Dataset Information

Proteomics of intracellular amastigotes and axenic culture amastigote-like life forms of Trypanosoma cruzi in replicative and non-replicative conditions

ABSTRACT: Analysis of replicative and non-replicative conditions of trypanosoma cruzi amastigote lifeform.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (ncbitaxon:9606) Trypanosoma Cruzi (ncbitaxon:5693)

SUBMITTER: Carlos Adnre Ornelas Ricart

PROVIDER: MSV000098494 | MassIVE | Sat Jul 12 15:03:00 BST 2025

SECONDARY ACCESSION(S): PXD066080

REPOSITORIES: MassIVE

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Quantitative proteomics of intracellular and axenic amastigote-like forms of Trypanosoma cruzi under replicative and non-replicative conditions.

Melo Reynaldo Magalhães RM de Souza Agnelo Rodrigues AR Dos Santos Júnior Agenor de Castro Moreira ACM Lopes Tarcila Zuleica Zaparolli TZZ Santana Jaime Martins JM Bastos Izabela Dourado ID Motta Flavia Nader FN de Souza Jaques Miranda Ferreira JMF Charneau Sébastien S de Sousa Marcelo Valle MV Fontes Wagner W de Lima Beatriz Dolabela BD Ricart Carlos André Ornelas CAO

Journal of proteomics 20260227

Trypanosoma cruzi, the etiologic agent of Chagas disease, has a complex life cycle that involves both arthropods and mammals. Amastigotes are the T. cruzi life forms capable of replication in mammalian hosts. Here we report a quantitative LC-MS/MS-based proteomics of intracellular amastigotes (AI) and amastigote-like forms produced in axenic cultures. AI were purified from T. cruzi-infected HeLa cells using DEAE-cellulose, whereas three different axenic amastigote-like forms were produced as fol ...[more]

PMID: 41765178

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Project description:Trypanosoma cruzi is a protozoan parasite etiological agent of the vector-borne disease American trypanosomiasis, also known as Chagas disease. During its life cycle, T. cruzi undergoes some fundamental processes: metacyclogenesis (transition from epimastigote to metacyclic trypomastigote form) – occurring in the invertebrate host, amastigogenesis (transition from trypomastigote to amastigote form) and trypomastigogenesis (transition from amastigote to trypomastigote form) – both occurring within nucleated cells of the mammalian host, and finally epimastigogenesis (transition from trypomastigote to epimastigote forms) – which occurs as soon as the invertebrate host ingests trypomastigote forms during the bloodmeal. The precise mechanisms that regulate these processes remain elusive but certainly depend on kinases. The canonical function of the inositol hexakisphosphate kinases (IP6Ks) is to phosphorylate the phosphate groups from inositol hexaphosphate (IP6), leading to the formation of inositol pyrophosphates (PP-IPs). However, recent studies have been describing non-canonical functions for this kinase family. Here, after disrupting a single IP6K allele of T. cruzi and confirming its downregulation, we observed that the life cycle of this parasite was profoundly impaired. Epimastigote forms of T. cruzi IP6K-deficient showed morphological alterations, increased population presenting a dormant-like state (quiescence), and a reduced differentiation capacity during metacyclogenesis. The restricted metacyclic forms of T. cruzi IP6K-deficient that were able to differentiate had reduced infective potential (invasion rate) in human cardiomyocytes. Interestingly, 120 h after infection, the amastigote forms of T. cruzi IP6K-deficient showed an impaired ability to transform into trypomastigotes, with most of the population egressing from human cardiomyocytes without completing trypomastigogenesis. Transcriptomic data show that the levels of surface proteins (mucins and trans-sialidases) were altered in both epimastigote and trypomastigote forms in response to the low levels of IP6K, which helps explain our findings. Finally, we observed that the few trypomastigote forms of T. cruzi IP6K-deficient that egressed from human cardiomyocytes could not complete the epimastigogenesis. Together, our findings strongly suggest that IP6K is critical to sustain the T. cruzi life cycle. Thus, as the disruption of both IP6K alleles did not generate viable parasites and the similarity relative to its human homolog is ~15%, this kinase could be a potential target for drug development against Chagas disease.