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      Independent Cis-Regulatory Modules within the Herpes Simplex Virus 1 Infected Cell Protein 0 (ICP0) Promoter Are Transactivated by Krüppel-like Factor 15 and Glucocorticoid Receptor.

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          Abstract

          A corticosteroid antagonist impairs Herpes Simplex Virus 1 (HSV-1) productive infection and explant-induced reactivation from latency, suggesting corticosteroids and the glucocorticoid receptor (GR) mediate certain aspects of these complex virus-host interactions. GR-hormone complexes regulate transcription positively and negatively, in part, by binding GR response elements (GREs). Recent studies revealed infected cell protein 0 (ICP0), ICP4, and ICP27 promoter/cis-regulatory modules (CRMs) are cooperatively transactivated by GR and Krüppel-like factor 15 (KLF15), which forms a feed-forward transcription loop. We hypothesized the ICP0 promoter contains independent CRMs that are transactivated by GR, KLF15, and the synthetic corticosteroid dexamethasone (DEX). This hypothesis is based on the finding that the ICP0 promoter contains multiple transcription factor binding sites, and GR and KLF15 cooperatively transactivate the full-length ICP0 promoter. ICP0 promoter sequences spanning -800 to -635 (fragment A) were efficiently transactivated by GR, KLF15, and DEX in monkey kidney cells (Vero), whereas GR and DEX significantly enhanced promoter activity in mouse neuroblastoma cells (Neuro-2A). Furthermore, ICP0 fragment B (-458 to -635) was efficiently transactivated by GR, KLF15, and DEX in Vero cells, but not Neuro-2A cells. Finally, fragment D (-232 to -24) was transactivated significantly in Vero cells by GR, KLF15, and DEX, whereas KLF15 and DEX were sufficient for transactivation in Neuro-2A cells. Collectively, these studies revealed efficient transactivation of three independent CRMs within the ICP0 promoter by GR, KLF15, and/or DEX. Finally, GC-rich sequences containing specificity protein 1 (Sp1) binding sites were essential for transactivation.

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          Author and article information

          Journal
          Viruses
          Viruses
          MDPI AG
          1999-4915
          1999-4915
          Jun 13 2022
          : 14
          : 6
          Affiliations
          [1 ] Department of Veterinary Pathobiology, College of Veterinary Medicine, Oklahoma State University, 208 N McFarland Street, RM 250 McElroy Hall, Stillwater, OK 74078, USA.
          [2 ] Experimental Pathology Program, University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555, USA.
          Article
          v14061284
          10.3390/v14061284
          9228413
          35746756
          700ca0be-1995-40c9-ad02-0cb3752b2559
          History

          Krüppel-like factor 15,stress,infected cell protein 0 (ICP0) expression,herpes simplex virus type 1 (HSV-1),glucocorticoid receptor (GR)

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