We have previously shown that long terminal repeats (LTRs) derived fro
m various isolates of SIVAGM share a unique functional property. In th
e absence of viral Tat, all SIVAGM LTRs act as much more efficient pro
moters than any of the other LTRs derived from representative primate
immunodeficiency viruses. In the presence of Tat, however, SIVAGM LTRs
are activated relatively inefficiently. To map the elements that conf
er these features on the SIVAGM LTR, a number of deletion mutants were
constructed, and their promoter activities were determined using a ba
cterial CAT gene as a marker. The results obtained indicated that vari
ous elements located in the U3 region may contribute to the high basal
promoter activity and that no negative elements are present in the re
gion. The Tat-responsive sequence TAR was localized to the R region as
observed for the other LTRs. A mutant carrying a single nucleotide de
letion in this region completely lost responsiveness to Tat protein.