Abstract
Trypanosoma cruzi is a flagellated protozoan that causes Chagas disease; it presents a complex life cycle comprising four morphological stages: epimastigote (EP), metacyclic trypomastigote (MT), cell-derived trypomastigote (CDT) and amastigote (AM). Previous transcriptomic studies on three stages (EPs, CDTs and AMs) have demonstrated differences in gene expressions among them; however, to the best of our knowledge, no studies have reported on gene expressions in MTs. Therefore, the present study compared differentially expressed genes (DEGs), and signaling pathway reconstruction in EPs, MTs, AMs and CDTs. The results revealed differences in gene expressions in the stages evaluated; these differences were greater between MTs and AMs-PTs. The signaling pathway that presented the highest number of DEGs in all the stages was associated with ribosomes protein profiles, whereas the other related pathways activated were processes related to energy metabolism from glucose, amino acid metabolism, or RNA regulation. However, the role of autophagy in the entire life cycle of T. cruzi and the presence of processes such as meiosis and homologous recombination in MTs (where the expressions of SPO11 and Rad51 plays a role) are crucial. These findings represent an important step towards the full understanding of the molecular basis during the life cycle of T. cruzi.
Highlights
Trypanosoma cruzi is a flagellated protozoan that causes Chagas disease, and it is estimated to affect approximately 8 million individuals worldwide (OMS, 2019; Rassi & De Rezende, 2012)
When cell-derived trypomastigote (CDT) were compared with metacyclic trypomastigote (MT), 2,108 genes were down-regulated and 1,972 were up-regulated, whereas when EPs were compared with MTs, 1,739 were down-regulated and 2,188 were up-regulated, and AMs compared to MTs, 1,732 were down-regulated and 1,917 were up-regulated (Table S2)
The distribution analysis of FPKM values across individual samples revealed that transcriptomes with the highest number of genes and the highest FPKM value corresponded to MTs, followed by AMs and CDTs, whereas the lowest FPKM value was observed for EPs and MTs (Fig. 1B)
Summary
Trypanosoma cruzi is a flagellated protozoan that causes Chagas disease, and it is estimated to affect approximately 8 million individuals worldwide (OMS, 2019; Rassi & De Rezende, 2012). T. cruzi has a complex life cycle comprising four well-differentiated morphological stages—epimastigote (EP), amastigote (AM), cell-derived trypomastigote (CDT) and metacyclic trypomastigote (MT), that circulate among several mammals, such as humans and vectors from the Reduviidae family (Goldenberg & Avila, 2011). In the rectal blister of the insect and because of nutritional stress, EPs adhere to the perimicrovilar film of the epithelial cells of the insect and transform into MTs, which are the infectious stages of T. cruzi. They are characterized by their mobility but not replication. The process through which EPs transform into MTs is called metacyclogenesis, and it involves multiple changes in the parasite such as modifications in nucleus and the kinetoplast location, increases in heterochromatin, elongation of the cytoplasm, increases in the flagellum pocket in the cytoplasm, and increases in the expressions of proteins mainly associated with virulence (e.g., transialidase-like GP63, mucins and mucin-associated surface proteins (MASP)) (Avila et al, 2003; Bayer-Santos et al, 2013; Contreras, Morel & Goldenberg, 1985; Ferreira et al, 2008)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
