Genetic blueprint of the zoonotic pathogen Toxocara canis

Abstract

Toxocara canis is a zoonotic parasite of major socioeconomic importance worldwide. In humans, this nematode causes disease (toxocariasis) mainly in the under-privileged communities in developed and developing countries. Although relatively well studied from clinical and epidemiological perspectives, to date, there has been no global investigation of the molecular biology of this parasite. Here we use next-generation sequencing to produce a draft genome and transcriptome of T. canis to support future biological and biotechnological investigations. This genome is 317 Mb in size, has a repeat content of 13.5% and encodes at least 18,596 protein-coding genes. We study transcription in a larval, as well as adult female and male stages, characterize the parasite's gene-silencing machinery, explore molecules involved in development or host-parasite interactions and predict intervention targets. The draft genome of T. canis should provide a useful resource for future molecular studies of this and other, related parasites.

Figure 1. Gene orthology.

Venn diagram showing the number of orthologs between Toxocara canis and four other nematode species, Ascaris suum, Brugia malayi, Caenorhabditis elegans and Pristionchus pacificus upon pairwise comparison.

Figure 2. Stage-, gut- and gender-enriched transcription.

Key biological pathways or processes in Toxocara canis, for which the gene transcription is enriched in adult females (red) and males (blue); in adults and third-stage larvae (L3; grey); and in the alimentary tract of the adult worms (black box, top left). Molecules enriched in L3s and involved in parasite–host interactions, such as immunomodulation, are also indicated (black box, bottom left; ANT, abundant new transcripts); the number of genes with significantly increased transcription are given in parentheses. The proposed arrested or dauer status of the L3 stage of T. canis (from embryontated eggs) is supported by the transcription profiles (heat-map, right) for gene homologues daf-9, daf-12 and osm-3, osm-6 (upregulation; yellow) and two mek-2 paralogs (downregulation; orange to red), which are all known to promote dauer in C. elegans; the biological replicates (1–4) studied are indicated to the right of the heat-map.