Background Spliced Leader trans-splicing is an important mechanism for the maturation of mRNAs in several lineages of eukaryotes, including several groups of parasites of great medical and economic importance. Nevertheless, its study across the tree of life is severely hindered by the problem of identifying the SL sequences that are being trans-spliced.

Results In this paper we present SLFinder, a four-step pipeline meant to identify de novo candidate SL sequences making very few assumptions regarding the SL sequence properties. The pipeline takes transcriptomic de novo assemblies and a reference genome as input and allows the user intervention on several points to account for unexpected features of the dataset. The strategy and its implementation were tested on real RNAseq data from species with and without SL Trans-Splicing.

Conclusions SLFinder is capable to identify SL candidates with good precision in a reasonable amount of time. It is especially suitable for species with unknown SL sequences, generating candidate sequences for further refining and experimental validation.

Raphidiopsis (Cylindrospermopsis) raciborskii, a globally distributed bloom-forming cyanobacterium, produces either the cytotoxin cylindrospermopsin (CYL) in Oceania, Asia and Europe or the neurotoxin saxitoxin (STX) and analogues (paralytic shellfish poison, PSP) in South America (encoded by sxt genetic cluster) and none of them in Africa. Nevertheless, this particular geographic pattern is usually overlooked in current hypotheses about the species dispersal routes. Here, we combined genomics, phylogenetic analyses, toxicity data and a literature survey to unveil the evolutionary history and spread of the species. Phylogenies based on 354 orthologous genes from all the available genomes and ribosomal ITS sequences of the taxon showed two well-defined clades: the American, having the PSP producers; and the Oceania/Europe/Asia, including the CYL producers. We propose central Africa as the original dispersion center (non-toxic populations), reaching North Africa and North America (in former Laurasia continent). The ability to produce CYL probably took place in populations that advanced to sub-Saharan Africa and then to Oceania and South America. According to the genomic context of the sxt cluster found in PSP-producer strains, this trait was acquired once by horizontal transfer in South America, where the ability to produce CYL was lost.

The CAP superfamily is a diverse group of proteins that are involved in different biological processes, yet their molecular functions are still incompletely understood. The α-β-α sandwich structure of the CAP domain is characteristic of this superfamily and several different domains may be found together with it. They are generally secreted proteins and in helminths many are secreted to the environment, and are related to the host-parasite interaction. In this work we mined cestode genomic data for members of this superfamily. Whereas in average 26 members with complete CAP domains were found in most cestodes, in Mesocestoides corti we strikingly found 271 members with complete domains, most of which show evidence of expression. We also found other truncated domains and putative pseudogenes. Interestingly, most of these genes were found in a monophyletic clade within a cestode-specific group of CAP domain containing proteins, and each cestode species has also developed independent duplications of these proteins. This pattern of extensive independent duplications can also be found in other parasitic and free-living flatworms, as well as in other metazoan phyla. Within the M. corti specific expansion, several sub-clades of these proteins showed evidence of evolution under positive selection. Our results suggest that the CAP domain containing proteins of animals evolve through a “birth and death” mechanism, and that different environmental pressures may drive this evolution in different species. In the case of helminth parasites, this could be related to the interaction between the parasite and the host, including mechanisms to evade and modulate the host immune system.