Publication

Genome of Rhodnius prolixus, an insect vector of Chagas disease, reveals unique adaptations to hematophagy and parasite infection.

Proc Natl Acad Sci U S A. 2015 Dec 1;112(48):14936-14941. Epub 2015 Nov 16.

Abstract

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.

Authors

Mesquita RD, Vionette-Amaral RJ, Lowenberger C, Rivera-Pomar R, Monteiro FA, Minx P, Spieth J, Carvalho AB, Panzera F, Lawson D, Torres AQ, Ribeiro JM, Sorgine MH, Waterhouse RM, Montague MJ, Abad-Franch F, Alves-Bezerra M, Amaral LR, Araujo HM, Araujo RN, Aravind L, Atella GC, Azambuja P, Berni M, Bittencourt-Cunha PR, Braz GR, Calderón-Fernández G, Carareto CM, Christensen MB, Costa IR, Costa SG, Dansa M, Daumas-Filho CR, De-Paula IF, Dias FA, Dimopoulos G, Emrich SJ, Esponda-Behrens N, Fampa P, Fernandez-Medina RD, da Fonseca RN, Fontenele M, Fronick C, Fulton LA, Gandara AC, Garcia ES, Genta FA, Giraldo-Calderón GI, Gomes B, Gondim KC, Granzotto A, Guarneri AA, Guigó R, Harry M, Hughes DS, Jablonka W, Jacquin-Joly E, Juárez MP, Koerich LB, Latorre-Estivalis JM, Lavore A, Lawrence GG, Lazoski C, Lazzari CR, Lopes RR, Lorenzo MG, Lugon MD, Majerowicz D, Marcet PL, Mariotti M, Masuda H, Megy K, Melo AC, Missirlis F, Mota T, Noriega FG, Nouzova M, Nunes RD, Oliveira RL, Oliveira-Silveira G, Ons S, Pagola L, Paiva-Silva GO, Pascual A, Pavan MG, Pedrini N, Peixoto AA, Pereira MH, Pike A, Polycarpo C, Prosdocimi F, Ribeiro-Rodrigues R, Robertson HM, Salerno AP, Salmon D, Santesmasses D, Schama R, Seabra-Junior ES, Silva-Cardoso L, Silva-Neto MA, Souza-Gomes M, Sterkel M, Taracena ML, Tojo M, Tu ZJ, Tubio JM, Ursic-Bedoya R, Venancio TM, Walter-Nuno AB, Wilson D, Warren WC, Wilson RK, Huebner E, Dotson EM, Oliveira PL.