Reevaluation of the Toxoplasma gondii and Neospora caninum genomes reveals misassembly, karyotype differences, and chromosomal rearrangements

  1. Carlos Robello1,4
  1. 1Laboratory of Host Pathogen Interactions–Molecular Biology Unit, Institut Pasteur de Montevideo, 11400 Montevideo, Uruguay;
  2. 2Laboratory of Apicomplexan Biology, Institut Pasteur de Montevideo, 11400 Montevideo, Uruguay;
  3. 3Departamento de Parasitología y Micología, Facultad de Medicina–Universidad de la República, 11600 Montevideo, Uruguay;
  4. 4Departamento de Bioquímica, Facultad de Medicina–Universidad de la República, 11300 Montevideo, Uruguay
  • Corresponding authors: mfrancia{at}pasteur.edu.uy; robello{at}pasteur.edu.uy
  • Abstract

    Neospora caninum primarily infects cattle, causing abortions, with an estimated impact of a billion dollars on the worldwide economy annually. However, the study of its biology has been unheeded by the established paradigm that it is virtually identical to its close relative, the widely studied human pathogen Toxoplasma gondii. By revisiting the genome sequence, assembly, and annotation using third-generation sequencing technologies, here we show that the N. caninum genome was originally incorrectly assembled under the presumption of synteny with T. gondii. We show that major chromosomal rearrangements have occurred between these species. Importantly, we show that chromosomes originally named Chr VIIb and VIII are indeed fused, reducing the karyotype of both N. caninum and T. gondii to 13 chromosomes. We reannotate the N. caninum genome, revealing more than 500 new genes. We sequence and annotate the nonphotosynthetic plastid and mitochondrial genomes and show that although apicoplast genomes are virtually identical, high levels of gene fragmentation and reshuffling exist between species and strains. Our results correct assembly artifacts that are currently widely distributed in the genome database of N. caninum and T. gondii and, more importantly, highlight the mitochondria as a previously oversighted source of variability and pave the way for a change in the paradigm of synteny, encouraging rethinking the genome as basis of the comparative unique biology of these pathogens.

    Footnotes

    • Received March 10, 2020.
    • Accepted December 16, 2020.

    This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see https://genome.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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