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5. Genome Size, Karyotype Polymorphism and Chromosomal Evolution in Trypanosoma cruzi.

Author

Souza, Renata T., Lima, F´bio M., Barros, Roberto Moraes, Cortez, Danielle R., Santos, Michele F., Cordero, Esteban M., Conceiçao Ruiz, Jeronimo, Goldenberg, Samuel, Teixeira, Marta M. G., and da Silveira, JoséFranco

Subjects
GENOMES, KARYOTYPES, GENETIC polymorphisms, CHROMOSOMES, BIOLOGICAL evolution, TRYPANOSOMA cruzi, RETROTRANSPOSONS, HOMOLOGY (Biology)
Abstract

Background: The Trypanosoma cruzi genome was sequenced from a hybrid strain (CL Brener). However, high allelic variation and the repetitive nature of the genome have prevented the complete linear sequence of chromosomes being determined. Determining the full complement of chromosomes and establishing syntenic groups will be important in defining the structure of T. cruzi chromosomes. A large amount of information is now available for T. cruzi and Trypanosoma brucei, providing the opportunity to compare and describe the overall patterns of chromosomal evolution in these parasites. Methodology/Principal Findings: The genome sizes, repetitive DNA contents, and the numbers and sizes of chromosomes of nine strains of T. cruzi from four lineages (TcI, TcII, TcV and TcVI) were determined. The genome of the TcI group was statistically smaller than other lineages, with the exception of the TcI isolate Tc1161 (José-IMT). Satellite DNA content was correlated with genome size for all isolates, but this was not accompanied by simultaneous amplification of retrotransposons. Regardless of chromosomal polymorphism, large syntenic groups are conserved among T. cruzi lineages. Duplicated chromosome-sized regions were identified and could be retained as paralogous loci, increasing the dosage of several genes. By comparing T. cruzi and T. brucei chromosomes, homologous chromosomal regions in T. brucei were identified. Chromosomes Tb9 and Tb11 of T. brucei share regions of syntenic homology with three and six T. cruzi chromosomal bands, respectively. Conclusions: Despite genome size variation and karyotype polymorphism, T. cruzi lineages exhibit conservation of chromosome structure. Several syntenic groups are conserved among all isolates analyzed in this study. The syntenic regions are larger than expected if rearrangements occur randomly, suggesting that they are conserved owing to positive selection. Mapping of the syntenic regions on T. cruzi chromosomal bands provides evidence for the occurrence of fusion and split events involving T. brucei and T. cruzi chromosomes. [ABSTRACT FROM AUTHOR]

Published
2011
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7. Identification of a domain of Trypanosoma cruzimetacyclic trypomastigote surface molecule gp82 required for attachment and invasion of mammalian cells

Author

Santori, Fabio R., Dorta, Miriam L., Juliano, Luiz, Juliano, Maria A., da Silveira, JoséFranco, Ruiz, Rita C., and Yoshida, Nobuko

Abstract

Recombinant proteins and synthetic peptides representing various sequences of gp82, a surface glycoprotein of Trypanosoma cruzimetacyclic trypomastigotes implicated in mammalian cell invasion, were used in this study aiming at the identification of the domain(s) of this molecule required for interaction with target cells. Invasion of cultured HeLa cells by metacyclic trypomastigotes was inhibited by about 80% in the presence of native gp82 or the corresponding recombinant construct J18. Inhibition by recombinant proteins J18a and J18b, containing respectively the N-terminal and the C-terminal portions of gp82, was on the order of 30% and 65%. As compared to J18b (amino acids 224–516), the truncated gp82 fragments J18b1 (amino acids 303–516) and J18b2 (amino acids 357–516) displayed lower inhibitory effect (∼40% and ∼15%, respectively). Compatible with these observations, we found that the recombinant protein J18b, but not J18a or J18b2, binds to HeLa cells in a dose-dependent and saturable fashion. Experiments with ten overlapping synthetic peptides, representing the gp82 portion spanning amino acids 224–333, showed that peptides 4 (amino acids 254–273) and 8 (amino acids 294–313) have significant inhibitory activity on HeLa cell invasion by metacyclic forms. All these results indicate that the portion of gp82 required for mammalian cell attachment and invasion is located in the central domain of the molecule.

Published
1996
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