Abstract
ABSTRACT Metacyclogenesis is one of the most important processes in the life cycle of Trypanosoma cruzi. In this stage, noninfective epimastigotes become infective metacyclic trypomastigotes. However, the transcriptomic changes that occur during this transformation remain uncertain. Illumina RNA-sequencing of epimastigotes and metacyclic trypomastigotes belonging to T. cruzi DTU I was undertaken. Sequencing reads were aligned and mapped against the reference genome, differentially expressed genes between the two life cycle stages were identified, and metabolic pathways were reconstructed. Gene expression differed significantly between epimastigotes and metacyclic trypomastigotes. The cellular pathways that were mostly downregulated during metacyclogenesis involved glucose energy metabolism (glycolysis, pyruvate metabolism, the Krebs cycle, and oxidative phosphorylation), amino acid metabolism, and DNA replication. By contrast, the processes where an increase in gene expression was observed included those related to autophagy (particularly Atg7 and Atg8 transcripts), corroborating its importance during metacyclogenesis, endocytosis, by an increase in the expression of the AP-2 complex subunit alpha, protein processing in the endoplasmic reticulum and meiosis. Study findings indicate that in T. cruzi metacyclic trypomastigotes, metabolic processes are decreased, and expression of genes involved in specific cell cycle processes is increased to facilitate transformation to this infective stage.
Highlights
Trypanosoma cruzi is a protozoan parasite that causes Chagas disease and is a serious public health problem in the Americas [1]
The T. cruzi life cycle in insects begins when a triatomine bug ingests blood from mammals with cell-derived trypomastigotes (CDTs) circulating in the per ipheral blood, which differentiate into noninfective replicative epimastigotes (EPs)
The highest meta cyclic trypomastigotes (MTs) concentration corresponded to an average of 5.35 × 108 trypomastigotes/mL on day 7 postculture; from day 7 onwards, the number of MTs decreased until reaching an average MT concen tration of 1.75 × 108 trypomastigotes/mL after 10 days post-infection (Figure S1)
Summary
Trypanosoma cruzi is a protozoan parasite that causes Chagas disease and is a serious public health problem in the Americas [1]. The T. cruzi life cycle in mammals begins when meta cyclic trypomastigotes (MTs), an infectious form, present in the vector’s feces reach peripheral blood through the skin wound caused by the triatomine during a blood meal and infect mononuclear cells, such as monocytes. MTs differentiate into amastigotes, which are non-mobile replicative forms that undergo multiple rounds of division until transforming into cell-derived trypomastigotes (CDTs). The latter lyses the cells and migrate to infect other cells or tissues for which they have a high tropism [2,3]. Some of the events carried out during metacy clogenesis remain unclear, the main stimulus is exposure of EPs to a poor nutritional environment that is rich in redox stress, leading to increased adenylate cyclase activ ity and consequent rise of intracellular cAMP levels in the parasite [4,5]
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