Pre-existing genome architecture partitions viral takeover in the smallest free-living eukaryote
- 1Living Systems Institute, University of Exeter, Exeter, UK
Abstract
Nuclear DNA viruses colonize host genomes already structured into complex spatial domains, yet whether established spatial boundaries dictate viral progression remains unresolved--in part because sequence composition and transcriptional output are intertwined in animal models. Here, we tracked productive lytic infection of the marine picoeukaryote Ostreococcus tauri by the giant double-stranded DNA prasinovirus OtV5, recording transcription, accessibility, and 3D contact dynamics across parallel time courses. Although total cellular transcript pools collapsed 18-fold by 10 h post-infection, the host transcriptional shutdown, decay of insulation, early chromatin opening, and viral DNA positioning were all bounded by architectural coordinates defined prior to viral arrival. Across two low-GC outlier domains, chromatin accessibility spiked rapidly, spatial insulation eroded, and loci exhibited relative upregulation by 6 hpi, with the smaller outlier region retaining elevated transcript levels per cell compared to the rest of the genome. Unexpectedly, viral DNA was preferentially depleted from these accessible outlier cores, contacting instead the standard-GC telomeric flanks situated immediately beyond the pre-existing spatial boundaries. Domain identity, rather than local accessibility or active host expression, thus governs viral positioning, demonstrating that pre-existing nuclear architecture partitions the physical and transcriptional takeover of the host cell.
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BibTeX
@misc{harrison2026preexisting,
title = {{Pre-existing genome architecture partitions viral takeover in the smallest free-living eukaryote}},
author = {K. Harrison and M. Valiadi and E. S. Kilias and Y. Loe-Mie and R. Ragheb and S. Kimmance and A. Monier},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.29.762491},
url = {https://www.biorxiv.org/content/10.64898/2026.10.29.762491v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Pre-existing genome architecture partitions viral takeover in the smallest free-living eukaryote
AU - K. Harrison
AU - M. Valiadi
AU - E. S. Kilias
AU - Y. Loe-Mie
AU - R. Ragheb
AU - S. Kimmance
AU - A. Monier
PY - 2026
DA - 2026/10/29
PB - bioRxiv
DO - 10.64898/2026.10.29.762491
UR - https://www.biorxiv.org/content/10.64898/2026.10.29.762491v1
AB - Nuclear DNA viruses colonize host genomes already structured into complex spatial domains, yet whether established spatial boundaries dictate viral progression remains unresolved--in part because sequence composition and transcriptional output are intertwined in animal models. Here, we tracked productive lytic infection of the marine picoeukaryote Ostreococcus tauri by the giant double-stranded DNA prasinovirus OtV5, recording transcription, accessibility, and 3D contact dynamics across parallel time courses. Although total cellular transcript pools collapsed 18-fold by 10 h post-infection, the host transcriptional shutdown, decay of insulation, early chromatin opening, and viral DNA positioning were all bounded by architectural coordinates defined prior to viral arrival. Across two low-GC outlier domains, chromatin accessibility spiked rapidly, spatial insulation eroded, and loci exhibited relative upregulation by 6 hpi, with the smaller outlier region retaining elevated transcript levels per cell compared to the rest of the genome. Unexpectedly, viral DNA was preferentially depleted from these accessible outlier cores, contacting instead the standard-GC telomeric flanks situated immediately beyond the pre-existing spatial boundaries. Domain identity, rather than local accessibility or active host expression, thus governs viral positioning, demonstrating that pre-existing nuclear architecture partitions the physical and transcriptional takeover of the host cell.
ER -