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Peer-reviewedCC BYNature Communications

Trypanosoma cruzi cell atlas as a single-cell resource for understanding parasite population heterogeneity and differentiation

  • Ross F Laidlaw1,2
  • Marta García-Sánchez3
  • Juliana da Silva Pacheco3
  • Luciana S. Paradela3
  • Thomas D. Otto4,5,6
  • Manu De Rycker7
7 affiliations
  1. 1Leiden University Medical Centre, Leiden, The Netherlands
  2. 2School of Infection and Immunity, University of Glasgow, Glasgow, UK
  3. 3Drug Discovery Unit, Faculty of Life Sciences, University of Dundee, Dundee, UK
  4. 4Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany. [email protected]
  5. 5School of Infection and Immunity, University of Glasgow, Glasgow, UK. [email protected]
  6. 6University of Hamburg, Hamburg, Germany. [email protected]
  7. 7Drug Discovery Unit, Faculty of Life Sciences, University of Dundee, Dundee, UK. [email protected]
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Abstract

Trypanosoma cruzi, the causative agent of Chagas disease, exhibits a complex life cycle with multiple hosts, stages and differentiation steps. We present a cell atlas for the T. cruzi life cycle, based on single cell transcriptomes for over 31,000 cells and population-based transcriptomics. The atlas reveals many life cycle associated genes and can be utilised to accurately annotate life cycle stages. It provides detailed insights into cell heterogeneity, including cell-specific repertoires of surface antigens in trypomastigotes, with key implications for immune responses. Enabled by single-cell resolution, we define the transcriptomic changes that occur across the epimastigote to metacyclic trypomastigote differentiation axis. Furthermore, we provide comprehensive UTR annotation, identifying previously unannotated transcripts as well as revealing alternative polyadenylation and an unanticipated complexity of reverse strand and antisense transcripts. This T. cruzi atlas provides a comprehensive resource and unlocks a range of new avenues for research on this important human pathogen.

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Cite

BibTeXRIS
BibTeX
@article{laidlaw2026trypanosoma,
  title = {{Trypanosoma cruzi cell atlas as a single-cell resource for understanding parasite population heterogeneity and differentiation}},
  author = {Ross F Laidlaw and Marta García-Sánchez and Juliana da Silva Pacheco and Luciana S. Paradela and Thomas D. Otto and Manu De Rycker},
  journal = {Nature Communications},
  year = {2026},
  month = may,
  doi = {10.1038/s41467-026-73098-w},
  url = {https://doi.org/10.1038/s41467-026-73098-w},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Trypanosoma cruzi cell atlas as a single-cell resource for understanding parasite population heterogeneity and differentiation
AU  - Ross F Laidlaw
AU  - Marta García-Sánchez
AU  - Juliana da Silva Pacheco
AU  - Luciana S. Paradela
AU  - Thomas D. Otto
AU  - Manu De Rycker
PY  - 2026
DA  - 2026/05/25
JO  - Nature Communications
DO  - 10.1038/s41467-026-73098-w
UR  - https://doi.org/10.1038/s41467-026-73098-w
AB  - Trypanosoma cruzi, the causative agent of Chagas disease, exhibits a complex life cycle with multiple hosts, stages and differentiation steps. We present a cell atlas for the T. cruzi life cycle, based on single cell transcriptomes for over 31,000 cells and population-based transcriptomics. The atlas reveals many life cycle associated genes and can be utilised to accurately annotate life cycle stages. It provides detailed insights into cell heterogeneity, including cell-specific repertoires of surface antigens in trypomastigotes, with key implications for immune responses. Enabled by single-cell resolution, we define the transcriptomic changes that occur across the epimastigote to metacyclic trypomastigote differentiation axis. Furthermore, we provide comprehensive UTR annotation, identifying previously unannotated transcripts as well as revealing alternative polyadenylation and an unanticipated complexity of reverse strand and antisense transcripts. This T. cruzi atlas provides a comprehensive resource and unlocks a range of new avenues for research on this important human pathogen.
SN  - 2041-1723
ER  -