Abstract
Trypanosoma cruzi, the etiologic agent of Chagas disease, cycles through different life stages characterized by defined molecular traits associated with the proliferative or differentiation state. In particular, T. cruzi epimastigotes are the replicative forms that colonize the intestine of the Triatomine insect vector before entering the stationary phase that is crucial for differentiation into metacyclic trypomastigotes, which are the infective forms of mammalian hosts. The transition from proliferative exponential phase to quiescent stationary phase represents an important step that recapitulates the early molecular events of metacyclogenesis, opening new possibilities for understanding this process. In this study, we report a quantitative shotgun proteomic analysis of the T. cruzi epimastigote in the exponential and stationary growth phases. More than 3000 proteins were detected and quantified, highlighting the regulation of proteins involved in different subcellular compartments. Ribosomal proteins were upregulated in the exponential phase, supporting the higher replication rate of this growth phase. Autophagy-related proteins were upregulated in the stationary growth phase, indicating the onset of the metacyclogenesis process. Moreover, this study reports the regulation of N-terminally acetylated proteins during growth phase transitioning, adding a new layer of regulation to this process. Taken together, this study reports a proteome-wide rewiring during T. cruzi transit from the replicative exponential phase to the stationary growth phase, which is the preparatory phase for differentiation.
Highlights
Cell proliferation is controlled by a series of environmental factors such as temperature, population density due to the presence of critical quantities of quorum-sensing molecules and specific growth factors, osmolarity, pH, the redox state of the environment, and the availability of essential nutrients [1,2]
This study aimed at dissecting the molecular pathways activated in T. cruzi epimastigotes upon transitioning from the exponential to the stationary phase
The parasite shows a slender shape with an elongated cellular body and flagellum (Figure 1C)
Summary
Cell proliferation is controlled by a series of environmental factors such as temperature, population density due to the presence of critical quantities of quorum-sensing molecules and specific growth factors, osmolarity, pH, the redox state of the environment, and the availability of essential nutrients [1,2]. Cells initially face a binary decision: proliferate or enter into a specialized non-dividing resting state, known as stationary/quiescent phase or G0 [3]. It is well demonstrated that under a severe metabolic stress condition known as starvation, yeasts arrest their cell cycle and enter into a G0/quiescence state that promotes persistence and survival [3]. This change is concomitant with deep modification of the cells’ structures that can yield resistance structures such as cysts or spores [4,5]. Quiescent cells become more thermotolerant and osmotolerant than their proliferating counterparts [7]
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
