Identification and control of the cis-acting elements of the immediate early gene of equid herpesvirus type 1

Purewal, A.S.; Smallwood, Andrea; Kaushal, A.; Adegboye, D. S.; Edington, N.

doi:10.1099/0022-1317-73-3-513

Cited by 45 publications

(22 citation statements)

References 37 publications

(27 reference statements)

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“…Purewal et al [34], Welch et al [45], Fortier et al [21], Jolly et al [28] and Nordengrahn et al [31] have linked EHV-2 with Streptococcus zooepidemicus, Rhodococcus equi, and S. equi. In our study, we could not establish a link between gammaherpesvirus infection and bacterial colonization as all swabs were transported to the laboratory in virus transport medium containing antibiotics and therefore unsuitable for bacteriology testing.…”

Section: Discussionmentioning

confidence: 99%

Equine herpesvirus infections in yearlings in South-East Queensland

et al. 2008

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SummaryTwelve nasal swabs were collected from yearling horses with respiratory distress and tested for Equid herpesvirus 1 (EHV-1) and Equid herpesvirus 4 (EHV-4) by realtime PCR targeting the glycoprotein B gene. All samples were negative for EHV-1; however 3 were positive for EHV-4. When these samples were tested for EHV-2 and EHV-5 by PCR all samples were negative for EHV-2 and 11 were positive for EHV-5. All three samples that were positive for EHV-4 were also positive for EHV-5.These three samples gave a limited CPE in ED cells reminiscent of EHV-4 CPE.EHV-4 CPE was obvious after 3 days and was characterised by syncytia. None of the samples produced cytopathic effect (CPE) on African green monkey kidney (Vero) cells or hamster kidney (BSR) cells. Four of the samples, which were positive in the EHV-5 PCR, produced CPE on rabbit kidney (RK13) cells and equine dermis (ED) cells. EHV-5 CPE on both cell lines was slow and was apparent after four 7-day passages. On RK13 cells the CPE was characteristic of equid herpesvirus with the formation of syncytia. However in ED cells, the CPE was characterised by ringshaped syncytia.For the first time a case of equine respiratory disease involving dual infection with EHV-4 and EHV-5 has been reported in Queensland. This was shown by simultaneously isolating EHV-4 and EHV-5 from clinical samples. EHV5 was recovered from all samples except one, suggesting that EHV5 was more prevalent in young horses than EHV2.

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Section: Discussionmentioning

confidence: 99%

Equine herpesvirus infections in yearlings in South-East Queensland

et al. 2008

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“…Like VP16, both of these proteins are packaged in the virus tegument and transactivate viral IE gene promoters (44,48). They have also been shown to be capable of activating transcription through a TAATGARAT element (44,48).…”

Section: Discussionmentioning

confidence: 99%

Transcriptional activation by herpes simplex virus type 1 VP16 in vitro and its inhibition by oligopeptides.

Wu¹,

Monokian²,

Mark³

et al. 1994

Mol. Cell. Biol.

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VP16 is a herpes simplex virus (HSV)-encoded transcriptional activator protein that is essential for efficient viral replication and as such may be a target for novel therapeutic agents directed against viral gene expression. We have reconstituted transcriptional activation by VP16 in an in vitro system that is dependent on DNA sequences from HSV immediate-early gene promoters and on protein-protein interactions between VP16 and Oct-i that are required for VP16 activation in vivo. Activation increased synergistically with the number of TAATGARAT elements (the cis-acting element for VP16 activation in vivo) upstream of the core promoter, and mutations of this element that reduce Oct-I or VP16 DNA binding reduced transactivation in vitro. A VP16 insertion mutant unable to interact with Oct-1 was inactive, but, surprisingly, a deletion mutant lacking the activation domain was -65% as active as the full-length protein. The activation domains of Oct-1 were necessary for activation in reactions containing the VP16 deletion mutant, and they contributed significantly to activation by full-length VP16. Addition of a GA-rich element present in many HSV immediate-early gene enhancers synergistically stimulated VP16-activated transcription. Finally, oligopeptides that are derived from a region of VP16 thought to contact a cellular factor known as HCF (host cell factor) and that inhibit efficient VP16 binding to the TAATGARAT element also specifically inhibited VP16-activated, but not basal, transcription. Amino acid substitutions in one of these peptides identified three residues that are absolutely required for inhibition and presumably for interaction of VP16 with HCF.Herpes simplex virus type 1 (HSV-1) and HSV-2 package a protein, VP16, also known as Vmw65 or a-TIF, that activates transcription of the viral immediate-early (IE) genes and is essential for efficient virus replication (1,2,7,13,24,61). Two features of this 65-kDa protein have made it the object of much interest in the study of eukaryotic gene regulation. Its highly acidic C-terminal activation domain, which is absolutely required for IE gene activation in vivo (22,59,62), is one of the most potent known and has been fused to heterologous DNA binding domains to create novel transactivators for both in vivo and in vitro studies (8,10,50). Investigations of wild-type and mutant forms of this domain have begun to shed light on its key structural features (14,17,22,49,59,62). Despite such intensive study, the mechanism of action of this prototypic activation domain-whether it acts directly on a basal transcription factor (27,39,40,57) proteins, Oct-1 and HCF (host cell factor; also known as Cl factor, VCAF, or CFF), which direct its binding to a sequence element, the TAATGARAT motif, found in all HSV-1 IE enhancers (20,23,29,32,33,46,56 TAATGARAT element. Although Oct-I and VP16 can form a low-affinity ternary complex with TAATGARAT (32,55,56), HCF stimulates complex formation by several orders of magnitude (32). HCF has no apparent sequence-specific DNA binding...

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“…Homologs of VP16 have now been identified in other herpesviruses, including varicella-zoster virus (7,27), equine herpesviruses (EHV) 1 and 4 (23,38,39), and bovine herpesvirus 1 (BHV-1) (3). The primary structural attributes of VP16, demonstrated to be important for interaction with Oct-1 and HCF, are retained in these homologs.…”

mentioning

confidence: 99%

Conformational Alteration of Oct-1 upon DNA Binding Dictates Selectivity in Differential Interactions with Related Transcriptional Coactivators

Misra

Walter

Yang

et al. 1996

Molecular and Cellular Biology

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VP16 (termed VP16-H here) of herpes simplex virus (HSV) belongs to a family of related regulatory proteins which includes VP16-B of bovine herpesvirus (BHV).We show that VP16-B, while also being a powerful transactivator of transcription dependent on Oct-1 binding sites in its target promoters, has virtually no activity on a defined VP16-H-responsive, octamer-containing target promoter. While Oct-1 binds equally well to the VP16-B-responsive and -nonresponsive sites, VP16-B interacts with Oct-1 only when Oct-1 is bound to the BHV octamer site and not when it is bound to the HSV site. We show from the analysis of chimeric proteins that the ability of VP16-B to discriminate between the Oct-1 forms depends on features of its N-terminal region. We also show from an analysis of chimeric DNA motifs that sequences that lie 3 to the POU domain-contacting region of the HSV octamer site play a role in making it unresponsive to VP16-B. Finally, we show by high-resolution hydroxyl radical footprint analysis that the conformation of Oct-1 is different on the two sites. These results augment our previous report on an allosteric effect of DNA signals on the conformation of bound proteins and indicate that different conformations of the same DNA binding protein can be recognized selectively by related members of interacting regulatory proteins. The possible implications of our observations for selective gene regulation by Oct-1, a ubiquitous transcription factor, and other multimember transcription families are discussed.A fundamental aspect of the proper orchestration of coordinate and differential gene expression is the assembly of multicomponent transcription complexes involving different combinations and spatial arrangements of transcription factors. Given the multiplicity of potential interactions between regulatory proteins and the identification of numerous large families of DNA binding proteins with related if not identical binding sites, an understanding of precisely how the appropriate combinations are selected and assembled is crucial to the elucidation of the basis of gene control.

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Identification and control of the cis-acting elements of the immediate early gene of equid herpesvirus type 1

Cited by 45 publications

References 37 publications

Equine herpesvirus infections in yearlings in South-East Queensland

Equine herpesvirus infections in yearlings in South-East Queensland

Transcriptional activation by herpes simplex virus type 1 VP16 in vitro and its inhibition by oligopeptides.

Conformational Alteration of Oct-1 upon DNA Binding Dictates Selectivity in Differential Interactions with Related Transcriptional Coactivators

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