Knockout of the CCCH zinc finger protein TcZC3H31 blocks Trypanosoma cruzi differentiation into the infective metacyclic form

Publication date: April 2018 Source:Molecular and Biochemical Parasitology, Volume 221 Author(s): Monica Visnieski Alcantara, Rafael Luis Kessler, Rosana Elisa Gonçalves Gonçalves, Newmar Pinto Marliére, Alessandra Aparecida Guarneri, Gisele Fernanda Assine Picchi, Stenio Perdigão Fragoso In the protozoan parasite Trypanosoma cruzi – the causative agent of Chagas disease − gene expression control is mainly post-transcriptional, where RNA-binding proteins (RBPs) play a central role, by controlling mRNA stability, distribution and translation. A large variety of RBPs are encoded in the T. cruzi genome, including the CCCH-type zinc finger (CCCH ZnF) protein family, which is characterized by the presence of the C-X7/8-C-X5-C-X3-H (CCCH) motif. In the related parasite T. brucei, CCCH ZnF proteins have been shown to control key differentiation steps in the parasite’s life cycle. However, little is known about the CCCH ZnF proteins in T. cruzi. We have worked on the generation of T. cruzi mutants for CCCH ZnF proteins in an effort to shed light on the functions of these proteins in this parasite. Here, we characterize the expression and function of the CCCH ZnF protein TcZC3H31 of T. cruzi. TcZC3H31 is almost exclusively expressed in epimastigotes and metacyclic trypomastigotes, the parasite forms found in the invertebrate host. Importantly, we show that the epimastigote form of the T. cruzi knockout for the TcZC3H31 gene (TcZC3H31 KO) is incapable, both in vitro ...
Source: Molecular and Biochemical Parasitology - Category: Parasitology Source Type: research