Comparative transcriptome analysis of geographically distinct virulent and attenuated Babesia bovis strains reveals similar gene expression changes through attenuation

BMC Genomics

Research Article

Ignacio Echaide¹  Monica J Pedroni²  Kerry S Sondgeroth²  Gina M Gallego-Lopez²  Audrey OT Lau³ 

[1] Laboratorio de Inmunología y Parasitología, Instituto Nacional de Tecnologia Agropecuaria (INTA), CP2300, Rafaela, Argentina;Program of Genomics, Department of Veterinary Microbiology & Pathology, College of Veterinary Medicine, Washington State University, ADBF 4043, 99164, Pullman, WA, USA;Program of Genomics, Department of Veterinary Microbiology & Pathology, College of Veterinary Medicine, Washington State University, ADBF 4043, 99164, Pullman, WA, USA;Paul G. Allen School for Global Animal Health, College of Veterinary Medicine, Washington State University, 99164, Pullman, WA, USA;

关键词: Babesia bovis;    Apicomplexans;    Virulence;    Attenuation;    Transcriptome;    Microarray;    RNA-sequencing;   

DOI  :  10.1186/1471-2164-14-763

 received in 2013-05-13, accepted in 2013-10-30,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundLoss of virulence is a phenotypic adaptation commonly seen in prokaryotic and eukaryotic pathogens. This mechanism is not well studied, especially in organisms with multiple host and life cycle stages such as Babesia, a tick-transmitted hemoparasite of humans and animals. B. bovis, which infects cattle, has naturally occurring virulent strains that can be reliably attenuated in vivo. Previous studies suggest the virulence loss mechanism may involve post-genomic modification. We investigated the transcriptome profiles of two geographically distinct B. bovis virulent and attenuated strain pairs to better understand virulence loss and to gain insight into pathogen adaptation strategies.ResultsExpression microarray and RNA-sequencing approaches were employed to compare transcriptome profiles of two B. bovis strain pairs, with each pair consisting of a virulent parental and its attenuated derivative strain. Differentially regulated transcripts were identified within each strain pair. These included genes encoding for VESA1, SmORFs, undefined membrane and hypothetical proteins. The majority of individual specific gene transcripts differentially regulated within a strain were not shared between the two strains. There was a disproportionately greater number of ves genes upregulated in the virulent parental strains. When compared with their attenuated derivatives, divergently oriented ves genes were included among the upregulated ves genes in the virulent strains, while none of the upregulated ves genes in the attenuated derivatives were oriented head to head. One gene family whose specific members were consistently and significantly upregulated in expression in both attenuated strains was spherical body protein (SBP) 2 encoding gene where SBP2 truncated copies 7, 9 and 11 transcripts were all upregulated.ConclusionsWe conclude that ves heterodimer pair upregulation and overall higher frequency of ves gene expressions in the virulent strains is consistent with the involvement of this gene family in virulence. This is logical given the role of VESA1 proteins in cytoadherence of infected cells to endothelial cells. However, upregulation of some ves genes in the attenuated derivatives suggests that the consequence of upregulation is gene-specific. Furthermore, upregulation of the spherical body protein 2 gene family may play a role in the attenuated phenotype. Exactly how these two gene families may contribute to the loss or gain of virulence is discussed.

【 授权许可】

Unknown   
© Pedroni et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.