Two modes of activation of a single surface antigen gene of trypanosoma brucei

Bernards, André; Lange, Titia de; Michels, Paul A.M.; Liu, Alvin Y.C.; Huisman, Marianne J.; Borst, Piet

doi:10.1016/0092-8674(84)90085-0

Cited by 114 publications

(76 citation statements)

References 42 publications

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“…The most striking observation reported here is that in trypanosomes which harbour the novel telomeric gene, AnTat 1.13 has become a predominant VAT, suggesting that a telomeric position is essential for predominance, in agree-ment with other predominant VATs being also encoded by telomeric genes (13,14,24,25). The telomeric location of a surface antigen gene could enhance its ability to recombine with an expression site.…”

Section: Discussionmentioning

confidence: 48%

Translocation alters the activation rate of a trypanosome surface antigen gene

et al. 1984

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Section: Discussionmentioning

confidence: 48%

Translocation alters the activation rate of a trypanosome surface antigen gene

et al. 1984

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“…brucei Transformants and Culturing Conditions-All trypanosomes used were T. brucei 427, and bloodstream form variants were all derived from T. brucei 427 VSG221a (25). Bloodstream form T. brucei was maintained at 37°C in HMI-9 medium with the addition of 10% fetal calf serum and 10% Serum Plus (JRH Biosciences) (26).…”

Section: Methodsmentioning

confidence: 99%

Bloodstream Form-specific Up-regulation of Silent VSG Expression Sites and Procyclin in Trypanosoma brucei after Inhibition of DNA Synthesis or DNA Damage

Sheader

Vruchte

Rudenko

2004

Journal of Biological Chemistry

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The African trypanosome Trypanosoma brucei transcribes the active variant surface glycoprotein (VSG) gene from one of about 20 VSG expression sites (ESs). In order to study ES control, we made reporter lines with a green fluorescent protein gene inserted behind the promoter of different ESs. We attempted to disrupt the silencing machinery, and we used fluorescence-activated cell sorter analysis for the rapid and sensitive detection of ES up-regulation. We find that a range of treatments that either block nuclear DNA synthesis, like aphidicolin, or modify DNA-like cisplatin and 1-methyl-3-nitro-1-nitrosoguanidine results in up-regulation of silent ESs. Aphidicolin treatment was the most effective, with almost 80% of the cells expressing green fluorescent protein from a silent ES. All of these treatments blocked the cells in S phase. In contrast, a range of toxic chemicals had little or no effect on expression. These included berenil and pentamidine, which selectively cleave the mitochondrial kinetoplast DNA, the metabolic inhibitors suramin and difluoromethylornithine, and the mitotic inhibitor rhizoxin. Up-regulation also affected other RNA polymerase I (pol I) transcription units, as procyclin genes were also up-regulated after cells were treated with either aphidicolin or DNA-modifying agents. Strikingly, this up-regulation of silent pol I transcription units was bloodstream form-specific and was not observed in insect form T. brucei. We postulate that the redistribution of a limiting bloodstream form-specific factor involved in both silencing and DNA repair results in the derepression of normally silenced pol I transcription units after DNA damage.

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“…The trypanosome can change the antigenic composition of its surface by switching the VSG gene expressed (see Borst and Cross, 1982). Switching occurs either by a duplicative transposition of an inactive VSG gene to a telomeric expression site (Hoeijmakers et al, 1980;Pays et al, 1981Pays et al, , 1983aBernards et al, 1981;Majiwa et al, 1982;Longacre et al, 1983), or by the activation of a new telomeric site and the inactivation of the old one (Laurent et al, 1984;Pays et al, 1983b;Bernards et al, 1984;Michels et al, 1984;Myler et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

Trypanosoma brucei: a surface antigen mRNA is discontinuously transcribed from two distinct chromosomes.

Guyaux¹,

Cornelissen²,

Pays³

et al. 1985

The EMBO Journal

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Communicated by M.SteinertThe mRNAs for variant surface glycoproteins (VSGs) and many other proteins in Trypanosoma brucei start with the same sequence of 35 nucleotides, encoded by a separate miniexon. There are -200 mini-exon genes per trypanosome and these are highly clustered on large chromosomes. We have found two trypanosome variants that express a VSG gene located on a small, 225-kb chromosome. Each gene yields a mRNA containing the 35-nucleotide sequence even though the 225-kb chromosome does not contain a complete mini-exon gene. These results provide a strong support for the hypothesis that transcription of protein-coding genes in trypanosomes is discontinuous.

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Two modes of activation of a single surface antigen gene of trypanosoma brucei

Cited by 114 publications

References 42 publications

Translocation alters the activation rate of a trypanosome surface antigen gene

Translocation alters the activation rate of a trypanosome surface antigen gene

Bloodstream Form-specific Up-regulation of Silent VSG Expression Sites and Procyclin in Trypanosoma brucei after Inhibition of DNA Synthesis or DNA Damage

Trypanosoma brucei: a surface antigen mRNA is discontinuously transcribed from two distinct chromosomes.

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