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| Author(s): |
Bruno Alves Santarossa
Total Authors: 1
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| Document type: | Master's Dissertation |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) |
| Defense date: | 2024-10-14 |
| Examining board members: |
Simone Guedes Calderano;
Rodrigo da Silva Galhardo;
Carlos Renato Machado
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| Advisor: | Simone Guedes Calderano |
| Abstract | |
Trypanosoma cruzi is a clinically relevant protozoan, causing Chagas disease. Its endemic characteristic in emerging countries is an important context for understanding why it is still, proportionally to other model eukaryotes, very poorly understood. The various changes that this parasite undergoes throughout its life cycle indicate a high degree of complexity in the regulation of cellular mechanisms, with cell cycle progression control being especially important for halting replication and during cell cycle progression in replicative forms. In model eukaryotes, CDK (cyclin-dependent kinase) cyclins regulate cell cycle progression, as well as lead to the halt of cell replication in situations of nutrient deprivation and mitogenic stimulus absence. In T. cruzi, homologous genes to CDK1 have been identified, named CRKs (Cdc2 related kinases), and among these, the enzyme CRK3 is involved in cell cycle regulation. This work will show the validation of CRISPR/Cas9-modified strains, CRK3 expression throughout the cell cycle, its localization during the cell cycle and metacyclogenesis, its expression during metacyclogenesis, and some attempts with the TurboID experiment. (AU) | |
| FAPESP's process: | 22/05264-5 - CRK3 (Cdc2 Related Kinase): Uncovering modulation pathways linked to cell cycle and metacyclogenesis in Trypanosoma cruzi |
| Grantee: | Bruno Alves Santarossa |
| Support Opportunities: | Scholarships in Brazil - Master |