KSHV episomes reveal dynamic chromatin loop formation with domain-specific gene regulation

Mel Campbell, Tadashi Watanabe, Kazushi Nakano, Ryan R. Davis, Yuanzhi Lyu, Clifford G. Tepper, Blythe Durbin-Johnson, Masahiro Fujimuro and Yoshihiro Izumiya ()
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Mel Campbell: University of California Davis (UC Davis)
Tadashi Watanabe: Kyoto Pharmaceutical University
Kazushi Nakano: University of California Davis (UC Davis)
Ryan R. Davis: School of Medicine, UC Davis
Yuanzhi Lyu: University of California Davis (UC Davis)
Clifford G. Tepper: UC Davis School of Medicine
Blythe Durbin-Johnson: UC Davis School of Medicine
Masahiro Fujimuro: Kyoto Pharmaceutical University
Yoshihiro Izumiya: University of California Davis (UC Davis)

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract The three-dimensional structure of chromatin organized by genomic loops facilitates RNA polymerase II access to distal promoters. The Kaposi’s sarcoma-associated herpesvirus (KSHV) lytic transcriptional program is initiated by a single viral transactivator, K-Rta. Here we report the KSHV genomic structure and its relationship with K-Rta recruitment sites using Capture Hi–C analyses. High-resolution 3D viral genomic maps identify a number of direct physical, long-range, and dynamic genomic interactions. Mutant KSHV chromosomes harboring point mutations in the K-Rta responsive elements (RE) significantly attenuate not only the directly proximate downstream gene, but also distal gene expression in a domain-specific manner. Genomic loops increase in the presence of K-Rta, while abrogation of K-Rta binding impairs the formation of inducible genomic loops, decreases the expression of genes networked through the looping, and diminishes KSHV replication. Our study demonstrates that genomic architectural dynamics plays an essential role in herpesvirus gene expression.

Date: 2018
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DOI: 10.1038/s41467-017-02089-9

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