PMID- 9614871
OWN - NLM
STAT- MEDLINE
DCOM- 19980624
LR  - 20071114
IS  - 0042-6822 (Print)
IS  - 0042-6822 (Linking)
VI  - 245
IP  - 1
DP  - 1998 May 25
TI  - Expression and mutational analysis of the baculovirus very late factor 1 (vlf-1) 
      gene.
PG  - 99-109
AB  - We have examined the expression and function of a gene, vlf-1, of Autographa 
      californica nuclear polyhedrosis virus that is known to encode a regulator of 
      very late gene transcription. Western blot analysis revealed that vlf-1 is 
      expressed during the late phase of infection, primarily from 15 to 24 h 
      postinfection. VLF-1 localized in the cell nucleus and was also present in the 
      nucleocapsids of virus particles. Mapping of vlf-1 mRNA by primer extension 
      showed that transcription initiates at a TAAG motif 71 bp upstream of the vlf-1 
      open reading frame. Disruption of this TAAG motif abolished the ability of vlf-1 
      to stimulate transcription from the very late polyhedrin gene (polh) promoter in 
      transient expression assays, suggesting that vlf-1 expression is controlled by 
      the TAAG motif. Using a highly efficient system to construct recombinant viruses 
      with modifications in vlf-1, we confirmed that the TAAG motif was essential. 
      Furthermore, efforts to construct null mutants of vlf-1 failed, suggesting that 
      vlf-1 is an essential gene for virus replication. Computer-assisted sequence 
      homology searches place vlf-1 in the lambda phage integrase family (McLachlin and 
      Miller, 1994). None of the strictly conserved residues of this family which are 
      found in vlf-1 could be changed in the viral genome, implying that the putative 
      integrase activity of VLF-1 is associated with the essential function of vlf-1. 
      However, mutation of a crucial active-site tyrosine did not affect the ability of 
      vlf-1 to transactivate the polh promoter in transient expression assays, 
      indicating that the very late transcriptional activity of VLF-1 does not require 
      the integrase activity.
FAU - Yang, S
AU  - Yang S
AD  - Department of Genetics, University of Georgia, Athens 30602, USA.
FAU - Miller, L K
AU  - Miller LK
LA  - eng
GR  - AI23719/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Virology
JT  - Virology
JID - 0110674
RN  - 0 (Ac-vlf-1 protein, Autographa californica nucleopolyhedrovirus)
RN  - 0 (Transcription Factors)
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Animals
MH  - Baculoviridae/*physiology
MH  - DNA Mutational Analysis
MH  - *Gene Expression Regulation, Viral
MH  - *Genes, Viral
MH  - Transcription Factors/*genetics
MH  - Viral Proteins/*genetics
MH  - Virus Replication/*genetics
EDAT- 1998/06/06 00:00
MHDA- 1998/06/06 00:01
CRDT- 1998/06/06 00:00
PHST- 1998/06/06 00:00 [pubmed]
PHST- 1998/06/06 00:01 [medline]
PHST- 1998/06/06 00:00 [entrez]
AID - S0042-6822(98)99152-8 [pii]
AID - 10.1006/viro.1998.9152 [doi]
PST - ppublish
SO  - Virology. 1998 May 25;245(1):99-109. doi: 10.1006/viro.1998.9152.