ChlR1 is required for loading papillomavirus E2 onto mitotic chromosomes and viral genome maintenance.

Joanna Louise Parish, AM Bean, RB Park, EJ Androphy

Research output: Contribution to journalArticlepeer-review

87 Citations (Scopus)

Abstract

Autonomously replicating DNA viruses must evade mitotic checkpoints and actively partition their genomes to maintain persistent infection. The E2 protein serves these functions by tethering papillomavirus episomes to mitotic chromosomes; however, the mechanism remains unresolved. We show that E2 binds ChIR1, a DNA helicase that plays a role in sister chromatid cohesion. The E2 mutation W130R falls to bind ChIR1 and correspondingly does not associate with mitotic chromosomes. Viral genomes encoding this E2 mutation are not episomally maintained in cell culture. Notably, E2 W130R binds Brd4, which reportedly acts as a mitotic tether, indicating this interaction is insufficient for E2 association with mitotic chromosomes. RNAi-induced depletion of ChIR1 significantly reduced E2 localization to mitotic chromosomes. These studies provide compelling evidence that ChIR1 association is required for loading the papillomavirus E2 protein onto mitotic chromosomes and represents a kinetochore-independent mechanism for viral genome maintenance and segregation.

Original languageEnglish
Pages (from-to)867-876
Number of pages10
JournalMolecular Cell
Volume24
Issue number6
DOIs
Publication statusPublished - 28 Dec 2006

Keywords

  • SISTER-CHROMATID COHESION
  • SARCOMA-ASSOCIATED HERPESVIRUS
  • TRANSCRIPTIONAL ACTIVATION FUNCTION
  • BROMODOMAIN PROTEIN BRD4
  • NUCLEAR ANTIGEN 1
  • BOVINE PAPILLOMAVIRUS
  • SACCHAROMYCES-CEREVISIAE
  • DNA HELICASE
  • TYPE-1 E2
  • TRANSACTIVATION DOMAIN

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