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Elife. 2017 Nov 4;6. pii: e29391. doi: 10.7554/eLife.29391.

Modifications at K31 on the lateral surface of histone H4 contribute to genome structure and expression in apicomplexan parasites.

Author information

1
Institute for Advanced Biosciences (IAB), Team Host-pathogen interactions and immunity to infection, INSERM U1209, CNRS UMR5309, Université Grenoble Alpes, Grenoble, France.
2
Unité de Biologie des Interactions Hôte-Parasite, Institut Pasteur, CNRS, ERL 9195, INSERM, Unit U1201, Paris, France.
3
Aix-Marseille Univ, CEA, CNRS, UMR 7265, BIAM-LEMIRE, St-Paul-lez-Durance, France.
4
Université Grenoble Alpes, CEA, INSERM, Grenoble, France.
5
Institute for Advanced Biosciences (IAB), Team Membrane and Cell Dynamics of Host Parasite Interactions, INSERM U1209, CNRS UMR5309, Université Grenoble Alpes, Grenoble, France.
6
Institute for Advanced Biosciences (IAB), Team ApicoLipid, INSERM U1209, CNRS UMR5309, Université Grenoble Alpes, Grenoble, France.

Abstract

An unusual genome architecture characterizes the two related human parasitic pathogens Plasmodium falciparum and Toxoplasma gondii. A major fraction of the bulk parasite genome is packaged as transcriptionally permissive euchromatin with few loci embedded in silenced heterochromatin. Primary chromatin shapers include histone modifications at the nucleosome lateral surface close to the DNA but their mode of action remains unclear. We now identify versatile modifications at Lys31 within the globular domain of histone H4 that crucially determine genome organization and expression in Apicomplexa parasites. H4K31 acetylation at the promoter correlates with, and perhaps directly regulates, gene expression in both parasites. By contrast, monomethylated H4K31 is enriched in the core body of T. gondii active genes but inversely correlates with transcription, whereas it is unexpectedly enriched at transcriptionally inactive pericentromeric heterochromatin in P. falciparum, a region devoid of the characteristic H3K9me3 histone mark and its downstream effector HP1.

KEYWORDS:

Toxoplasma gondii; acetylation; chromatin; gene expression; histone core modifications; infectious disease; methylation; microbiology

PMID:
29101771
PMCID:
PMC5685513
DOI:
10.7554/eLife.29391
[Indexed for MEDLINE]
Free PMC Article

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