As early divergers from other eukaryotes, kinetoplastids have several unusual features of gene regulation. For example, genes are post-transcriptionally processed from polycistronic transcription units and contain a hypermodified base, base J (β-D-glucosyl-hydroxymethyluracil), that demarcates the sites of transcription initiation and termination. In Leishmania spp., the loss of base J results in genome-wide defects in the termination of transcription, but only a partial defect is observed in Trypanosoma brucei. Two new studies now establish that the histone mark H3.V is required in addition to base J to terminate transcription by RNA polymerase II in T. brucei. Furthermore, the studies found that H3.V, but not base J, mediates the termination of transcription by RNA polymerase I at telomeric loci that encode variant surface glycoproteins. Therefore, H3.V may contribute to the antigen switching that occurs at these loci, which hides T. brucei from the host immune system.
References
Reynolds, D. et al. Histone H3 variant regulates RNA polymerase II transcription termination and dual strand transcription of siRNA loci in Trypanosoma brucei. PLoS Genet. 12, e1005758 (2016)
Schulz, D. et al. Base J and H3.V regulate transcriptional termination in Trypanosoma brucei. PLoS Genet. 12, e1005762 (2016)
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Attar, N. Putting a stop to kinetoplastid transcription. Nat Rev Microbiol 14, 130 (2016). https://doi.org/10.1038/nrmicro.2016.19
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DOI: https://doi.org/10.1038/nrmicro.2016.19