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Effect of the Disruption of RNA Pol II on the Transcription by RNA Pol l by Trypanosoma brucei
Author(s) -
DEVAUX S.,
LECORDIER L.,
VANHAMME L.,
PAYS E.
Publication year - 2005
Publication title -
journal of eukaryotic microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.067
H-Index - 77
eISSN - 1550-7408
pISSN - 1066-5234
DOI - 10.1111/j.1550-7408.2005.05202003_3_8.x
Subject(s) - rna polymerase ii , biology , rna polymerase iii , transcription (linguistics) , rna , rna polymerase i , transcription factor ii d , transcription factor ii f , microbiology and biotechnology , rna silencing , rna polymerase , transcription factor ii b , rna dependent rna polymerase , rna polymerase ii holoenzyme , rna interference , gene expression , genetics , gene , promoter , linguistics , philosophy
Trypanosomes exist in two major distinct forms: the procyclic form in insects in which the surface molecule is procyclin and the bloodstream form in mammals in which the surface molecule is VSG. The promoter of these locus recruits RNA Pol I. Despite the use of this polymerase, the transcripts are spliced and polyadenylated exactly as the mRNAs synthesised by RNA Pol II. The fact that mRNA production from these sites must involve a concerted action between RNA Pol I and a “RNA factory” normally linked to RNA Pol II, led to the proposal that the control of these Pol I transcription units would involve a limiting component bridging RNA Pol I and an elongation/processing complex normally associated with RNA Pol II. To study the effects of the disruption of RNA Pol II on VSG expression level, we cloned the T. brucei homologue of the rpb9 subunit of RNA Pol II, which plays a role in RNA elongation in other eukaryotic cells. In PF, disruption of Tbrpb9 by conditional RNAi led to a strong transcriptional stimulation in the beginning of the ESs. This effect was linked to the inhibition of procyclin transcription. Thus, the disruption of RNA Pol II abolished the stage‐specific regulation of the transcription units for the two major surface antigens, both of which recruit RNA Pol I.