Author: Ella N Hartenian; Britt A Glaunsinger
Title: Herpesvirus infection reduces Pol II occupancy of host promoters but spares viral promoters Document date: 2019_3_26
ID: i51almnu_4
Snippet: Pol II signal throughout Srsf2 in the MHV68 condition of two replicate ChIP experiments. We 108 independently validated the ChIP-seq results by ChIP-qPCR at the Rplp0 and Fus promoters, 109 both of which showed a significant reduction of Pol II occupancy in cells infected with WT but 110 not R443I MHV68 (Fig 1C) , as did a validation using a second antibody that recognizes the N-111 terminus of the major subunit of Pol II, Rpb1 (Fig1D). The genom.....
Document: Pol II signal throughout Srsf2 in the MHV68 condition of two replicate ChIP experiments. We 108 independently validated the ChIP-seq results by ChIP-qPCR at the Rplp0 and Fus promoters, 109 both of which showed a significant reduction of Pol II occupancy in cells infected with WT but 110 not R443I MHV68 (Fig 1C) , as did a validation using a second antibody that recognizes the N-111 terminus of the major subunit of Pol II, Rpb1 (Fig1D). The genome-wide reduction in poised Pol 112 II in WT but not R443I infected cells was also evident when the sequencing reads from positions 113 -2000 to +4000 around the transcription start sites (TSS) were plotted as a histogram (Fig 1G and 114 S1 Fig B) . The variability between replicates in R443I recovery (Fig 1B) is likely due to 115 differences in the extent of host shutoff reduction between replicates due to R443I reducing 116 muSOX activity while not being a catalytic mutant. 117
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