PMID- 2545916
OWN - NLM
STAT- MEDLINE
DCOM- 19890818
LR  - 20200724
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 63
IP  - 8
DP  - 1989 Aug
TI  - Phorbol ester-inducible T-cell-specific expression of variant mouse mammary tumor 
      virus long terminal repeats.
PG  - 3466-71
AB  - Acquired proviruses of mouse mammary tumor virus (MMTV) in T-cell leukemias of 
      male GR mice have rearrangements in the U3 region of their long terminal repeats 
      (LTR). In contrast to the endogenous nonrearranged MMTV proviruses, these mutated 
      copies are highly expressed in leukemic T cells. To investigate whether the 
      sequence alterations in the LTR are responsible for the high expression of 
      rearranged MMTV proviruses, we made constructs in which normal and variant LTRs 
      drive the bacterial reporter gene chloramphenicol acetyltransferase (CAT). Two 
      different rearranged LTRs were used, one containing a 420-base-pair (bp) deletion 
      (L13) and another carrying a 456-bp deletion plus an 82-bp insertion (L42). These 
      constructs were transfected into murine (GRSL) and human (MOLT-4) T-cell lines 
      that either had or had not been treated with phorbol ester 
      (12-O-tetradecanoylphorbol-13-acetate [TPA]). In GRSL cells, the L13-LTR-CAT 
      construct showed transcriptional activity that was further enhanced by TPA. In 
      MOLT-4 cells, both variant LTRs were active, but only after stimulation with TPA. 
      In contrast, normal(N)-LTR-CAT constructs were not expressed, irrespective of TPA 
      addition. In XC rat fibrosarcoma cells, neither normal nor variant LTRs gave rise 
      to detectable CAT activity, either in the presence or in the absence of TPA, but 
      dexamethasone strongly stimulated CAT activity driven by N and L42 LTRs. The L13 
      LTR was considerably less active, probably caused by the deletion of the distal 
      part of the glucocorticoid responsive element. We conclude that the LTR 
      rearrangements generate TPA responsiveness and contribute to T-cell-specific 
      expression of MMTV variants.
FAU - Theunissen, H J
AU  - Theunissen HJ
AD  - Division of Molecular Biology, Antoni van Leeuwenhoekhuis, Netherlands Cancer 
      Institute, Amsterdam.
FAU - Paardekooper, M
AU  - Paardekooper M
FAU - Maduro, L J
AU  - Maduro LJ
FAU - Michalides, R J
AU  - Michalides RJ
FAU - Nusse, R
AU  - Nusse R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (DNA, Viral)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - DNA, Viral/genetics
MH  - *Gene Expression Regulation
MH  - Gene Rearrangement
MH  - Humans
MH  - Leukemia, T-Cell/*microbiology
MH  - Mammary Tumor Virus, Mouse/*genetics
MH  - Mice
MH  - Proviruses/*genetics
MH  - Repetitive Sequences, Nucleic Acid
MH  - Tetradecanoylphorbol Acetate/*pharmacology
MH  - Transcription, Genetic
MH  - Transfection
MH  - Tumor Cells, Cultured
PMC - PMC250923
EDAT- 1989/08/01 00:00
MHDA- 1989/08/01 00:01
PMCR- 1989/08/01
CRDT- 1989/08/01 00:00
PHST- 1989/08/01 00:00 [pubmed]
PHST- 1989/08/01 00:01 [medline]
PHST- 1989/08/01 00:00 [entrez]
PHST- 1989/08/01 00:00 [pmc-release]
AID - 10.1128/JVI.63.8.3466-3471.1989 [doi]
PST - ppublish
SO  - J Virol. 1989 Aug;63(8):3466-71. doi: 10.1128/JVI.63.8.3466-3471.1989.