TY - JOUR
T1 - Genome of the avirulent human-infective Trypanosome—Trypanosoma rangeli
AU - Stoco, Patrícia Hermes
AU - Wagner, Glauber
AU - Talavera-Lopez, Carlos
AU - Gerber, Alexandra
AU - Zaha, Arnaldo
AU - Thompson, Claudia Elizabeth
AU - Bartholomeu, Daniella Castanheira
AU - Lückemeyer, Débora Denardin
AU - Bahia, Diana
AU - Loreto, Elgion
AU - Prestes, Elisa Beatriz
AU - Lima, Fábio Mitsuo
AU - Rodrigues-Luiz, Gabriela
AU - Vallejo, Gustavo Adolfo
AU - Filho, José Franco Da Silveira
AU - Schenkman, Sérgio
AU - Monteiro, Karina Mariante
AU - Tyler, Kevin Morris
AU - Almeida, Luiz Gonzaga Paula De
AU - Ortiz, Mauro Freitas
AU - Chiurillo, Miguel Angel
AU - Moraes, Milene Höehr De
AU - Cunha, Oberdan De Lima
AU - Mendonça-Neto, Rondon
AU - Silva, Rosane
AU - Teixeira, Santuza Maria Ribeiro
AU - Murta, Silvane Maria Fonseca
AU - Sincero, Thais Cristine Marques
AU - Mendes, Tiago Antonio De Oliveira
AU - Urmenyi, Turán Peter
AU - Silva, Viviane Grazielle
AU - DaRocha, Wanderson Duarte
AU - Andersson, Björn
AU - Romanha, Álvaro José
AU - Steindel, Mário
AU - Vasconcelos, Ana Tereza Ribeiro De
AU - Grisard, Edmundo Carlos
N1 - © 2014 Stoco et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2014/9/18
Y1 - 2014/9/18
N2 - 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 heatshock 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.
AB - 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 heatshock 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.
U2 - 10.1371/journal.pntd.0003176
DO - 10.1371/journal.pntd.0003176
M3 - Article
VL - 8
JO - PLoS Neglected Tropical Diseases
JF - PLoS Neglected Tropical Diseases
SN - 1935-2727
IS - 9
M1 - e3176
ER -
