Search Results
Aspergillus niger is a common pathogenic fungus causing postharvest rot of fruit and vegetable, whereas the knowledge on virulence factors is very limited. Superoxide dismutase [SOD (EC 1.15.1.10)] is an important metal enzyme in fungal defense against oxidative damage. Thus, we try to study whether Cu/Zn-SOD is a virulence factor in A. niger. Cu/Zn-SOD encoding gene sodC was deleted in A. niger [MA70.15 (wild type)] by homologous recombination. The deletion of sodC led to decreased SOD activity in A. niger, suggesting that sodC did contribute to full enzyme activity. ΔsodC strain showed normal mycelia growth and sporulation compared with wild type. However, sodC deletion markedly increased the cell’s sensitivity to intracellular superoxide anion generator menadione. Besides, spore germination under menadione and H2O2 stresses were significantly retarded in ΔsodC mutant compared with wild type. Further results showed that sodC deletion induced higher superoxide anion production and higher content of H2O2 and malondialdehyde (MDA) compared with wild type, supporting the role of SOD in metabolism of reactive oxygen species (ROS). Furthermore, ΔsodC mutant had a reduced virulence on chinese white pear (Pyrus bretschneideri) as lesion development by ΔsodC was significantly less than wild type. The determination of superoxide anion, H2O2, and MDA in A. niger-infected pear showed that chinese white pear infected with ΔsodC accumulated less superoxide anion, H2O2, and MDA compared with that of wild type A. niger, implying that ΔsodC induced an attenuated response in chinese white pear during fruit–pathogen interaction. Our results indicate that sodC gene contributes to the full virulence of A. niger during infection on fruit. Aspergillus niger is one of the most common species found in fungal communities. It is an important fermentation industrial strain and is also known to cause the most severe symptoms in fruit during long-term storage (Pel et al., 2007). Meanwhile, plants activate their signaling pathways to trigger defense responses to limit pathogen expansion. One of the earliest host responses after pathogen attack is oxidative burst, during which large quantities of ROS are generated by different host enzyme systems, such as glucose oxidase (Govrin and Levine, 2000). ROS such as singlet oxygen, superoxide anion, hydroxyl (OH−), and H2O2 are released to hinder the advance of pathogens (Gara et al., 2003). ROS can react with and damage cellular molecules, such as DNA, protein, and lipids, which will limit fungal propagation in the host plant (Apel and Hirt, 2004).
Hydrogen sulfide (H2S) has been proven to be a multifunctional signaling molecule in plants. In this study, we attempted to explore the effects of H2S on the climacteric fruit tomato during postharvest storage. H2S fumigation for 1 d was found to delay the peel color transition from green to red and decreased fruit firmness induced by ethylene. Further investigation showed that H2S fumigation downregulated the activities and gene expressions of cell wall–degrading enzymes pectin lyase (PL), polygalacturonase (PG), and cellulase. Furthermore, H2S fumigation downregulated the expression of ethylene biosynthesis genes SlACS2 and SlACS3. Ethylene treatment for 1 d was found to induce the expression of SlACO1, SlACO3, and SlACO4 genes, whereas the increase was significantly inhibited by H2S combined with ethylene. Furthermore, H2S decreased the transcript accumulation of ethylene receptor genes SlETR5 and SlETR6 and ethylene transcription factors SlCRF2 and SlERF2. The correlation analysis suggested that the fruit firmness was negatively correlated with ethylene biosynthesis and signaling pathway. The current study showed that exogenous H2S could inhibit the synthesis of endogenous ethylene and regulate ethylene signal transduction, thereby delaying fruit softening and the ripening process of tomato fruit during postharvest storage.