Exploring the interaction between aminobutyric acid and epigenetics in modulating ash dieback response in european ash (Fraxinus excelsior)

Abstract

European ash populations face a significant threat from the invasive fungus Hymenoscyphus fraxineus, leading to ash dieback disease. The absence of resistant individuals and restrictions on biotechnological solutions hinder the ability to combat this widespread illness in the near term. Priming strategies offer an alternative approach to boost stress tolerance not only in this scenario but also in other endangered tree species by triggering plant defense mechanisms. The non-proteinogenic amino acid β-aminobutyric acid (BABA) has demonstrated potential in enhancing resistance to diverse stressors in plants. Despite limited research on forest tree species, the current study evaluated BABA’s effectiveness in mitigating ash dieback disease severity and explored potential correlations between priming treatments and epigenetic modifications. The results indicated that BABA enhanced stress tolerance in ash seedlings following inoculation with Hymenoscyphus fraxineus. BABA effectively decreased the development of necrosis associated with ash dieback disease in seedlings five months post-inoculation. Additionally, treatments involving BABA were linked to observed epigenetic alterations. Elevated levels of the non-canonical deoxynucleosides 5-(hydroxymethyl)-2'-deoxycytidine (5-hmdC) and 5-(hydroxymethyl)-2'-deoxyuridine (5-hmdU) were confirmed subsequent to the treatments. This study highlights the potential of BABA and other priming strategies in enhancing disease tolerance in forest tree species like European ash. Short-term improved stress tolerance and epigenetic changes were confirmed. Yet, the exact priming conditions for inducing long-term effects in plants, including long-living forest trees, remain unknown, posing a challenge for applying priming strategies to manage ash dieback and protect many other endangered tree species.