A biparental Vicia faba mapping population was screened under glasshouse conditions for resistance to a mixture of Fusarium avenaceum and Fusarium oxysporum, revealing several families with moderate to high resistance. Using the Vfaba_v2 Axiom SNP array, a high-density linkage map of 6,755 SNPs was constructed, enabling the identification of a major QTL on linkage group 4 associated with partial resistance to foot and root rot.
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 investigates how miR394 influences flowering time in Arabidopsis thaliana by combining transcriptomic profiling of mir394a mir394b double mutants with histological analysis of reporter lines. Bioinformatic analysis identified a novel lncRNA overlapping MIR394B (named MIRAST), and differential promoter activity of MIR394A and MIR394B suggests miR394 fine‑tunes flower development through transcription factor and chromatin remodeler regulation.
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.