Project description:Trypanosoma brucei gambiense is the causative agent of the fatal human disease African sleeping sickness. Here we have compared the transcriptome of two different life cycle stages, the potentially human-infective bloodstream form and the non-human-infective procyclic stage, using digital gene expression (DGE) analysis.
Project description:Cy3 and Cy5 direct labelled RNA from Bloodstream MiTat1.1 trypanosomes and Procyclic 427 Lister were hybridized onto JCVI Trypanosoma brucei oligoarrays (version2). Procyclic RNA were used as control for data analysis.
Project description:Trypanosoma brucei gambiense is the causative agent of the fatal human disease African sleeping sickness. Here we have compared the transcriptome of two different life cycle stages, the potentially human-infective bloodstream form and the non-human-infective procyclic stage, using digital gene expression (DGE) analysis. Digital gene expression analysis was performed on RNA from 3 biological replicates of bloodstream cultured T.b. gambiense strain STIB 386 and compared to that from 3 biological replicates of procyclic cultured T.b. gambiense strain STIB 386.
Project description:A procyclic form Trypansome brucei RNAi line (PTT parental line, transfected with pALC14 incorporating a TbNMD3 gene fragment) capable of inducing depletion of TbNMD3 was analysed for mRNA expression by RNAseq
Project description:T. brucei PF cells were treated with several chemical reagents and anti-trypanosomatid drugs. The effect of each chemical perturbation on the transcriptome of T. brucei was examined by transcript profiling of treated vs. control cells. The results indicated widespread changes, suggesting that the transcriptome of T. brucei is highly responsive to environmental factors that perturb its metabolic and biological pathways.
Project description:Purpose: Acoziborole is a recently developed benzoxaborole class compound, currently in clinical trials, for stage 1 and stage 2 treatment of Human African Trypanosomiasis. Recent studies have made significant progress in determining the molecular mode of action of acoziborole. However, less is known about the potential mechanisms leading to acoziborole resistance in trypanosomes. By characterising in vitro drug-resistance, this study aimed to gain a better understanding of the mechanisms involved in acoziborole resistance in the clinicaly relevant Trypanosoma brucei Methods: Drug resistance was generated in vitro through incremental dosage of acoziborole. RNA was isolated from axenic cultures of drug-resistant and parental drug sensitive cells and submitted for RNA-seq Results: Transcriptomics analysis revealed widepread downregulation of transcripts associated with mammalian-infective bloodstream-form parasites. Conversely, transcripts associated with insect-stage procyclic form parasites were increased, indicating that the resistant cells had undergone an unspecified "differentiation event", albeit on a transcriptomic level Conclusions: Trypanosoma brucei resistance to acoziborole can be generated under in vitro axenic conditions, and "transcriptional differentiation" is a mechanism of resistance. However, it is unknown whether this phenomenon is relevant to an in vivo setting
