Project name: Trypanosoma brucei

Description: Histone variant 3 (H3V) is a kinetoplastid specific histone variant that is enriched at RNA polymerase II termination sites and telomeres. We previously found that the DNA modification base J, which co-localizes with H3V, functions to prevent readthrough transcription within gene clusters in T. brucei. We now demonstrate a similar role for H3V, where the loss of this histone variant results in increased expression of downstream genes. The effect is larger when both H3V and J are lost. Additionally, removal of H3V results in increased siRNAs from dual strand transcribed loci as well as increased expression of silent VSGs, indicating a role of H3V in the regulation of antigenic variationOverall design: The role of H3V in regulating transcription termination was investigated using WT and H3V KO T. brucei cell lines. The role of J was also studied by treating each of these cell lines with DMOG, an inhibitor of J synthesis. We used 4 RNA seq libraries to determine gene expression changes following the loss of H3V and J

Data type: Transcriptome or Gene expression

Sample scope: Multiisolate

Relevance: Medical

Last updated: 2015-06-16