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Logo of bmcgenoBioMed Centralsearchsubmit a manuscriptregisterthis articleBMC Genomics
 
BMC Genomics. 2009; 10: 482.
Published online Oct 19, 2009. doi:  10.1186/1471-2164-10-482
PMCID: PMC2771046
Widespread variation in transcript abundance within and across developmental stages of Trypanosoma brucei
Bryan C Jensen,1 Dhileep Sivam,1,2 Charles T Kifer,1 Peter J Myler,1,2,3 and Marilyn Parsonscorresponding author1,3
1Seattle Biomedical Research Institute, 307 Westlake Ave. North, Seattle, WA, 98109 USA
2Department of Medical Education and Biomedical Informatics, University of Washington, Seattle, WA, 98195 USA
3Department of Global Health, University of Washington, Seattle, WA, 98195 USA
corresponding authorCorresponding author.
Bryan C Jensen: bryan.jensen/at/sbri.org; Dhileep Sivam: dhileep.sivam/at/sbri.org; Charles T Kifer: charles.kifer/at/sbri.org; Peter J Myler: peter.myler/at/sbri.org; Marilyn Parsons: marilyn.parsons/at/sbri.org
Received July 13, 2009; Accepted October 19, 2009.
Abstract
Background
Trypanosoma brucei, the causative agent of African sleeping sickness, undergoes a complex developmental cycle that takes place in mammalian and insect hosts and is accompanied by changes in metabolism and cellular morphology. While differences in mRNA expression have been described for many genes, genome-wide expression analyses have been largely lacking. Trypanosomatids represent a unique case in eukaryotes in that they transcribe protein-coding genes as large polycistronic units, and rarely regulate gene expression at the level of transcription initiation.
Results
Here we present a comprehensive analysis of mRNA expression in several stages of parasite development. Utilizing microarrays that have multiple copies of multiple probes for each gene, we were able to demonstrate with a high degree of statistical confidence that approximately one-fourth of genes show differences in mRNA expression levels in the stages examined. These include complex patterns of gene expression within gene families, including the large family of variant surface glycoproteins (VSGs) and their relatives, where we have identified a number of constitutively expressed family members. Furthermore, we were able to assess the relative abundance of all transcripts in each stage, identifying the genes that are either weakly or highly expressed. Very few genes show no evidence of expression.
Conclusion
Despite the lack of gene regulation at the level of transcription initiation, our results reveal extensive regulation of mRNA abundance associated with different life cycle and growth stages. In addition, analysis of variant surface glycoprotein gene expression reveals a more complex picture than previously thought. These data provide a valuable resource to the community of researchers studying this lethal agent.
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