Nucleic Acids Research, Vol 26, Issue 15 3480-3485, Copyright © 1998 by Oxford University Press
L Wang, KE Hunt, GM Martin and J Oshima
The Werner syndrome (WS) is an autosomal recessive segmental progeroid
syndrome caused by mutations in a novel member ( WRN ) of the RecQ family
of helicases. Somatic WS cells are hypermutable and have elongated S
phases, suggesting possible defects in DNA replication and/or repair. As an
initial approach to the investigation of how this locus might be responsive
to DNA damage, we determined the structure of the human WRN promoter. The
WRN promoter region has two transcription initiation sites and exhibits
several features characteristic of so- called constitutive promoters,
including the absence of TATA and CAAT boxes. A luciferase reporter assay
revealed that the upstream promoter was used 2-10-fold less frequently than
the downstream promoter, the variation being a function of cell type. The
activity of the WRN promoter was dramatically reduced in cells from WS
patients. The reduction of activity was not seen in three other promoters
tested, including one TATA-less promoter and one TATA-containing promoter.
This is consistent with the presence of a positive regulatory mechanism of
WRN expression.
ARTICLES
Structure and function of the human Werner syndrome gene promoter: evidence for transcriptional modulation
Department of Genetics and Department of Pathology, University of Washington, Seattle, WA 98195, USA.
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