The study examined how osmotic stress and cytosolic Ca²⁺ signaling regulate autophagy in plants by monitoring the dynamics of RFP‑tagged ATG8i. Both stimuli altered the accumulation of RFP‑ATG8i‑labeled autophagosomes in an organ‑specific way, and colocalization with the ER marker HDEL indicated that ATG8i participates in ER‑phagy during stress.

The study shows that the SnRK1 catalytic subunit KIN10 directs tissue-specific growth‑defense programs in Arabidopsis thaliana by reshaping transcriptomes. kin10 knockout mutants exhibit altered root transcription, reduced root growth, and weakened defense against Pseudomonas syringae, whereas KIN10 overexpression activates shoot defense pathways, increasing ROS and salicylic acid signaling at the cost of growth.

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 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 reveals that the bacterial pathogen Pseudomonas syringae suppresses host plant translation by targeting processing bodies (P‑bodies) through two liquid-like effectors, linking this repression to the ER stress response. It further demonstrates that autophagic clearance of P‑bodies is essential for balancing translationally active and inactive mRNAs, uncovering new connections among translation, ER stress, and autophagy during plant immunity.

The study investigated melatonin priming on methylglyoxal detoxification and autophagy during PEG‑induced drought stress in seed germination of drought‑sensitive (L‑799) and tolerant (Suraj) upland cotton. Melatonin increased endogenous melatonin, reduced MGO and AGEs, up‑regulated glyoxalase enzymes and autophagy markers, and improved cell viability in the sensitive variety, while the tolerant variety showed limited response.

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.