The transcription factor AP-1 regulates the catalase family and oxidative stress adaptation in the dermatophyte Trichophyton rubrum.

Oxidative stress results from an imbalance between the production of reactive oxygen species and cellular antioxidant activity, thereby causing cellular damage. In Saccharomyces cerevisiae, the Basic Leucine Zipper (bZIP) transcription factor AP-1 plays a key regulatory role in antioxidant responses. In Trichophyton rubrum, oxidative stress is countered by antioxidant enzymes and three main regulators: the HOG pathway, AP-1, and SKN7. Here, we investigated the role of AP-1 using a Δap1 mutant of T. rubrum exposed to hydrogen peroxide or menadione. RT-qPCR revealed higher expression of HOG-pathway genes and lower expression of skn7 and catalase genes in the Δap1 mutant under oxidative stress conditions, together with reduced catalase activity. Lipid peroxidation assays indicated greater oxidative damage in the mutants, particularly after menadione exposure. In silico analysis identified an AP-1 consensus binding site in the catalase gene TERG_02005. Post-transcriptional analysis revealed alternative splicing events, specifically intron retention, both in TERG_02005 and in genes related to the spliceosome machinery, which also contained predicted AP-1 binding sites. These findings indicate that AP-1 plays a role in regulating oxidative stress-responsive genes in T. rubrum, particularly those that code for catalase. Additionally, AP-1 may influence spliceosome function, linking transcriptional and post-transcriptional responses to oxidative stress.