The study used Arabidopsis thaliana mutants with low (vtc2, vtc4) and high (vtc2/OE-VTC2) ascorbate levels to examine how ascorbate concentration affects gene expression and cellular homeostasis. Transcriptomic analysis revealed that altered ascorbate levels modulate defense and stress pathways, and that TAA1/TAR2‑mediated auxin biosynthesis is required for coping with elevated ascorbate in a light‑dependent manner.

The study examines how autophagy-related genes AtATG5 and AtATG7 influence Arabidopsis seed germination and ABA responses, revealing that atg5 and atg7 mutants germinate more slowly and display altered lipid droplet and protein storage vacuole organization. Transcriptomic and immunolocalization analyses show delayed ABI5 decay and a direct interaction between ATG8 and the autophagy machinery, implicating autophagy in seed reserve mobilization via transcription factor turnover.

The study compares transcriptional, proteomic, and metabolomic responses of wild‑type Arabidopsis and a cyp71A27 mutant to a plant‑growth‑promoting Pseudomonas fluorescens strain and a pathogenic Burkholderia glumeae strain, revealing distinct reprogramming and an unexpected signaling role for the non‑canonical P450 CYP71A27. Mutant analysis showed that loss of CYP71A27 alters gene and protein regulation, especially during interaction with the PGP bacterium, while having limited impact on root metabolites and exudates.

The study reveals that root hair cells rely on elevated autophagy to extend their lifespan, and that loss-of-function mutations in autophagy genes ATG2, ATG5, or ATG7 trigger premature, cell-autonomous death mediated by NAC transcription factors ANAC046 and ANAC087. This uncovers an antagonistic interaction between autophagy and a developmentally programmed cell death pathway that controls root hair longevity, highlighting a potential target for improving nutrient and water uptake in crops.

The study reveals that root hair-forming trichoblast cells in Arabidopsis thaliana display higher autophagic flux than adjacent atrichoblast cells, a difference linked to cell fate determination. Elevated autophagy in trichoblasts is required for vacuolar sodium sequestration, contributing to salt‑stress tolerance, whereas disrupting autophagy in these cells impairs ion accumulation and survival. Cell‑type‑specific genetic complementation restores both autophagy and stress resilience, highlighting a developmental program that tailors autophagy for environmental adaptation.

The study investigates how miR394 influences flowering time in Arabidopsis thaliana by combining transcriptomic profiling of mir394a mir394b double mutants with histological analysis of reporter lines. Bioinformatic analysis identified a novel lncRNA overlapping MIR394B (named MIRAST), and differential promoter activity of MIR394A and MIR394B suggests miR394 fine‑tunes flower development through transcription factor and chromatin remodeler regulation.

The study demonstrates that loss of Arabidopsis metacaspase 1 (AtMC1) triggers autoimmunity reliant on downstream NLR and PRR signaling, and that overexpressing a catalytically dead AtMC1 exacerbates this effect. Overexpression of the E3 ligase SNIPER1 restores normal immunity, suggesting that AtMC1 regulates NLR protein turnover, possibly via autophagic degradation of the inactive protein.