PMID- 1531277
OWN - NLM
STAT- MEDLINE
DCOM- 19920312
LR  - 20190714
IS  - 0042-6822 (Print)
IS  - 0042-6822 (Linking)
VI  - 187
IP  - 1
DP  - 1992 Mar
TI  - Impaired transcription of the poly rI:rC- and interferon-activatable 202 gene in 
      mice and cell lines from the C57BL/6 strain.
PG  - 115-23
AB  - Activation of 202 and (2'-5')(A)n synthetase genes after injection of interferon 
      (IFN)-inducing, double-stranded, poly rI:rC was compared in various mouse 
      strains. The 202 mRNA level increased 4.5- to 10-fold in DBA/2, BALB/c, and 
      C3H/HeJ mice, whereas in C57BL/6 mice it rose only to about that in untreated 
      DBA/2, BALB/c, and C3H/HeJ mice. To determine whether this low level was due to a 
      reduced transcription rate, a nuclear "run-on" assay was performed with NIH 3T3 
      cells or BLK cells derived from C57BL/6 mice. IFN-alpha increased the 202 mRNA 
      transcription severalfold in NIH 3T3 cells only, and that of a (2'-5')(A)n 
      synthetase gene in both cell lines. The possibility that an alteration in 
      transacting factors could be responsible for this difference was examined. For 
      this purpose the 5' terminal flanking region (called the b segment, about 0.8 kb) 
      of the 202 gene was linked to a heterologous reporter 
      gene--chloramphenicolacetyl-transferase (CAT) and transfected into normal or 
      transformed NIH 3T3 cells and into various C57BL/6-derived cell lines. IFN-alpha 
      induced strong CAT activity in transfected normal or transformed NIH 3T3 cells, 
      but a much lower activity in those from C57BL/6 mice. The b segment contains an 
      IFN-responsive element (ISRE) (35 bp) homologous to that present in several other 
      IFN-inducible genes. Three tandem copies of the 202 ISRE were linked to an 
      enhancerless SV40 early promoter driving an influenza virus hemagglutinin (HA) 
      cDNA segment. No increase in HA mRNA expression was detected in the transfected 
      BLK cell line derived from C57BL/6 mice following IFN treatment, whereas in the 
      NIH 3T3 cell line, the IFN treatment resulted in a 2.5-fold increase. These and 
      other results suggest that C57BL/6 mice and cell lines derived from them might 
      carry defective transacting factors impairing the ability of IFN-alpha to 
      activate the 202 gene without impairing its ability to activate a (2'-5')(A)n 
      synthetase gene.
FAU - Gariglio, M
AU  - Gariglio M
AD  - Institute of Microbiology, Medical School, University of Torino, Italy.
FAU - Panico, S
AU  - Panico S
FAU - Cavallo, G
AU  - Cavallo G
FAU - Divaker, C
AU  - Divaker C
FAU - Lengyel, P
AU  - Lengyel P
FAU - Landolfo, S
AU  - Landolfo S
LA  - eng
GR  - AI 12320/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Virology
JT  - Virology
JID - 0110674
RN  - 0 (Interferon Type I)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Transcription Factors)
RN  - EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase)
RN  - O84C90HH2L (Poly I-C)
SB  - IM
MH  - 2',5'-Oligoadenylate Synthetase/genetics
MH  - Animals
MH  - Base Sequence
MH  - Blotting, Northern
MH  - Female
MH  - Gene Expression Regulation/*drug effects
MH  - Interferon Type I/*pharmacology
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Molecular Sequence Data
MH  - Plasmids/genetics
MH  - Poly I-C/*pharmacology
MH  - Recombinant Proteins
MH  - Specific Pathogen-Free Organisms
MH  - Transcription Factors/genetics
MH  - Transcription, Genetic/drug effects
MH  - Tumor Cells, Cultured
EDAT- 1992/03/01 00:00
MHDA- 1992/03/01 00:01
CRDT- 1992/03/01 00:00
PHST- 1992/03/01 00:00 [pubmed]
PHST- 1992/03/01 00:01 [medline]
PHST- 1992/03/01 00:00 [entrez]
AID - 10.1016/0042-6822(92)90300-e [doi]
PST - ppublish
SO  - Virology. 1992 Mar;187(1):115-23. doi: 10.1016/0042-6822(92)90300-e.