Genetius

The study demonstrates that salicylic acid (SA) restricts plant root growth through a mechanism requiring the transmembrane kinase TMK1, which leads to apoplastic alkalinization and inhibition of plasma membrane H⁺-ATPase phosphorylation. This SA effect operates independently of the auxin receptor ABP1, suggesting a novel SA-mediated pathway that balances stress responses with growth.

The study created transgenic Arabidopsis lines enabling inducible plasmodesmal closure via an overactive CALLOSE SYNTHASE3 allele (icals3m) and the C‑terminal domain of PDLP1, independent of pathogen signals. Induced closure triggered stress‑responsive gene expression, elevated salicylic acid levels, and enhanced resistance to Pseudomonas syringae, while also causing starch accumulation, reduced growth, and increased susceptibility to Botrytis cinerea, indicating that plasmodesmal closure itself can activate immune signaling.

The study demonstrates that elevated endogenous salicylic acid (SA) levels suppress anthocyanin accumulation in Arabidopsis thaliana under anthocyanin‑inducing conditions, a effect confirmed by exogenous SA applications. Microscopic analysis of the 5gt mutant further reveals that high SA reduces the abundance of anthocyanin vesicular inclusions, suggesting that SA downstream signaling, independent of NPR1, mediates this inhibition.

The study investigated how varying concentrations of salicylic acid (SA) and jasmonic acid (JA) together shape transcriptional responses, identifying 43 distinct expression patterns including novel combination-specific responses. A machine‑learning pipeline generated transcriptomic biomarkers that accurately estimate SA/JA response states, and these markers were validated using npr3/4 double mutants. The approach enables quantitative dissection of hormone signaling from large‑scale and single‑cell transcriptomic datasets.

The study reveals that the mobile immune signals azelaic acid (AzA) and N‑hydroxy‑pipecolic acid (NHP) differentially modulate salicylic acid (SA)–driven transcription, with NHP stabilizing the SA receptor NPR1 and dramatically enhancing SA‑mediated bacterial resistance via WRKY38/62 transcription factors. Loss of WRKY38/62 abolishes NHP’s potentiation of SA‑induced gene expression and immunity, indicating these WRKYs integrate mobile signals with SA signaling during systemic acquired resistance.

The study combines phylogenetic, structural, and functional analyses to trace the origin of the isochorismate (IC) pathway for salicylic acid biosynthesis to the Brassicales order, occurring between the divergence of Carica papaya and Capparis spinosa. It identifies three evolutionary adaptations—enhanced ICS enzymatic activity, neofunctionalization of the EDS5 transporter after gene duplication, and specialization of PBS3 for glutamate‑conjugation to IC—supported by salt‑bridge network modeling and amino‑acid substitution assessments.

The study investigates how glucose and salicylic acid (SA) interact to regulate primary root growth, revealing that SA inhibits growth through auxin signaling, TOR pathway activity, and down‑regulation of the cell‑cycle transcription factor E2Fa. Disruption of auxin signaling or transport reduces SA’s inhibitory effect, highlighting a complex cross‑talk among glucose, auxin, and TOR pathways in root development.