Maintenance of the DNA puff expanded state is independent of active replication and transcription

Mok, Eric H.; Smith, Heidi S.; DiBartolomeis, Susan M.; Kerrebrock, Anne W.; Rothschild, Lynn J.; Lange, Thilo S.; Gerbi, Susan A.

doi:10.1007/s004120000119

Cited by 15 publications

(9 citation statements)

References 107 publications

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“…Heat shock is another cellular stress that causes global changes in Pol II transcription in eukaryotic cells. Although some genes, such as those encoding heat shock proteins, are significantly activated in response to heat shock, most mRNA genes are thought to be transcriptionally repressed (36)(37)(38)(39). We were interested in learning whether the genes repressed during HSV-1 infection also showed a profound loss in Pol II occupancy in response to heat shock, which would suggest similarities in how Pol II transcription is downregulated in response to the two different stresses.…”

Section: Resultsmentioning

confidence: 99%

Infection by Herpes Simplex Virus 1 Causes Near-Complete Loss of RNA Polymerase II Occupancy on the Host Cell Genome

Abrisch

Eidem

Yakovchuk

et al. 2016

J Virol

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Lytic infection by herpes simplex virus 1 (HSV-1) triggers a change in many host cell programs as the virus strives to express its own genes and replicate. Part of this process is repression of host cell transcription by RNA polymerase II (Pol II), which also transcribes the viral genome. Here, we describe a global characterization of Pol II occupancy on the viral and host genomes in response to HSV-1 infection using chromatin immunoprecipitation followed by deep sequencing (ChIP-seq). The data reveal near-complete loss of Pol II occupancy throughout host cell mRNA genes, in both their bodies and promoter-proximal regions. Increases in Pol II occupancy of host cell genes, which would be consistent with robust transcriptional activation, were not observed. HSV-1 infection induced a more potent and widespread repression of Pol II occupancy than did heat shock, another cellular stress that widely represses transcription. Concomitant with the loss of host genome Pol II occupancy, we observed Pol II covering the HSV-1 genome, reflecting a high level of viral gene transcription. Interestingly, the positions of the peaks of Pol II occupancy at HSV-1 and host cell promoters were different. The primary peak of Pol II occupancy at HSV-1 genes is ϳ170 bp upstream of where it is positioned at host cell genes, suggesting that specific steps in transcription are regulated differently at HSV-1 genes than at host cell mRNA genes. IMPORTANCE We investigated the effect of herpes simplex virus 1 (HSV-1) infection on transcription of host cell and viral genes by RNA polymerase II (Pol II). The approach we used was to determine how levels of genome-bound Pol II changed after HSV-1 infection.We found that HSV-1 caused a profound loss of Pol II occupancy across the host cell genome. Increases in Pol II occupancy were not observed, showing that no host genes were activated after infection. In contrast, Pol II occupied the entire HSV-1 genome. Moreover, the pattern of Pol II at HSV-1 genes differed from that on host cell genes, suggesting a unique mode of viral gene transcription. These studies provide new insight into how HSV-1 causes changes in the cellular program of gene expression and how the virus coopts host Pol II for its own use. Herpes simplex virus 1 (HSV-1) is a double-stranded DNA virus that proliferates in the nuclei of host cells during lytic infection (reviewed in reference 1). HSV-1 can cause lifelong infection by establishing asymptomatic latency in host sensory neurons, where it remains in a transcriptionally silenced state until it is stimulated by stress to reactivate and replicate in epithelial cells (2). The majority of the population are infected with HSV-1, which is largely responsible for oral cold sores; however, in rarer cases, it can cause severe conditions, such as blindness and encephalitis (3, 4). Recent experimental and epidemiological evidence also suggests a role for recurrent HSV-1 infection in Alzheimer's disease (5). Despite its clear medical significance, the relationship between the virus ...

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Section: Resultsmentioning

confidence: 99%

Infection by Herpes Simplex Virus 1 Causes Near-Complete Loss of RNA Polymerase II Occupancy on the Host Cell Genome

Abrisch

Eidem

Yakovchuk

et al. 2016

J Virol

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“…In situ hybridization of pSc-hsp70/2.3 (Mok et al, 2001) to polytene chromosomes of R. americana. The consistently positive site, A14/15, is indicated by an arrow in both fluorescent and phase contrast photographs.…”

Section: The Development Of the Heat Shock Reactionmentioning

confidence: 99%

“…The plasmid DNA containing the hsp70 gene from Sciara coprophila (Mok et al, 2001) was nick translated using the BioNick System (Invitrogen). Hybridization was carried out overnight at 32°C according to the protocol of Stocker and Gorab (2000) and visualized by reactions with anti-biotin and a secondary antibody containing rhodamine as described above.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

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The Effects of Temperature Shock on Transcription and Replication in Rhynchosciara americana (Diptera: Sciaridae)

2006

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The chromosomal response to temperature shock in Rhynchosciara americana is similar to that observed in other Diptera. After a 33 degrees C/90 min or a 36 degrees C/30 min shock the reaction for RNA polymerase II (RpII) is enhanced at five loci. The most prominent of these was identified by in situ hybridization as the site of the hsp70 gene. At 33 degrees C, an accumulation of heat shock factor (HSF) and an increase in the level of RpII was observed at some heat shock loci after 5 min and reached a maximum after 15 min at most loci. The pattern of accumulation of HSF and RpII at individual heat shock loci was similar and their increases were generally coordinated among the loci. RpII gradually decreased at sites active prior to shock, the rate of decrease varying with the site. The B2 DNA puff retained RpII for a significant length of time while the histone locus still contained RpII after a shock of 90 min. With a 36 degrees C/30 min shock, the size of the heat shock puffs and the intensities of HSF and RpII peaked at 1-4 h post stress. The level of HSF declined rapidly after 1 h while the level of RpII remained high for an additional 4 h. The reaction of the DNA puffs to heat shock varied. Usually they did not regress completely and retained traces of RpII. BrdU incorporation continued at both amplifying and non-amplifying bands after shock but on average it appeared depressed for about 24 h post stress.

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“…Transcriptional activity is traditionally invoked to explain polytene chromosome banding patterns. Although general correlation between transcription and the decondensed state of multiple polytene chromosome regions is well established (reviewed in Zhimulev et al 2004), a number of independent observations indicate that under certain conditions decondensation and transcriptional activity of a locus could be uncoupled (Crowley et al 1984;Mok et al 2001;Petesch and Lis 2008;Winegarden et al 1996).…”

Section: Introductionmentioning

confidence: 99%

Functional analysis of Drosophila polytene chromosomes decompacted unit: the interband

et al. 2009

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Differential compaction of the interphase chromosomes is important for proper functioning of the eukaryotic genome. Such non-uniform compaction is most easily observed in Drosophila salivary gland polytene chromosomes as a reproducible banding pattern. Functional mechanisms underlying the establishment and maintenance of the banding pattern remain unclear but have been hypothesized to involve transcription and chromatin insulators. We tested functional properties of DNA fragments from several transcriptionally inert interband regions that behave as autonomous decompacted units of polytene chromosomes. Our results suggest that, in the absence of transcription, the decondensed state of interband regions does not depend on the presence of insulator elements but instead correlates with the presence of transcriptional enhancers.

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Maintenance of the DNA puff expanded state is independent of active replication and transcription

Cited by 15 publications

References 107 publications

Infection by Herpes Simplex Virus 1 Causes Near-Complete Loss of RNA Polymerase II Occupancy on the Host Cell Genome

Infection by Herpes Simplex Virus 1 Causes Near-Complete Loss of RNA Polymerase II Occupancy on the Host Cell Genome

The Effects of Temperature Shock on Transcription and Replication in Rhynchosciara americana (Diptera: Sciaridae)

Functional analysis of Drosophila polytene chromosomes decompacted unit: the interband

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