Genome replication affects transcription factor binding mediating the cascade of herpes simplex virus transcription

Proceedings of the National Academy of Sciences of the United States of America
Sarah E Dremel, N A DeLuca

Abstract

In herpes simplex virus type 1 (HSV-1) infection, the coupling of genome replication and transcription regulation has been known for many years; however, the underlying mechanism has not been elucidated. We performed a comprehensive transcriptomic assessment and factor-binding analysis for Pol II, TBP, TAF1, and Sp1 to assess the effect genome replication has on viral transcription initiation and elongation. The onset of genome replication resulted in the binding of TBP, TAF1, and Pol II to previously silent late promoters. The viral transcription factor, ICP4, was continuously needed in addition to DNA replication for activation of late gene transcription initiation. Furthermore, late promoters contain a motif that closely matches the consensus initiator element (Inr), which robustly bound TAF1 postreplication. Continued DNA replication resulted in reduced binding of Sp1, TBP, and Pol II to early promoters. Therefore, the initiation of early gene transcription is attenuated following DNA replication. Herein, we propose a model for how viral DNA replication results in the differential utilization of cellular factors that function in transcription initiation, leading to the delineation of kinetic class in HSV-productive infection.

References

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Citations

Oct 28, 2019·Critical Reviews in Biochemistry and Molecular Biology·Ella Hartenian, Britt A Glaunsinger

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Datasets Mentioned

BETA
SRP172783

Methods Mentioned

BETA
RNA-Seq
ChIP-Seq

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