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Summary    T   rypanosoma brucei  is a unicellular parasite that causes sleeping sickness in humans. Most of its transcription is constitutive and driven by  RNA  polymerase  II .  RNA  polymerase  I  ( Pol I ) transcribes not only ribosomal  RNA  genes, but also protein‐encoding genes, including variant surface glycoproteins (  VSGs  ) and procyclins. In   T   . brucei , histone  H 1 ( H 1) is required for   VSG   silencing and chromatin condensation. However, whether  H 1 has a genome‐wide role in transcription is unknown. Here, using  RNA  sequencing we show that  H 1 depletion changes the expression of a specific cohort of genes. Interestingly, the predominant effect is partial loss of silencing of  Pol I  loci, such as   VSG   and procyclin genes. Labelling of nascent transcripts with 4‐thiouridine showed that  H 1 depletion does not alter the level of labelled  Pol II  transcripts. In contrast, the levels of 4 sU ‐labelled  Pol I  transcripts were increased by two‐ to sixfold, suggesting that  H 1 preferentially blocks transcription at  Pol I  loci. Finally, we observed that parasites depleted of  H 1 grow almost normally in culture but they have a reduced fitness in mice, suggesting that  H 1 is important for host–pathogen interactions.

T rypanosoma brucei histone H 1 inhibits RNA polymerase I transcription and is important for parasite fitness in vivo