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Complement C2 receptor inhibitor trispanning: from man to schistosome
1Immunonephrology, Department of Research, University Hospital Basel, Basel, Switzerland. jameel.inal@unibas.ch
Springer Seminars in Immunopathology
|October 20, 2005
Summary
Horizontal gene transfer (HGT) may explain how the CRIT gene, found in humans and parasites like Schistosoma, evolved. This genetic transfer between hosts and parasites is a poorly understood but significant evolutionary mechanism.
Area of Science:
- Genetics
- Evolutionary Biology
- Parasitology
Background:
- The complement inhibitor CRIT was initially identified in human parasites like Schistosoma and Trypanosoma cruzi.
- CRIT gene distribution spans diverse species, including fish, rodents, and humans, suggesting a broader evolutionary role.
Purpose of the Study:
- To investigate the evolutionary origins of the CRIT gene in humans and parasites.
- To test the hypothesis of host-to-parasite horizontal gene transfer (HGT) as the mechanism for CRIT acquisition in schistosomes.
Main Methods:
- Phylogenetic analysis of CRIT genes at the nucleotide level to assess evolutionary distances.
- Comparative analysis of CRIT gene function, protein structure, and genomic organization between species.
Main Results:
- Phylogenetic analysis revealed significant evolutionary proximity between human and Schistosoma CRIT genes.
- Identical function, high nucleotide/amino acid identity, and similar secondary protein structures were observed for CRIT across species.
- Genomic organization of CRIT was found to be identical between human and schistosome parasites.
Conclusions:
- The data strongly support the hypothesis that CRIT in humans and schistosomes is orthologous.
- Host-to-parasite HGT is proposed as the likely mechanism for the presence of CRIT in schistosomes.
- This study highlights HGT as a significant, yet under-described, factor in host-parasite co-evolution.