The bovine papillomavirus type 1 genome contains multiple loci of static DNA bending, but bends are absent from the functional origin of replication

Twenty-four overlapping restriction fragments spanning the entire bovine papillomavirus type 1 (BPV-1) genome were analyzed by electrophoresis to determine the extent of static DNA bending in the BPV-1 genome. Thirteen of 24 fragments contained static bends. Based on known locations of previously ma...

Full description

Saved in:
Bibliographic Details
Published in:Virus research Vol. 31; no. 2; p. 203
Main Authors: Schuller, G, Holt, S E, Hsu, J, Wilson, V G
Format: Journal Article
Language:English
Published: Netherlands 01-02-1994
Subjects:
Online Access:Get more information
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Twenty-four overlapping restriction fragments spanning the entire bovine papillomavirus type 1 (BPV-1) genome were analyzed by electrophoresis to determine the extent of static DNA bending in the BPV-1 genome. Thirteen of 24 fragments contained static bends. Based on known locations of previously mapped bend loci and the overlapping pattern of these 13 fragments, we estimate that there are 8-11 distinct static bend loci in the BPV-1 genome. The bend loci were not uniformly distributed on the genome and with one exception, were clustered from nucleotides 5816 to 2621 on the BPV-1 map. This portion of the BPV-1 genome contains most of the transcriptional regulatory sequences as well as the origin of replication. The concordance between the genomic distribution of DNA bends and cis-active elements is consistent with the possibility that bent sequences may contribute to the function of at least some of these elements. However, unlike SV40, there was no static bend at that functional origin of replication for BPV-1. The nearest bends to the origin were approximately 120 bp to the 5' side and 300 bp to the 3' side. As both of these bends were outside of the sequences required for origin function, it is unlikely that static bending plays a critical role in BPV-1 replication.
ISSN:0168-1702
DOI:10.1016/0168-1702(94)90004-3