Transcriptional responses of Solanum lycopersicum to three distinct parasites reveal host hubs and networks underlying parasitic successes
Authors: Truch, J., Jaouannet, M., Da Rocha, M., Kulhanek-Fontanille, E., Van Ghelder, C., Rancurel, C., Migliore, O., Pere, A., Jaubert, S., Coustau, C., Galiana, E., Favery, B.
The study used transcriptomic profiling to compare tomato (Solanum lycopersicum) responses to three evolutionarily distant pathogens—nematodes, aphids, and oomycetes—during compatible interactions, identifying differentially expressed genes and key host hubs. Integrating public datasets and performing co‑expression and GO enrichment analyses, the authors mapped shared dysregulation clusters and employed Arabidopsis interactome data to place tomato candidates within broader networks, highlighting potential targets for multi‑pathogen resistance.
Phosphite (Phi) and phosphate (Pi) share the same root uptake system, but Phi acts as a biostimulant that modulates plant growth and disease resistance in a species‑ and Pi‑dependent manner. In Arabidopsis, Phi induces hypersensitive‑like cell death and enhances resistance to Plectosphaerella cucumerina, while in rice it counteracts Pi‑induced susceptibility to Magnaporthe oryzae and Fusarium fujikuroi, accompanied by extensive transcriptional reprogramming.
The study created a system that blocks root‑mediated signaling between wheat varieties in a varietal mixture and used transcriptomic and metabolomic profiling to reveal that root chemical interactions drive reduced susceptibility to Septoria tritici blotch, with phenolic compounds emerging as key mediators. Disruption of these root signals eliminates both the disease resistance phenotype and the associated molecular reprogramming.
A novel pathosystem between Aeschynomene evenia and Aphanomyces euteiches reveals new immune components in quantitative legume root-rot resistance.
Authors: Baker, M., Martinez, Y., Keller, J., Sarrette, B., Pervent, M., Libourel, C., Le Ru, A., Bonhomme, M., Gough, C., Castel, B., ARRIGHI, J.-F., Jacquet, C.
The study establishes Aeschynomene evenia as a new model for dissecting legume immunity against the soilborne pathogen Aphanomyces euteiches and its relationship with Nod factor-independent symbiosis. Quantitative resistance was assessed through inoculation assays, phenotypic and cytological analyses, and RNA‑seq identified thousands of differentially expressed genes, highlighting immune signaling and specialized metabolism, with mutant analysis confirming dual‑function kinases that modulate resistance. Comparative transcriptomics with Medicago truncatula revealed conserved and unique immune responses, positioning the A. evenia–A. euteiches system as a valuable platform for exploring quantitative resistance and symbiosis integration.
The study characterizes the chloroplast‑localized protein AT4G33780 in Arabidopsis thaliana using CRISPR/Cas9 knockout and overexpression lines, revealing tissue‑specific expression and context‑dependent effects on seed germination, seedling growth, vegetative development, and root responses to nickel stress. Integrated transcriptomic (RNA‑seq) and untargeted metabolomic analyses show extensive transcriptional reprogramming—especially of cell‑wall genes—and altered central energy metabolism, indicating AT4G33780 coordinates metabolic state with developmental regulation rather than controlling single pathways.
Root-Suppressed Phenotype of Tomato Rs Mutant is Seemingly Related to Expression of Root-Meristem-Specific Sulfotransferases
Authors: Kumari, A., Gupta, P., Santisree, P., Pamei, I., Valluri,, S., Sharma, K., Venkateswara Rao, K., Shukla, S., Nama, S., Sreelakshmi, Y., Sharma, R.
The study characterizes a radiation‑induced root‑suppressed (Rs) mutant in tomato that displays dwarfism and pleiotropic defects in leaves, flowers, and fruits. Metabolite profiling and rescue with H2S donors implicate disrupted sulfur metabolism, and whole‑genome sequencing identifies promoter mutations in two root‑meristem‑specific sulfotransferase genes as likely contributors to the root phenotype.
The study examined how elevated atmospheric CO₂ (550 ppm) affects immunity in the C₄ cereal maize (Zea mays L.) by exposing plants grown under ambient and elevated CO₂ to a range of pathogens. Elevated CO₂ increased susceptibility to sugarcane mosaic virus, decreased susceptibility to several bacterial and fungal pathogens, and left susceptibility to others unchanged, with reduced bacterial disease linked to heightened basal immune responses. These findings provide a baseline for future investigations into CO₂‑responsive defense mechanisms in C₄ crops.
The study shows that maize plants carrying autophagy-defective atg10 mutations exhibit delayed flowering and significant reductions in kernel size, weight, and number, culminating in lower grain yield. Reciprocal crossing experiments reveal that the maternal genotype, rather than the seed genotype, primarily drives the observed kernel defects, suggesting impaired nutrient remobilization from maternal tissues during seed development.
The interplay between autophagy and the carbon/nitrogen ratio as key modulator of the auxin-dependent chloronema-caulonema developmental transition in Physcomitrium patens.
Authors: Pettinari, G., Liberatore, F., Mary, V., Theumer, M., Lascano, R., Saavedra, L. L.
Using the bryophyte Physcomitrium patens, the study shows that loss of autophagy enhances auxin‑driven caulonemata differentiation and colony expansion under low nitrogen or imbalanced carbon/nitrogen conditions, accompanied by higher internal IAA, reduced PpPINA expression, and up‑regulated RSL transcription factors. Autophagy appears to suppress auxin‑induced differentiation during nutrient stress, acting as a hub that balances metabolic cues with hormonal signaling.
Thermopriming enhances heat stress tolerance by orchestrating protein maintenance pathways: it activates the heat shock response (HSR) via HSFA1 and the unfolded protein response (UPR) while modulating autophagy to clear damaged proteins. Unprimed seedlings cannot mount these responses, leading to proteostasis collapse, protein aggregation, and death, highlighting the primacy of HSR and protein maintenance over clearance mechanisms.