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T rypanosoma brucei histone H 1 inhibits RNA polymerase I transcription and is important for parasite fitness in vivo
Author(s) -
Pena Ana C.,
Pimentel Mafalda R.,
Manso Helena,
VazDrago Rita,
PintoNeves Daniel,
ArestaBranco Francisco,
RijoFerreira Filipa,
Guegan Fabien,
Pedro Coelho Luis,
CarmoFonseca Maria,
BarbosaMorais Nuno L.,
Figueiredo Luisa M.
Publication year - 2014
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12677
Subject(s) - biology , rna polymerase ii , transcription (linguistics) , rna polymerase iii , chromatin , microbiology and biotechnology , rna , rna polymerase , gene , rna polymerase i , gene expression , genetics , promoter , linguistics , philosophy
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.