The bZIP Ap1 transcription factor is a negative regulator of virulence attributes of the anthropophilic dermatophyte .

is a fungus that causes chronic skin and nail infections in healthy individuals and immunocompromised patients. During infection, invades host cutaneous tissues by adapting to the acidic pH and the innate immune response of the host. Several genes are upregulated during the growth of in substrates found in human tissue, including the gene, which codes for the transcription factor Ap1. Here, we generated a null mutant strain by deleting the gene and performed a functional analysis of this gene. Our results showed that the Δmutant increased its growth in nail fragments and co-cultures with keratinocytes compared to the wild type. Furthermore, the mutant displayed hyperpigmentation, thickening of the conidia cell wall, increased conidia susceptibility to calcofluor-white compared to the wild type, and loss of control of the keratinolytic activity. Although the gene was upregulated during exposure to the antifungal drugs amphotericin B, nystatin, and terbinafine, its deletion did not alter the fungal susceptibility to these drugs, revealing the role of the gene in the physiological response to the stress caused by these drugs, but not in their resistance. Moreover, was also involved in the oxidative stress response caused by menadione, but not paraquat or hydrogen peroxide. These findings indicate that the gene plays a role in the negative control of virulence-related attributes and may contribute to the chronicity of nail infection caused by .