Chromosomal copy number variation reveals differential levels of genomic plasticity in distinct Trypanosoma cruzi strains.
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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 16 (-) 499 [2015-07-04; online 2015-07-04]
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. 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. 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.
PubMed 26141959
DOI 10.1186/s12864-015-1680-4
Crossref 10.1186/s12864-015-1680-4
pii: 10.1186/s12864-015-1680-4
pmc: PMC4491234
SRA: SRR058509
SRA: SRR058510
SRA: SRR058511
SRA: SRR058512
SRA: SRR058513
SRA: SRR058514
SRA: SRR058515
SRA: SRR058516
SRA: SRR058517
SRA: SRR058518
SRA: SRR058519
SRA: SRR058520
SRA: SRR833799
SRA: SRR833800
SRA: SRS838181
SRA: SRS841912
SRA: SRS842149