14 research outputs found

    Long-lasting memory of jasmonic acid-dependent immunity requires DNA demethylation and ARGONAUTE1

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    Stress can have long-lasting impacts on plants. Here we report the long-term effects of the stress hormone jasmonic acid (JA) on the defence phenotype, transcriptome and DNA methylome of Arabidopsis. Three weeks after transient JA signalling, 5-week-old plants retained induced resistance (IR) against herbivory but showed increased susceptibility to pathogens. Transcriptome analysis revealed long-term priming and/or upregulation of JA-dependent defence genes but repression of ethylene- and salicylic acid-dependent genes. Long-term JA-IR was associated with shifts in glucosinolate composition and required MYC2/3/4 transcription factors, RNA-directed DNA methylation, the DNA demethylase ROS1 and the small RNA (sRNA)-binding protein AGO1. Although methylome analysis did not reveal consistent changes in DNA methylation near MYC2/3/4-controlled genes, JA-treated plants were specifically enriched with hypomethylated ATREP2 transposable elements (TEs). Epigenomic characterization of mutants and transgenic lines revealed that ATREP2 TEs are regulated by RdDM and ROS1 and produce 21 nt sRNAs that bind to nuclear AGO1. Since ATREP2 TEs are enriched with sequences from IR-related defence genes, our results suggest that AGO1-associated sRNAs from hypomethylated ATREP2 TEs trans-regulate long-lasting memory of JA-dependent immunity

    Inhibition by fatty acyl esters of adenine nucleotide translocation in rat-liver mitochondria

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    At low substrate concentrations linoleate oxidation in isolated rat-liver mitochondria can be stimulated by addition of phosphate and phosphate acceptor. With ADP as phosphate acceptor this State-3 linoleate oxidation is strongly inhibited after addition of CoASH. Inhibition by CoASH itself seems rather unlikely. However, in media containing ADP and Mg²+ the longchain acyl-CoA synthetase present in the outer mitochondrial membrane can form linoleyl-CoA, ATP being derived from ADP through the action of adenylate kinase
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