The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes

Lara Djakovic, Thomas Hennig, Katharina Reinisch, Andrea Milić, Adam W. Whisnant, Katharina Wolf, Elena Weiß, Tobias Haas, Arnhild Grothey, Christopher S. Jürges, Michael Kluge, Elmar Wolf, Florian Erhard, Caroline C. Friedel () and Lars Dölken ()
Additional contact information
Lara Djakovic: Julius-Maximilians-University Würzburg
Thomas Hennig: Julius-Maximilians-University Würzburg
Katharina Reinisch: Ludwig-Maximilians-Universität München
Andrea Milić: Julius-Maximilians-University Würzburg
Adam W. Whisnant: Julius-Maximilians-University Würzburg
Katharina Wolf: Julius-Maximilians-University Würzburg
Elena Weiß: Ludwig-Maximilians-Universität München
Tobias Haas: Julius-Maximilians-University Würzburg
Arnhild Grothey: Julius-Maximilians-University Würzburg
Christopher S. Jürges: Julius-Maximilians-University Würzburg
Michael Kluge: Ludwig-Maximilians-Universität München
Elmar Wolf: University of Würzburg
Florian Erhard: Julius-Maximilians-University Würzburg
Caroline C. Friedel: Ludwig-Maximilians-Universität München
Lars Dölken: Julius-Maximilians-University Würzburg

Nature Communications, 2023, vol. 14, issue 1, 1-17

Abstract: Abstract Herpes simplex virus 1 (HSV-1) infection and stress responses disrupt transcription termination by RNA Polymerase II (Pol II). In HSV-1 infection, but not upon salt or heat stress, this is accompanied by a dramatic increase in chromatin accessibility downstream of genes. Here, we show that the HSV-1 immediate-early protein ICP22 is both necessary and sufficient to induce downstream open chromatin regions (dOCRs) when transcription termination is disrupted by the viral ICP27 protein. This is accompanied by a marked ICP22-dependent loss of histones downstream of affected genes consistent with impaired histone repositioning in the wake of Pol II. Efficient knock-down of the ICP22-interacting histone chaperone FACT is not sufficient to induce dOCRs in ΔICP22 infection but increases dOCR induction in wild-type HSV-1 infection. Interestingly, this is accompanied by a marked increase in chromatin accessibility within gene bodies. We propose a model in which allosteric changes in Pol II composition downstream of genes and ICP22-mediated interference with FACT activity explain the differential impairment of histone repositioning downstream of genes in the wake of Pol II in HSV-1 infection.

Date: 2023
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DOI: 10.1038/s41467-023-40217-w

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