Dataset Information

Small proteome in trypanosomes

ABSTRACT: Although technical advances in genomics and proteomics research have yielded a better understanding of the coding capacity of a genome, one major challenge remaining is the identification of all expressed proteins, especially those less than 100 amino acids in length. Such information can be particularly relevant to human pathogens, like Trypanosoma brucei, the causative agent of African trypanosomiasis, since it will provide further insight into the parasite biology and life cycle.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Trypanosoma Brucei

SUBMITTER: F Butter

LAB HEAD: Mann

PROVIDER: PXD000712 | Pride | 2014-04-16

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	20110826_Orbi6_FB_trypansome_10kD.RAW	Raw
	20110826_Orbi6_FB_trypansome_10kD_denatured.RAW	Raw
	20110826_Orbi6_FB_trypansome_30kD.RAW	Raw
	20110826_Orbi6_FB_trypansome_30kD_denatured.RAW	Raw
	20110826_Orbi6_FB_trypansome_3kD.RAW	Raw

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Publications

On the extent and role of the small proteome in the parasitic eukaryote Trypanosoma brucei.

Ericson Megan M Janes Michael A MA Butter Falk F Mann Matthias M Ullu Elisabetta E Tschudi Christian C

BMC biology 20140219

<h4>Background</h4>Although technical advances in genomics and proteomics research have yielded a better understanding of the coding capacity of a genome, one major challenge remaining is the identification of all expressed proteins, especially those less than 100 amino acids in length. Such information can be particularly relevant to human pathogens, such as Trypanosoma brucei, the causative agent of African trypanosomiasis, since it will provide further insight into the parasite biology and li ...[more]

PMID: 24552149

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Project description:Variant Surface Glycoproteins (VSG) coat parasitic African trypanosomes and underpin antigenic variation and immune evasion. This VSG is a super-abundant virulence factor that is subject to post-transcriptional gene expression controls mediated via the VSG 3’-untranslated region (3’-UTR). To identify positive VSG regulators in bloodstream form cells, we used prior genome-scale screening data to prioritise mRNA binding protein (mRBPs) knockdowns that phenocopy VSG mRNA knockdown, displaying both loss-of-fitness and pre-cytokinesis accumulation. The top three candidate VSG regulators were CFB2 (cyclin F-box protein 2, Tb927.1.4650), MKT1 (Tb927.6.4770) and PBP1 (polyadenylate binding-protein binding-protein, Tb927.8.4540). Notably, CFB2 was recently found to regulate VSG transcript stability, and all three proteins were found to associate with each other. We used data-independent acquisition for accurate label-free quantification and deep proteome coverage to quantify expression profiles following depletion of each mRBP. Only CFB2 knockdown significantly reduced VSG expression and the expression of a reporter under the control of a VSG 3’-untranslated region (3’-UTR). CFB2 knockdown also triggered depletion of cytoplasmic ribosomal proteins, consistent with translation arrest observed when VSG synthesis is blocked. In contrast, PBP1 knockdown triggered depletion of CFB2, MKT1, and other components of the PBP1-complex. Finally, all three knockdowns triggered depletion of cytokinesis initiation factors, consistent with the cytokinesis defect that was confirmed here for all three knockdowns. Thus, genome-scale knockdown datasets facilitate the triage and prioritisation of candidate regulators. Quantitative proteomic analysis confirms 3’-UTR dependent positive control of VSG expression by CFB2 and interactions with additional mRBPs. Our results also reveal connections between VSG expression control by CFB2, ribosomal protein expression, and cytokinesis.