PMID- 9338008
OWN - NLM
STAT- MEDLINE
DCOM- 19971119
LR  - 20081121
IS  - 0969-7128 (Print)
IS  - 0969-7128 (Linking)
VI  - 4
IP  - 8
DP  - 1997 Aug
TI  - beta-Gal enzyme activity driven by the HSV LAT promoter does not correspond to 
      beta-gal RNA levels in mouse trigeminal ganglia.
PG  - 797-807
AB  - beta-Galactosidase enzyme expression can be detected in only a small percentage 
      of trigeminal ganglia (TG) neurons acutely and latently infected with herpes 
      simplex virus (HSV), in which the lacZ reporter gene was placed down-stream of 
      the latency associated transcript (LAT) promoter at the LAT locus. However, DNA 
      quantification suggests that a larger percentage of cells is infected than is 
      expressing beta-galactosidase enzyme. To investigate the mechanism involved in 
      regulation of genes expressed from the LAT promoter in trigeminal ganglia, in 
      situ hybridization and histochemical staining assays were employed to determine 
      on a cell-by-cell basis beta-gal gene expression both at the RNA and protein 
      level. Using a LAT promoter-driven beta-gal construct in HSV-1 strain HFEM, it 
      was found that there were 89-fold more cells positive for beta-gal transcript 
      than cells positive for beta-gal enzyme in acutely infected trigeminal ganglia 
      and a 10-fold difference in latently infected trigeminal ganglia. Thus, there is 
      a discordance between beta-gal mRNA and beta-gal enzyme levels in HFEM/LAT-lacZ 
      infected cells during acute and latent infection, and the beta-gal reporter gene 
      activity does not faithfully compare the LAT promoter activity between acute and 
      latently infected tissue. In contrast, in situ hybridization and histochemical 
      staining assays were performed in mice acutely infected with a virus in which 140 
      bp of the LAT promoter sequences flanking the TATA element were replaced by 1.8 
      kbp of the neurofilament promoter (HSV-1 HFEM/NF-lacZ). This construct showed a 
      correlation between beta-gal mRNA and enzyme expression in trigeminal ganglia in 
      acute and latent infections. These findings suggest that sequences at the 5' end 
      of the beta-gal transcript influence translation of the beta-gal message.
FAU - Huang, Q S
AU  - Huang QS
AD  - Wistar Institute, Philadelphia, PA 19104, USA.
FAU - Valyi-Nagy, T
AU  - Valyi-Nagy T
FAU - Kesari, S
AU  - Kesari S
FAU - Fraser, N W
AU  - Fraser NW
LA  - eng
GR  - CA09171/CA/NCI NIH HHS/United States
GR  - NS 29390/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Gene Ther
JT  - Gene therapy
JID - 9421525
RN  - 63231-63-0 (RNA)
RN  - EC 3.2.1.23 (beta-Galactosidase)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Gene Expression
MH  - Genetic Vectors
MH  - Histocytochemistry
MH  - In Situ Hybridization
MH  - Lac Operon
MH  - Mice
MH  - Molecular Sequence Data
MH  - *Promoter Regions, Genetic
MH  - RNA/*analysis
MH  - Simplexvirus/*genetics
MH  - Trigeminal Ganglion/*enzymology
MH  - beta-Galactosidase/*genetics/*metabolism
EDAT- 1997/08/01 00:00
MHDA- 1997/10/24 00:01
CRDT- 1997/08/01 00:00
PHST- 1997/08/01 00:00 [pubmed]
PHST- 1997/10/24 00:01 [medline]
PHST- 1997/08/01 00:00 [entrez]
AID - 10.1038/sj.gt.3300476 [doi]
PST - ppublish
SO  - Gene Ther. 1997 Aug;4(8):797-807. doi: 10.1038/sj.gt.3300476.