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 generated a high-quality genome assembly for Victoria cruziana and used comparative transcriptomics to identify anthocyanin biosynthesis genes and their transcriptional regulators that are differentially expressed between white and light pinkish flower stages. Differential expression of structural genes (VcrF3H, VcrF35H, VcrDFR, VcrANS, VcrarGST) and transcription factors (VcrMYB123, VcrMYB-SG6_a, VcrMYB-SG6_b, VcrTT8, VcrTTG1) correlates with the observed flower color change.

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 RNA extracted from herbarium specimens can be used to generate high‑quality transcriptomes, comparable to those from fresh or silica‑dried samples. By assembling and comparing transcriptomes across specimen types, the authors validated a plant immune receptor synthesized from a 1956 collection, proving archival RNA’s utility for functional genomics. These findings challenge the prevailing view that herbarium RNA is unsuitable for transcriptomic analyses.

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.