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Fusarium culmorum is a soilborne fungal pathogen, agent of crown and root rot disease (FCRR), responsible of major economic losses in wheat plants. This host—pathogen interaction, following methyl jasmonate (MeJA) application at the beginning of the necrotrophic stage of infection, has not been previously studied at molecular level. In this study, using real-time quantitative PCR, the emerging role of MeJA in the basal resistance of two bread wheat cultivars against F. culmorum has been investigated. MeJA treatment was dispensed 6 hours after pathogen inoculation (6 hai) to detect the defense response at the beginning of the necrotrophic stage. The expression of phenylalanine ammonia-lyase (PAL), lipoxygenase (LOX), cytochrome P450 (CYP709C1) genes and of some pathogenesis related (PR) genes, including PR3, PR4 and PR9, was examined in both root and crown tissues of the susceptible wheat cultivar Falat and the tolerant cultivar Sumai3. The pathogen responsive defense genes were induced in both cultivars, with a higher level of induction in Sumai3 than in Falat. MeJA treatment reduced the symptoms in cv Falat, whereas no significant effects have been detected in cv Sumai3. In fact, MeJA treatment caused a striking difference in defense gene induction. The genetic change was present in root and crown tissues of both wheat cultivars, demonstrating a systemic signaling pathway. The chemically induced protection correlated with induction of the F. culmorum-responsive genes supports a possible role of jasmonate signaling in regulating basal resistance in wheat–F. culmorum interaction.
Absztrakt
Az oxidatív stressz fontos szerepet játszik a szívelégtelenség kialakulásában. A szívizomzatban megtalálható összes sejttípus részt vesz az oxigén- és a nitrogén-szabadgyökök termelésében. A reaktívoxigén-származékok potenciális forrásának a szívben a NADPH-oxidáz, a nitrogén-oxid-szintázok, a lipoxigenázok, a ciklooxigenázok, a xantinoxidáz, a citokróm P450 enzimek, illetve a mitokondriális légzési lánc elemei tekinthetők. A reaktívoxigén-származékok okozta károsodás magában foglalja mind a vascularis rendszer (endotheldiszfunkció, atherosclerosis), mind a myocardium direkt károsodását (bal kamrai remodelling). A reaktívoxigén-származékok sejtszinten fehérje-, lipid- és DNS-károsodáshoz, valamint számos jelátviteli út modifikációjához vezetnek, amelyek központi szerepet töltenek be a remodelling, a hypertrophia és a kamrai dilatatio kialakulásában. Orv. Hetil., 2015, 156(47), 1916–1920.
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