Sclerotinia sclerotiorum catalase SCAT1 affects oxidative stress tolerance, regulates ergosterol levels and controls pathogenic development

• Sclerotinia sclerotiorum catalase 1 (Scat1) is required for normal pathogenic development.
• Scat1 function does not involve hydrogen peroxide detoxification.
• Scat1 modulates cell membrane integrity in S. sclerotiorum.
• Inactivation of Scat1 results in decreased ergosterol content.

Reactive oxygen species (ROS) are essential for pathogenic development of Sclerotinia sclerotiorum. A key question for S. sclerotiorum and many other pathogens concerns how fungi tolerate/dampen the oxidative environment during growth and pathogenesis. Regulatory components of oxidative stress include both enzymatic and non-enzymatic antioxidants. Catalases are a ubiquitous family of enzymes that play an important role in the enzymatic detoxification of ROS by converting hydrogen peroxide (H2O2) to water and molecular oxygen. The genome of the omnivorous pathogen S. sclerotiorum contains seven predicted catalase genes. In this study we evaluate and functionally characterize the type A catalase (Scat1) in S. sclerotiorum, whose expression is highly induced during host infection. Insertional inactivation of Scat1 (ΔScat1) resulted in hyperbranching of hyphae accompanied by slower growth and smaller sclerotia. ΔScat1 strains were attenuated in pathogenicity and rendered the fungus hypersensitive to Sodium dodecyl sulfate (SDS), as w