The study investigated how Arabidopsis thaliana SR protein kinases (AtSRPKs) regulate alternative RNA splicing by using chemical inhibitors of SRPK activity. Inhibition with SPHINX31 and SRPIN340 caused reduced root growth and loss of root hairs, accompanied by widespread changes in splicing and phosphorylation of genes linked to root development and other cellular processes. Multi‑omics analysis (transcriptomics and phosphoproteomics) revealed that AtSRPKs modulate diverse splicing factors and affect the splicing landscape of numerous pathways.
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.
Bacteria use processing body condensates to attenuate host translation during infection
Authors: Gonzalez-Fuente, M., Schulz, N., Abdrakhmanov, A., Izzati, G., Zhu, S., Langin, G., Gouguet, P., Franz-Wachtel, M., Macek, B., Hafren, A., Dagdas, Y., Üstün, S.
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 investigates the role of the Arabidopsis transcription factor AtMYB93 in sulfur (S) signaling and root development, revealing that AtMYB93 mutants exhibit altered expression of S transport and metabolism genes and increased shoot S levels, while tomato plants overexpressing SlMYB93 show reduced shoot S. Transcriptomic profiling, elemental analysis, and promoter activity assays indicate that AtMYB93 contributes to root responses to S deprivation, though functional redundancy masks clear phenotypic effects on lateral and adventitious root formation.
The study investigates the Arabidopsis ribosomal protein RPS6A and its role in auxin‑related root growth, revealing that rps6a mutants display shortened primary roots, fewer lateral roots, and defective vasculature that are not rescued by exogenous auxin. Cell biological observations and global transcriptome profiling show weakened auxin signaling and reduced levels of PIN auxin transporters in the mutant, indicating a non‑canonical function of the ribosomal subunit in auxin pathways.
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.
Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability
Authors: Salguero-Linares, J., Armengot, L., Ayet, J., Ruiz-Solani, N., Saile, S., Salas-Gomez, M., Fernandez, E., Denolf, L., Navarrete, F., Krumbach, J., Kaiser, M., Stael, S., Van Breusegem, F., Gevaert, K., Kaschani, F., petersen, m., El Kasmi, F., Valls, M., Coll, N. S.
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.