23 research outputs found
Transcription initiation of transfected mouse mammary tumor virus LTR DNA is regulated by glucocorticoid hormones.
A chimeric gene, recombined in vitro, containing a long terminal repeat (LTR) sequence from the proviral DNA of mouse mammary tumor virus and the thymidine kinase (tk) gene of Herpes Simplex Virus was introduced into L tk- cells. No transcription of LTR RNA was observed in transfected cells when glucocorticoid hormones were absent from the growth medium. Accumulation of LTR initiated RNA was measured upon hormone addition by the single strand specific nuclease RNA mapping procedure. The accumulation was rapid (detectable after 7.5 minutes), independent of simultaneous protein synthesis and mediated by a functional glucocorticoid receptor complex. Glucocorticoid hormones affect LTR transcription at the level of initiation. The rate of initiation (1.8 X 10(-2) molecules/cell/sec) and a half life of about 30 minutes could be calculated for LTR RNA. The half life of LTR RNA is independent of the presence of hormone
12-O-tetradecanoylphorbol 13-acetate-inducible proteins are synthesized at an increased rate in Bloom syndrome fibroblasts.
The endogenous proviral mouse mammary tumor virus genes of the GR mouse are not identical and only one corresponds to the exogenous virus.
The endogenous proviral copies of mouse mammary tumor virus (MMTV) were selected from a gene library of GR mouse DNA. We obtained five different lambda. MMTV recombinant clones. Four of them correspond to the 3' Eco RI fragments of the endogenous proviruses an one comprises an intact MMTV provirus with 2 to 3 kb of flanking mouse genomic DNA. Heteroduplex formation followed by S1 digestion under stringent conditions shows that there is nucleotide sequence heterology among the cloned endogenous proviral copies. Only one endogenous proviral copy, associated with the mtv-2 locus, was found to be totally homologous to the exogenous proviral DNA