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Trypanosoma brucei brucei

ABSTRACT: Genome wide dissection of the quorum sensing signalling pathway in Trypanosoma brucei

PROVIDER: PRJNA200686 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1029480_1.fastq.gz	Fastqsanger.gz
	SRR1029480_2.fastq.gz	Fastqsanger.gz
	SRR1029481_1.fastq.gz	Fastqsanger.gz
	SRR1029481_2.fastq.gz	Fastqsanger.gz
	SRR1029482_1.fastq.gz	Fastqsanger.gz

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Extracellular release of two peptidases dominates generation of the quorum sensing signal in Trypanosoma brucei

Project description:Trypanosomes causing African sleeping sickness use quorum sensing to control the production of transmission-competent stumpy forms in their mammalian hosts. This density-dependent process is signalled by the release of parasite peptidases whose action generates oligopeptides that stimulate the signal transduction pathway leading to stumpy formation. Using mass spectrometry analysis, we have characterised the peptidases released by Trypanosoma brucei brucei.

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Genome wide dissection of the quorum sensing signalling pathway in Trypanosoma brucei

Project description:The protozoan parasites Trypanosoma brucei spp. are responsible for important human and livestock diseases in sub Saharan Africa. In the mammalian blood, two developmental forms of the parasite exist: proliferative ?slender? forms and transmissible ?stumpy? forms that are quiescent, awaiting uptake in a tsetse fly bloodmeal. The slender to stumpy differentiation is a density-dependent response that resembles quorum sensing in microbial systems and is crucial for the parasite life cycle, ensuring both infection chronicity and disease transmission. The response is triggered by an elusive ?stumpy induction factor? (SIF) whose intracellular signaling pathway is also completely uncharacterized. Laboratory-adapted (monomorphic) trypanosome strains cannot respond to SIF, but can generate forms with stumpy characteristics when exposed to cell permeable cAMP and AMP analogues. Exploiting this, we have used a genome-wide RNAi library screen to identify the signaling components driving stumpy formation. In separate screens, monomorphic parasites were exposed to cell permeable cAMP or AMP analogues to select cells that remained proliferative and so were unresponsive to these signals. Genome-wide ion torrent-based RNA interference Target sequencing (RIT-seq) identified a cohort of genes implicated in all steps of the signaling pathway, from purine metabolism, through signal transducers (kinases, phosphatases) to gene expression regulators. The identified genes at each step have been validated in cells naturally capable of stumpy formation, confirming their role in SIF-induced density sensing and cellular quiescence.

2013-12-16 | GSE46501 | GEO

Digital Gene Expression data of a group 1 Trypanosoma brucei gambiense vs a Trypanosoma brucei brucei

Project description:Trypanosoma brucei gambiense is the causative agent of the fatal human disease African sleeping sickness. Using Digital Gene Expression we have compared the transcriptome of a group 1 T.b.gambiense (Eliane) and a T.b.brucei (STIB 247).

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Project description:Trypanosoma brucei brucei edited mRNA transcriptomes

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Project description:Trypanosoma brucei brucei Raw sequence reads

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In vitro generation of human high-density-lipoprotein-resistant Trypanosoma brucei brucei

Project description:The host range of African trypanosomes is influenced by innate protective molecules in the blood of primates. A subfraction of human high-density lipoprotein (HDL) containing apolipoprotein A-I, apolipoprotein L-I, and haptoglobin-related protein is toxic to Trypanosoma brucei brucei but not the human sleeping sickness parasite Trypanosoma brucei rhodesiense. It is thought that T. b. rhodesiense evolved from a T. b. brucei-like ancestor and expresses a defense protein that ablates the antitrypanosomal activity of human HDL. To directly investigate this possibility, we developed an in vitro selection to generate human HDL-resistant T. b. brucei. Here we show that conversion of T. b. brucei from human HDL sensitive to resistant correlates with changes in the expression of the variant surface glycoprotein (VSG) and abolished uptake of the cytotoxic human HDLs. Complete transcriptome analysis of the HDL-susceptible and -resistant trypanosomes confirmed that VSG switching had occurred but failed to reveal the expression of other genes specifically associated with human HDL resistance, including the serum resistance-associated gene (SRA) of T. b. rhodesiense. In addition, we found that while the original active expression site was still utilized, expression of three expression site-associated genes (ESAG) was altered in the HDL-resistant trypanosomes. These findings demonstrate that resistance to human HDLs can be acquired by T. b. brucei. Keywords: Trypanosoma, VSG, antigenic switching, HDL-resistance

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Project description:Trypanosoma brucei brucei Raw gRNA sequence reads

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