Prion Proteins and HSPs Involved in the Stress Control Response in Trichophyton rubrum

• Grant number: 25/14311-5
• Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
• Start date: December 01, 2025
• End date: January 31, 2029
• Field of knowledge: Biological Sciences - Genetics - Molecular Genetics and Genetics of Microorganisms
• Principal Investigator: Nilce Maria Martinez-Rossi
• Grantee: Maria Júlia Santos Saboya Pereira
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

Trichophyton rubrum is currently the main cause of dermatophytosis worldwide. Understanding the molecular pathways that coordinate its biology is fundamental to understanding and expanding knowledge about pathogenicity in fungi. Some important characteristics, such as the differential expression of stress response genes, provide adaptive value for fungi to be able to maintain themselves and proliferate in the presence of conditions imposed by the parasite-host dynamic. Knowing this, the choice of molecules central to the processes of resistance, virulence and response to stress becomes essential as a target for study. Heat Shock Proteins (HSPs) are used by fungi to respond to stress, since their main functions are related to signal transduction, disaggregation of protein complexes and correct folding of proteins. In addition, Prion Proteins are becoming increasingly relevant due to their properties as infection-causing proteins that do not follow the Mendelian genetic model in their replication in yeasts and filamentous fungi. These protein classes are associated due to the disaggregase action of HSPs, mainly the Hsp104 complex with Hsp70/Hsp40, which also act on aggregates formed by prions.Therefore, the integrated study between them is of paramount importance for understanding new stress response pathways. We will carry out an in-depth investigation into the mechanisms involved in controlling the gene expression of HSPs and prion proteins in T. rubrum in response to abiotic cellular stress and in infection models. (AU)