while the pathogen effector PBZF1 interferes with SnRK1 nuclear translocation.

Using the bryophyte Physcomitrium patens, the study shows that loss of autophagy enhances auxin‑driven caulonemata differentiation and colony expansion under low nitrogen or imbalanced carbon/nitrogen conditions, accompanied by higher internal IAA, reduced PpPINA expression, and up‑regulated RSL transcription factors. Autophagy appears to suppress auxin‑induced differentiation during nutrient stress, acting as a hub that balances metabolic cues with hormonal signaling.

Thermopriming enhances heat stress tolerance by orchestrating protein maintenance pathways: it activates the heat shock response (HSR) via HSFA1 and the unfolded protein response (UPR) while modulating autophagy to clear damaged proteins. Unprimed seedlings cannot mount these responses, leading to proteostasis collapse, protein aggregation, and death, highlighting the primacy of HSR and protein maintenance over clearance mechanisms.

Arabidopsis pub41 mutants display reduced root hair number and length, while auxin up‑regulates PUB41 transcript and protein levels. A catalytically inactive PUB41ΔU construct rescues the mutant phenotype and makes plants hyper‑responsive to auxin, localizing preferentially to trichoblasts and colocalizing with the auxin exporter PIN2. Biochemical and microscopy analyses reveal that PUB41 physically interacts with the cytoplasmic loop of PIN2, stabilizing its abundance, indicating that PUB41 modulates root hair development through PIN2 regulation.