How are parasite genomes adapted for a parasitic way of life?

 

The genome includes all the genetic material in a single living cell. Although we do not understand all of the functions of a given parasite genome, they nonetheless have the potential to explain how and why the parasite behaves as it does.

The genome is also a historical document, a record of the important events that have happened in the deep evolutionary past, which have shaped the organism we see today. So, we produce genome sequences, and study their contents, in order to understand how the parasite causes disease, but also how these mechanisms evolved in the first place.

We use the latest long-read DNA sequencing technologies to produce highly complete and contiguous genome sequences, and by curating these sequences to a high standard using a range of manual and automated techniques that locate and identify genes.

In the past we produced genome and transcriptome sequences for African trypanosomes (Trypanosoma spp.), blood parasites that cause diseases in humans and animals across sub-Saharan African, and across the world. To explore the qualities of trypanosome genomes that enable parasitism, we added genome sequences for the related kinetoplastids Bodo saltans and Trypanoplasma borreli.

Similar projects exploring the genomic origins of other types of eukaryotic parasite are in progress. We are studying Proteromonas lacertae, a commensal organism of lizards to examine the evolution of the human intestinal parasite Blastocystis hominii, and the free-living Mastigella sp. to illuminate the origins of another intestinal pathogen, Entamoeba histolytica. A genome sequence for the bovine parasite Tritrichomonas foetus, a distinct relative of the human pathogen Trichomonas vaginalis, is being developed to design vaccine candidates for bovine trichomoniasis.

Our genomic studies have revealed unique features of parasites that play vital roles in pathogenesis and virulence. Features like the enigmatic VSG genes in African trypanosomes, and pir and sicaVAR genes in malaria parasites (Plasmodium spp.), which play pivotal roles in the immune interaction between host and pathogen. Our comparison of parasitic and free-living kinetoplastids discovered how a single ancestral gene family (‘bodonin’) gave rise to diverse, and now virtually incomparable, parasite-specific gene families with very distinct functions.

Even before the advent of parasite genome sequences, we would have predicted that they would be finely adapted to exploit and manipulate their hosts. So it has proven. The structures and contents of parasite genomes reflect their needs: to survive host immunity, scavenge nutrients and transmit to the next host.

Enquiries:

Jackson Laboratory
Institute of Infection and Global Health
University of Liverpool
146 Brownlow Hill
Liverpool L3 5RF
United Kingdom

a.p.jackson@liv.ac.uk
+44 (0) 151 795 0225