Publication | Open Access
Genome of <i>Rhodnius prolixus</i> , an insect vector of Chagas disease, reveals unique adaptations to hematophagy and parasite infection
358
Citations
59
References
2015
Year
Unique AdaptationsTandem ExpansionsMicrobial PathogensGeneticsEntomologyImmunologyInsect VectorInnate Immune SystemInnate ImmunityGenomicsImmune SystemParasite GenomicsChagas DiseaseHost ResponsePublic HealthRhodnius ProlixusParasitologyHost-pathogen InteractionsHost-parasite RelationshipParasitic ProtozoaEvolutionary ImmunologyAutoimmunityImmune FunctionHost-microbe InteractionMicrobiomeBiologyImd PathwayMucosal ImmunologyImmune Cell DevelopmentPathogenesisHost ResistanceMedicine
Rhodnius prolixus is a key model for insect physiology and a major vector of Chagas disease, affecting about seven million people worldwide. The authors sequenced 95 % of its 702 Mb genome, identified 15 456 protein‑coding genes, and performed comprehensive genomic analyses of this obligate blood‑feeding insect. The genome shows a restructured IMD pathway lacking key components, extensive loss of selenoproteins, horizontally transferred Wolbachia genes, and lineage‑specific expansions in chemoreception, feeding, and digestion genes, while Toll/IMD effectors control microbiota but not Trypanosoma cruzi, providing insights for vector control.
Rhodnius prolixus not only has served as a model organism for the study of insect physiology, but also is a major vector of Chagas disease, an illness that affects approximately seven million people worldwide. We sequenced the genome of R. prolixus, generated assembled sequences covering 95% of the genome (∼ 702 Mb), including 15,456 putative protein-coding genes, and completed comprehensive genomic analyses of this obligate blood-feeding insect. Although immune-deficiency (IMD)-mediated immune responses were observed, R. prolixus putatively lacks key components of the IMD pathway, suggesting a reorganization of the canonical immune signaling network. Although both Toll and IMD effectors controlled intestinal microbiota, neither affected Trypanosoma cruzi, the causal agent of Chagas disease, implying the existence of evasion or tolerance mechanisms. R. prolixus has experienced an extensive loss of selenoprotein genes, with its repertoire reduced to only two proteins, one of which is a selenocysteine-based glutathione peroxidase, the first found in insects. The genome contained actively transcribed, horizontally transferred genes from Wolbachia sp., which showed evidence of codon use evolution toward the insect use pattern. Comparative protein analyses revealed many lineage-specific expansions and putative gene absences in R. prolixus, including tandem expansions of genes related to chemoreception, feeding, and digestion that possibly contributed to the evolution of a blood-feeding lifestyle. The genome assembly and these associated analyses provide critical information on the physiology and evolution of this important vector species and should be instrumental for the development of innovative disease control methods.
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