Fusarium infections in Pisum sativum L. crops present a major constraint to cultivation, leading to substantial yield losses. However, effective disease management strategies, particularly the implementation of biological control methods, offer promising approaches for mitigating infection severity and limiting pathogen spread. In P. sativum cultivation, pathogen control is particularly challenging due to the limited penetration of pesticides into the leaves. This is attributed to the dense crystalline plate structure within the leaf cuticle, which acts as a barrier, reducing the efficacy of conventional chemical treatments. Therefore, optimizing the formulation of biopesticides and plant conditioning agents is essential to improve the absorption and bioavailability of active ingredients, ensuring more effective disease management in P. sativum cultivation. This study examined the exogenous effects of garlic extracts in different formulations, including EliceVakcina (liposomal formulation), Garlic-lipo (liposomal formulation), and Garlic-oil (oil-based formulation), which contained high concentrations of abscisic acid (ABA) at 6.3, 81, and 80.4 µg g⁻¹, respectively. Transcriptomic profiling, including the identification of Differentially expressed genes (DEGs) and KEGG pathway analysis of EliceVakcina-treated field samples, revealed a significant upregulation of stress- and defence-related genes, as well as pathways associated with thiamine metabolism and ABA signalling. Notably, key defence genes, including pathogenesis-related (PR1, PR2, PR4, PR5) and SnRK2, were overexpressed, indicating an enhanced stress response. HPLC-DAD analytical investigations confirmed the activation of the thiamine biosynthesis pathway, demonstrating a 14.3% increase in vitamin B1 content. Furthermore, the absence of Fusarium infection in the treated small-plot field cultures suggests that the tested garlic extracts formulation functions as a promising preventive biostimulant against plant fungal diseases.

Manganese superoxide dismutases (MnSODs) play a pivotal role in the preservation of mitochondrial integrity and function in fungi under various endogenous and exogenous stresses. Deletion of Aspergillus nidulans mnSOD/SodB increased oxidative stress sensitivity and apoptotic cell death rates as well as affected antioxidant enzyme and sterigmatocystin productions, respiration, conidiation and the stress tolerance of conidiospores. The physiological consequences of the lack of sodB were more pronounced during carbon starvation than in the presence of glucose. Lack of SodB also affected the changes in the transcriptome, recorded by high-throughput RNA sequencing, in menadione sodium bisulfite (MSB)-exposed, submerged cultures supplemented with glucose. Surprisingly, the difference between the global transcriptional changes of the ΔsodB mutant and the control strain were relatively small, indicating that the SodB-dependent maintenance of mitochondrial integrity was not essential under these experimental conditions. Owing to the outstanding physiological flexibility of the Aspergilli, certain antioxidant enzymes and endogenous antioxidants together with the reduction in mitochondrial functions compensated well for the lack of SodB. The lack of sodB reduced the growth of surface cultures more than of the submerged culture, which should be considered in future development of fungal disinfection methods.

The importance of manganese superoxide dismutase (Mn-SOD), an evolutionarily ancient metalloenzyme that maintains the integrity and function of mitochondria, was studied in oxidative stress-treated Aspergillus fumigatus cultures. Deletion of the Mn-SOD gene (sodB) increased both the menadione sodium bisulfite (MSB)-elicited oxidative stress and the deferiprone (DFP)-induced iron limitation stress sensitivity of the strain. Moreover, DFP treatment enhanced the MSB sensitivity of both the gene deletion mutant and the reference strain. The lack of SodB also increased the susceptibility of conidia to killing by human macrophages. Concurring with the stress sensitivity data, RNS sequencing data also demonstrated that the deletion of sodB largely altered the MSB-induced oxidative stress response. The difference between the oxidative stress responses of the two strains manifested mainly in the intensity of the response. Importantly, upregulation of “Ribosome protein”, “Iron uptake”, and “Fe-S cluster assembly” genes, alterations in the transcription of “Fe-S cluster protein” genes, and downregulation of “Heme binding protein” genes under MSB stress were characteristic only for the ΔsodB gene deletion mutant. We assume that the elevated superoxide level generated by MSB treatment may have destroyed Fe-S cluster proteins of mitochondria in the absence of SodB. This intensified the resynthesis of Fe-S cluster proteins, which was accompanied with enhanced translation and iron acquisition, leading to increased DFP sensitivity.