TY - JOUR
T1 - Identification of sequences encoding the equine infectious anemia virus tat gene
AU - Noiman, Silvia
AU - Gazit, Arnona
AU - Tori, Orli
AU - Sherman, Levana
AU - Miki, Toru
AU - Tronick, Steven R.
AU - Yaniv, Abraham
N1 - Funding Information:
We thank Dr. S. Aaronson for his continued support and encouragement. T.M. was partially supported by a Japanese Overseas Cancer Fellowship from the Foundation for Promotion of Cancer Research.
PY - 1990/5
Y1 - 1990/5
N2 - Equine infectious anemia virus (EIAV), a lentivirus, encodes a trans-activator (tat) which stimulates gene expression directed by the viral long terminal repeat (LTR). This function has been previously shown by us and others to be encoded by sequences within the middle region of the EIAV genome in which two short open reading frames, S1 and S2, reside. In the present study, by using in vitro mutagenesis, we show that disruption of S1, but not S2, completely abolished trans-activation. Addition of oligonucleotides complementary to S1 to cells transfected with a tat expression vector resulted in inhibition of trans-activation. EIAV cDNAs were isolated from a library of EIAV-infected cells constructed by using a eukaryotic expression vector. One cDNA clone which contained S1 sequences was able to trans-activate the EIAV LTR. Sequence analysis of this cDNA clone revealed that, in addition to S1, two other open reading frames were present. The cDNA still retained its activity when the latter two sequences were deleted.
AB - Equine infectious anemia virus (EIAV), a lentivirus, encodes a trans-activator (tat) which stimulates gene expression directed by the viral long terminal repeat (LTR). This function has been previously shown by us and others to be encoded by sequences within the middle region of the EIAV genome in which two short open reading frames, S1 and S2, reside. In the present study, by using in vitro mutagenesis, we show that disruption of S1, but not S2, completely abolished trans-activation. Addition of oligonucleotides complementary to S1 to cells transfected with a tat expression vector resulted in inhibition of trans-activation. EIAV cDNAs were isolated from a library of EIAV-infected cells constructed by using a eukaryotic expression vector. One cDNA clone which contained S1 sequences was able to trans-activate the EIAV LTR. Sequence analysis of this cDNA clone revealed that, in addition to S1, two other open reading frames were present. The cDNA still retained its activity when the latter two sequences were deleted.
UR - http://www.scopus.com/inward/record.url?scp=0025278072&partnerID=8YFLogxK
U2 - 10.1016/0042-6822(90)90254-O
DO - 10.1016/0042-6822(90)90254-O
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AN - SCOPUS:0025278072
SN - 0042-6822
VL - 176
SP - 280
EP - 288
JO - Virology
JF - Virology
IS - 1
ER -