Formation of a cruciform structure at the simian virus 40 replication origin abolishes T-antigen binding to the origin in vitro.
Heteroduplex DNA molecules were formed by annealing an intact simian virus replication origin-containing fragment to a mutant derivative lacking the indigenous wild-type 27-base-pair (bp) inverted repeat within this structure and containing a nonhomologous 26-bp inverted repeat sequence in its place. Results of restriction enzyme and S1 endonuclease cleavage analyses strongly suggested that a 13-bp stem-loop structure formed at the site of nonhomology between these two DNAs. This structure lies within the boundary of simian virus 40 T-antigen-binding site 2, and its presence inhibited T-antigen binding to that sequence but not to an adjacent higher-affinity binding site (site 1). Therefore, the conformation of sequences within an otherwise intact T-antigen-binding site can have major effects upon T-antigen binding there.
Tenen
D G
DG
Haines
L L
LL
Hansen
U M
UM
Martin
R G
RG
Livingston
D M
DM
D000957:Antigens, Viral, Tumor / Q000378:metabolism*; D001483:Base Sequence; D001665:Binding Sites; D004261:DNA Replication; D004279:DNA, Viral / Q000235:genetics* / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D009154:Mutation; D009690:Nucleic Acid Conformation; D013539:Simian virus 40 / Q000235:genetics*; D013329:Structure-Activity Relationship
D000957:Antigens, Viral, Tumor; D004279:DNA, Viral; D004268:DNA-Binding Proteins