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CRKs (Cdc2 Related Kinases) in Trypanosoma cruzi: unraveling their role in proliferation, metacyclogenesis and crosstalk between proliferation and cellular metabolism


Chagas Disease is caused by the protozoan parasite Trypanosoma cruzi which has the same drug of treatment since 1970, benznidazole. The lack of new drugs of treatment reflects the complexity of this parasite biology that is found in four distinct life forms with differences regarding their metabolism and replicative capacity. Infective forms are unable to replicate and this changes among life forms are triggered by environmental conditions, such as nutritional stress during metacyclogenesis. However it is not clear how this parasite blocks cellular proliferation when transitioning from replicative forms to infective/non-replicative forms. In model eukaryotes CDKs (cyclin dependent kinases) coordinate cellular proliferation and quiescence entrance. Additionally, CDKs are central in cellular metabolism crosstalk and can regulate and be regulated by cellular sensors that dictates the replicative status of the cell according to environmental conditions. In T. cruzi ten genes homologous to CDKs, which are denominated CRKs (Cdc2 related kinases), are identified in the genome sequence. From them, only two have been partially characterized regarding cell cycle regulation (CRK1 and 3). Once cellular proliferation control is essential for T. cruzi differentiation among life forms and knowing that these transitions are connected with changes in cellular metabolism, this proposal aims to unveil CRK1 and 3 functions in controlling cellular proliferation, entrance in quiescence during metacyclogenesis and its possible role in metabolism crosstalk. Using cutting-edge techniques such as CRISPR/Cas9 and TurboID will be possible to establish CRKs expression, location and interactors through cell cycle and metacyclogenesis. (AU)

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