Deletion of Cu/Zn superoxide dismutase gene sodC reduces aspergillus niger virulence on Chinese white pear

Abstract

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 importantmetal 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-SODencoding 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 undermenadione 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 ofH2O2 andmalondialdehyde (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, andMDA 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-), andH2 O2 are released to hinder the advance of pathogens (Gara et al., 2003). ROS can react with and damage cellularmolecules, such as DNA, protein, and lipids, which will limit fungal propagation in the host plant (Apel and Hirt, 2004).