Putting a stop to kinetoplastid transcription

Attar, Naomi

doi:10.1038/nrmicro.2016.19

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Published: 15 February 2016

Parasite genetics

Putting a stop to kinetoplastid transcription

Naomi Attar

Nature Reviews Microbiology volume 14, page 130 (2016)Cite this article

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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.

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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)
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Schulz, D. et al. Base J and H3.V regulate transcriptional termination in Trypanosoma brucei. PLoS Genet. 12, e1005762 (2016)
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