Mono-allelic VSG expression by RNA polymerase I in Trypanosoma brucei: expression site control from both ends?
| Autor: | Justin K. Kirkham, Sung Hee Park, Nitika Badjatia, Tu N. Nguyen, Arthur Günzl |
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| Jazyk: | angličtina |
| Rok vydání: | 2014 |
| Předmět: |
Genes
Protozoan Trypanosoma brucei brucei Trypanosoma brucei Allelic Imbalance Article Transcription (biology) RNA Polymerase I parasitic diseases Genetics RNA polymerase I Antigenic variation Gene silencing Gene Silencing Promoter Regions Genetic Gene Alleles Regulation of gene expression Messenger RNA biology General Medicine Telomere biology.organism_classification Gene Expression Regulation Transcription Initiation Site Variant Surface Glycoproteins Trypanosoma |
| Popis: | Trypanosoma brucei is a vector borne, lethal protistan parasite of humans and livestock in sub-Saharan Africa. Antigenic variation of its cell surface coat enables the parasite to evade adaptive immune responses and to live freely in the blood of its mammalian hosts. The coat consists of ten million copies of variant surface glycoprotein (VSG) that is expressed from a single VSG gene, drawn from a large repertoire and located near the telomere at one of fifteen so-called bloodstream expression sites (BESs). Thus, antigenic variation is achieved by switching to the expression of a different VSG gene. A BES is a tandem array of expression site-associated genes and a terminal VSG gene. It is polycistronically transcribed by a multifunctional RNA polymerase I (RNAPI) from a short promoter that is located 45–60 kb upstream of the VSG gene. The mechanism(s) restricting VSG expression to a single BES are not well understood. There is convincing evidence that epigenetic silencing and transcription attenuation play important roles. Furthermore, recent data indicated that there is regulation at the level of transcription initiation and that, surprisingly, the VSG mRNA appears to have a role in restricting VSG expression to a single gene. Here, we review BES expression regulation and propose a model in which telomere-directed, epigenetic BES silencing is opposed by BES promoter-directed, activated RNAPI transcription. |
| Databáze: | OpenAIRE |
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