How did free-living organisms evolve into parasites?
Many living things are parasitic, perhaps the majority of organisms on Earth. Certainly, parasitism is, and always has been, a major force determining how organisms evolve and how ecosystems work. So the origin of parasitism, or origins as there have been many, is a fundamental question in biology.
We try to reconstruct how genomes changed at the moment in time when parasitism evolved by studying the differences between parasitic genomes, and between parasites and those of their closest, free-living relatives. Using this comparative approach, we examine how changes in the number of genes, their functional diversity and their distribution in the genome can be related to the process of becoming parasitism.
Our comparison of trypanosomatid genomes with that of the free-living Bodo saltans demonstrated how parasites such as Trypanosoma and Leishmania have undergone widespread genomic streamlining, as well as the origins of enigmatic cell surface glycoproteins associated with pathogenesis and life cycle transmission. Using a similar comparative approach, we are exploring the origins of Blastocystis hominis and the causes of genomic and ultrastructural reduction in this species, as well as the evolution of horizontal gene transfer in Entamoeba genomes.
Comparative genomics has in recent years stimulated a reassessment of long-cherished ideas, indeed dogmas like reductive evolution, and of ideas about how a parasitic life strategy can emerge, and what consequences this might then have.
Genomic reduction does indeed accompany the evolution of parasitism, but it is nearly always accompanied by the elaboration of pathogen-specific functions also. Genomic streamlining, the dynamic of genome-wide canalization of function, may be one typical response to a biotrophic life strategy and the narrowing of environmental stimuli that this often brings about.