ORIGINAL RESEARCH article
Front. Cell. Infect. Microbiol.
Sec. Parasite and Host
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1584812
Stage-Specific MCM Protein Expression in Trypanosoma cruzi: Insights Into Metacyclogenesis and G1 Arrested epimastigotes
Provisionally accepted
Bruno Alves Santarossa1
Évelin Mariani1Artur da Paixão Corrêa1
Fernanda Cristina Costa2
Martin Craig Taylor2
John Kelly2
Maria Carolina Elias1
Simone Guedes Calderano1*- 1Laboratório de Ciclo Celular, Instituto Butantan, São Paulo, Rio Grande do Sul, Brazil
- 2Department of Infection Biology, Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom
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Trypanosoma cruzi is a protozoan parasite that is the etiological agent of Chagas disease, which is endemic to Latin America with reported cases in non-endemic regions such as Europe, Asia, and Oceania due to migration. During its lifecycle, T. cruzi alternates between replicative and non-replicative infective lifeforms. Metacyclogenesis is the most studied transition of T. cruzi life cycle, wherein which replicative epimastigotes differentiate into infective metacyclic trypomastigotes inside the gut of the triatomine vector. This early-branching organism presents a divergent pre-replication complex (pre-RC) where the only conserved component is the MCM2-7 protein family. Given the role of pre-RC components in cell cycle regulation, we investigated whether MCM expression and location could be involved in proliferation control in epimastigotes and during metacyclogenesis. Our findings reveal that MCM subunits are consistently expressed and localized to the nucleus throughout the epimastigote cell cycle, including in G1/G0arrested cells. However, MCM subunitsproteins are degraded during metacyclogenesis as Formatted: Font: Italic cells enter the G0 state, marking the transition to replication arrest. Therefore, epimastigotes arrested in G1/G0 can either maintain MCM complex expression and resume the cell cycle when conditions become favorable, or they can undergo metacyclogenesis, exiting the cell cycle and entering a G0 state, where MCM subunits are degraded as part of the replication repression mechanism.
Keywords: mini-chromosome maintenance, MCM, Trypanosoma cruzi, Metacyclogenesis, replication control, G0, G1 arrest, cell cycle arrest
Received: 27 Feb 2025; Accepted: 16 Apr 2025.
Copyright: © 2025 Santarossa, Mariani, Corrêa, Costa, Taylor, Kelly, Elias and Calderano. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Simone Guedes Calderano, Laboratório de Ciclo Celular, Instituto Butantan, São Paulo, Rio Grande do Sul, Brazil
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