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Chromosomal copy number variation reveals differential levels of genomic plasticity in distinct Trypanosoma cruzi strains.

Reis-Cunha JL, Rodrigues-Luiz GF, Valdivia HO, Baptista RP, Mendes TA, de Morais GL, Guedes R, Macedo AM, Bern C, Gilman RH, Lopez CT, Andersson B, Vasconcelos AT, Bartholomeu DC - BMC Genomics (2015)

Bottom Line: Although the T. cruzi karyotype is not well defined, several studies have demonstrated a significant variation in the size and content of chromosomes between different T. cruzi strains.Chromosome 31, which is the only chromosome that is supernumerary in all six T. cruzi samples evaluated in this study, is enriched with genes related to glycosylation pathways, highlighting the importance of glycosylation to parasite survival.Increased gene copy number due to chromosome amplification may contribute to alterations in gene expression, which represents a strategy that may be crucial for parasites that mainly depend on post-transcriptional mechanisms to control gene expression.

View Article: PubMed Central - PubMed

Affiliation: Laboratório de Imunologia e Genômica de Parasitos, Departamento deParasitologia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. jaumlrc@gmail.com.

ABSTRACT

Background: Trypanosoma cruzi, the etiologic agent of Chagas disease, is currently divided into six discrete typing units (DTUs), named TcI-TcVI. CL Brener, the reference strain of the T. cruzi genome project, is a hybrid with a genome assembled into 41 putative chromosomes. Gene copy number variation (CNV) is well documented as an important mechanism to enhance gene expression and variability in T. cruzi. Chromosomal CNV (CCNV) is another level of gene CNV in which whole blocks of genes are expanded simultaneously. Although the T. cruzi karyotype is not well defined, several studies have demonstrated a significant variation in the size and content of chromosomes between different T. cruzi strains. Despite these studies, the extent of diversity in CCNV among T. cruzi strains based on a read depth coverage analysis has not been determined.

Results: We identify the CCNV in T. cruzi strains from the TcI, TcII and TcIII DTUs, by analyzing the depth coverage of short reads from these strains using the 41 CL Brener chromosomes as reference. This study led to the identification of a broader extent of CCNV in T. cruzi than was previously speculated. The TcI DTU strains have very few aneuploidies, while the strains from TcII and TcIII DTUs present a high degree of chromosomal expansions. Chromosome 31, which is the only chromosome that is supernumerary in all six T. cruzi samples evaluated in this study, is enriched with genes related to glycosylation pathways, highlighting the importance of glycosylation to parasite survival.

Conclusions: Increased gene copy number due to chromosome amplification may contribute to alterations in gene expression, which represents a strategy that may be crucial for parasites that mainly depend on post-transcriptional mechanisms to control gene expression.

No MeSH data available.


Related in: MedlinePlus

Competitive mapping and SNP content of the T. cruzi strains from different DTUs. In competitive mapping, whole-genome shotgun reads from the T. cruzi Arequipa, Colombiana, Sylvio, Esmeraldo, Y and 231 strains were simultaneously mapped to the 41 chromosomal sequences from Esmeraldo-like (Esmo-like) and non-Esmeraldo-like (Non-Esmo) CL Brener haplotypes, and their mean read depth coverage (RDC) was estimated. Each black bar corresponds to the mean RDC of each of the 41 CL Brener chromosomes (a). For each T. cruzi strain, the mean RDC of the CL Brener haplotype with the highest RDC in the competitive mapping (non-Esmeraldo for Arequipa, Sylvio and 231; Esmeraldo-like for Esmeraldo and Y) was divided by the mean RDC of the CL Brener haplotype with the lower RDC (Esmeraldo-like for Arequipa, Sylvio and 231; non-Esmeraldo for Esmeraldo and Y) (b). The SNP density of each T. cruzi strain and the 1563 Esmeraldo-like/non-Esmeraldo-like single-copy genes are shown (c)
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Fig1: Competitive mapping and SNP content of the T. cruzi strains from different DTUs. In competitive mapping, whole-genome shotgun reads from the T. cruzi Arequipa, Colombiana, Sylvio, Esmeraldo, Y and 231 strains were simultaneously mapped to the 41 chromosomal sequences from Esmeraldo-like (Esmo-like) and non-Esmeraldo-like (Non-Esmo) CL Brener haplotypes, and their mean read depth coverage (RDC) was estimated. Each black bar corresponds to the mean RDC of each of the 41 CL Brener chromosomes (a). For each T. cruzi strain, the mean RDC of the CL Brener haplotype with the highest RDC in the competitive mapping (non-Esmeraldo for Arequipa, Sylvio and 231; Esmeraldo-like for Esmeraldo and Y) was divided by the mean RDC of the CL Brener haplotype with the lower RDC (Esmeraldo-like for Arequipa, Sylvio and 231; non-Esmeraldo for Esmeraldo and Y) (b). The SNP density of each T. cruzi strain and the 1563 Esmeraldo-like/non-Esmeraldo-like single-copy genes are shown (c)

Mentions: To select the CL Brener haplotype most suitable as a reference in the mapping of the reads from the distinct T. cruzi strains, their quality-filtered reads were mapped simultaneously to the 41 chromosomal sequences from the CL Brener Esmeraldo-like and non-Esmeraldo-like haplotypes (Fig. 1a). As expected, the reads from the TcII strains (Esmeraldo and Y) mapped preferentially with chromosomes from the Esmeraldo-like haplotype, and the reads from the TcIII strain (231) mapped preferentially with chromosomes from the non-Esmeraldo-like haplotype. The reads from the strains from TcI DTU (Arequipa, Colombiana and Sylvio) mapped slightly better to the non-Esmeraldo-like than to the Esmeraldo-like CL Brener haplotype (Fig. 1b).Fig. 1


Chromosomal copy number variation reveals differential levels of genomic plasticity in distinct Trypanosoma cruzi strains.

Reis-Cunha JL, Rodrigues-Luiz GF, Valdivia HO, Baptista RP, Mendes TA, de Morais GL, Guedes R, Macedo AM, Bern C, Gilman RH, Lopez CT, Andersson B, Vasconcelos AT, Bartholomeu DC - BMC Genomics (2015)

Competitive mapping and SNP content of the T. cruzi strains from different DTUs. In competitive mapping, whole-genome shotgun reads from the T. cruzi Arequipa, Colombiana, Sylvio, Esmeraldo, Y and 231 strains were simultaneously mapped to the 41 chromosomal sequences from Esmeraldo-like (Esmo-like) and non-Esmeraldo-like (Non-Esmo) CL Brener haplotypes, and their mean read depth coverage (RDC) was estimated. Each black bar corresponds to the mean RDC of each of the 41 CL Brener chromosomes (a). For each T. cruzi strain, the mean RDC of the CL Brener haplotype with the highest RDC in the competitive mapping (non-Esmeraldo for Arequipa, Sylvio and 231; Esmeraldo-like for Esmeraldo and Y) was divided by the mean RDC of the CL Brener haplotype with the lower RDC (Esmeraldo-like for Arequipa, Sylvio and 231; non-Esmeraldo for Esmeraldo and Y) (b). The SNP density of each T. cruzi strain and the 1563 Esmeraldo-like/non-Esmeraldo-like single-copy genes are shown (c)
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4491234&req=5

Fig1: Competitive mapping and SNP content of the T. cruzi strains from different DTUs. In competitive mapping, whole-genome shotgun reads from the T. cruzi Arequipa, Colombiana, Sylvio, Esmeraldo, Y and 231 strains were simultaneously mapped to the 41 chromosomal sequences from Esmeraldo-like (Esmo-like) and non-Esmeraldo-like (Non-Esmo) CL Brener haplotypes, and their mean read depth coverage (RDC) was estimated. Each black bar corresponds to the mean RDC of each of the 41 CL Brener chromosomes (a). For each T. cruzi strain, the mean RDC of the CL Brener haplotype with the highest RDC in the competitive mapping (non-Esmeraldo for Arequipa, Sylvio and 231; Esmeraldo-like for Esmeraldo and Y) was divided by the mean RDC of the CL Brener haplotype with the lower RDC (Esmeraldo-like for Arequipa, Sylvio and 231; non-Esmeraldo for Esmeraldo and Y) (b). The SNP density of each T. cruzi strain and the 1563 Esmeraldo-like/non-Esmeraldo-like single-copy genes are shown (c)
Mentions: To select the CL Brener haplotype most suitable as a reference in the mapping of the reads from the distinct T. cruzi strains, their quality-filtered reads were mapped simultaneously to the 41 chromosomal sequences from the CL Brener Esmeraldo-like and non-Esmeraldo-like haplotypes (Fig. 1a). As expected, the reads from the TcII strains (Esmeraldo and Y) mapped preferentially with chromosomes from the Esmeraldo-like haplotype, and the reads from the TcIII strain (231) mapped preferentially with chromosomes from the non-Esmeraldo-like haplotype. The reads from the strains from TcI DTU (Arequipa, Colombiana and Sylvio) mapped slightly better to the non-Esmeraldo-like than to the Esmeraldo-like CL Brener haplotype (Fig. 1b).Fig. 1

Bottom Line: Although the T. cruzi karyotype is not well defined, several studies have demonstrated a significant variation in the size and content of chromosomes between different T. cruzi strains.Chromosome 31, which is the only chromosome that is supernumerary in all six T. cruzi samples evaluated in this study, is enriched with genes related to glycosylation pathways, highlighting the importance of glycosylation to parasite survival.Increased gene copy number due to chromosome amplification may contribute to alterations in gene expression, which represents a strategy that may be crucial for parasites that mainly depend on post-transcriptional mechanisms to control gene expression.

View Article: PubMed Central - PubMed

Affiliation: Laboratório de Imunologia e Genômica de Parasitos, Departamento deParasitologia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. jaumlrc@gmail.com.

ABSTRACT

Background: Trypanosoma cruzi, the etiologic agent of Chagas disease, is currently divided into six discrete typing units (DTUs), named TcI-TcVI. CL Brener, the reference strain of the T. cruzi genome project, is a hybrid with a genome assembled into 41 putative chromosomes. Gene copy number variation (CNV) is well documented as an important mechanism to enhance gene expression and variability in T. cruzi. Chromosomal CNV (CCNV) is another level of gene CNV in which whole blocks of genes are expanded simultaneously. Although the T. cruzi karyotype is not well defined, several studies have demonstrated a significant variation in the size and content of chromosomes between different T. cruzi strains. Despite these studies, the extent of diversity in CCNV among T. cruzi strains based on a read depth coverage analysis has not been determined.

Results: We identify the CCNV in T. cruzi strains from the TcI, TcII and TcIII DTUs, by analyzing the depth coverage of short reads from these strains using the 41 CL Brener chromosomes as reference. This study led to the identification of a broader extent of CCNV in T. cruzi than was previously speculated. The TcI DTU strains have very few aneuploidies, while the strains from TcII and TcIII DTUs present a high degree of chromosomal expansions. Chromosome 31, which is the only chromosome that is supernumerary in all six T. cruzi samples evaluated in this study, is enriched with genes related to glycosylation pathways, highlighting the importance of glycosylation to parasite survival.

Conclusions: Increased gene copy number due to chromosome amplification may contribute to alterations in gene expression, which represents a strategy that may be crucial for parasites that mainly depend on post-transcriptional mechanisms to control gene expression.

No MeSH data available.


Related in: MedlinePlus