Article
Genome of the Avirulent Human-Infective Trypanosome—Trypanosoma rangeli
Registro en:
STOCO, Patrıcia Hermes et al. Genome of the Avirulent Human-Infective Trypanosome—Trypanosoma rangeli. PLoS Negl Trop Dis, v. 8, n. 9, p. e3176.
1553-7366
Public Library of Science
Autor
Stoco, Patrícia Hermes
Wagner, Glauber
Talavera-Lopez, Carlos
Gerber, Alexandra
Zaha, Arnaldo
Thompson, Claudia Elizabeth
Bartholomeu, Daniella Castanheira
Luckemeyer, Debora Denardin
Bahia, Diana
Loreto, Elgion
Prestes, Elisa Beatriz
Lima, Fabio Mitsuo
Rodrigues Luiz, Gabriela
Vallejo, Gustavo Adolfo
Silveira Filho, Jose Franco da
Schenkman, Sergio
Monteiro, Karina Mariante
Tyler, Kevin Morris
Almeida, Luiz Gonzaga Paula de
Ortiz, Mauro Freitas
Chiurillo, Miguel Angel
Moraes, Milene Hoehr de
Cunha, Oberdan de Lima
Mendonça Neto, Rondon
Silva, Rosane
Teixeira, Santuza Maria Ribeiro
Murta, Silvane Maria Fonseca
Sincero, Thais Cristine Marques
Mendes, Tiago Antonio de Oliveira
Urmenyi, Turan Peter
Silva, Viviane Grazielle
Rocha, Wanderson Duarte Da
Andersson, Bjorn
Romanha, Alvaro Jose
Steindel, Mario
Vasconcelos, Ana Tereza Ribeiro de
Grisard, Edmundo Carlos
Resumen
BACKGROUND:Trypanosoma rangeli is a hemoflagellate protozoan parasite infecting humans and other wild and domestic mammals across Central and South America. It does not cause human disease, but it can be mistaken for the etiologic agent of Chagas disease, Trypanosoma cruzi. We have sequenced the T. rangeli genome to provide new tools for elucidating the distinct and intriguing biology of this species and the key pathways related to interaction with its arthropod and mammalian hosts.
METHODOLOGY/PRINCIPAL FINDINGS:The T. rangeli haploid genome is ∼ 24 Mb in length, and is the smallest and least repetitive trypanosomatid genome sequenced thus far. This parasite genome has shorter subtelomeric sequences compared to those of T. cruzi and T. brucei; displays intraspecific karyotype variability and lacks minichromosomes. Of the predicted 7,613 protein coding sequences, functional annotations could be determined for 2,415, while 5,043 are hypothetical proteins, some with evidence of protein expression. 7,101 genes (93%) are shared with other trypanosomatids that infect humans. An ortholog of the dcl2 gene involved in the T. brucei RNAi pathway was found in T. rangeli, but the RNAi machinery is non-functional since the other genes in this pathway are pseudogenized. T. rangeli is highly susceptible to oxidative stress, a phenotype that may be explained by a smaller number of anti-oxidant defense enzymes and heat-shock proteins.
CONCLUSIONS/SIGNIFICANCE: Phylogenetic comparison of nuclear and mitochondrial genes indicates that T. rangeli and T. cruzi are equidistant from T. brucei. In addition to revealing new aspects of trypanosome co-evolution within the vertebrate and invertebrate hosts, comparative genomic analysis with pathogenic trypanosomatids provides valuable new information that can be further explored with the aim of developing better diagnostic tools and/or therapeutic targets.