The remarkable diversity of action and specificity exerted by animal venoms is tightly linked to the prevalence of the different component toxins. The evolution of venoms is thus the story of how toxins arise and the processes that generate and maintain their diversity. For animal venoms these processes include recruitment for expression in the venom gland, neofunctionalization, paralogous expansions and functional divergence1. The systematic study of these processes requires the reliable identification the venom components involved in antagonistic interactions. While -omic approaches have the potential of uncovering the entire set of toxins in a given organism, the existence of non-venom toxin homologs and the misleading effect of partial census of the intragenome molecular diversity of toxins make necessary to collect complementary evidence to distinguish true toxins from their non-venom homologs. Here we analyzed the whole genomes of two scorpions, one spider and one snake aiming at the identification of the full repertoire of toxin-like protein coding genes. We classified the entire set protein coding genes into paralogous groups and monotypic genes, identified the toxin-like protein coding genes based on known toxin families, and quantified their expression in both venom-glands and pooled tissues. Our results confirm that toxin-like protein coding genes in a range of venomous animals are part of multigene families originated by recruitment events from non-toxin paralogs and followed by expansions of the toxin-like protein coding genes. However, we also show that failing to account for sequence similarity with non-toxin proteins has a considerable misleading effect that can be greatly reduced by comparative transcriptomics.
Acknowledgments: Research funded by a Marie Skowldowska-Curie / Pres-SUD grant (Cofund No. 246556). This contribution greatly benefited from discussions carried out at a NESCent catalysis meeting and the SICB’s symposium on Integrative and Comparative Biology of Venom organized by M. Daly and L. Gibbs.