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Journal of Virology, February 1999, p. 948-957, Vol. 73, No. 2
Department of Microbiology and Immunology and
Comprehensive Cancer Center, University of Michigan Medical School,
Ann Arbor, Michigan 48109-0620
Received 30 July 1998/Accepted 21 October 1998
A conserved purine-rich motif located near the 3' end of retroviral
genomes is involved in the initiation of plus-strand DNA synthesis. We
mutated sequences both within and flanking the Moloney murine leukemia
virus polypurine tract (PPT) and determined the effects of these
alterations on viral DNA synthesis and replication. Our results
demonstrated that both changes in highly conserved PPT positions and a
mutation that left only the cleavage-proximal half of the PPT intact
led to delayed replication and reduced the colony-forming titer of
replication defective retroviral vectors. A mutation that altered the
cleavage proximal half of the PPT and certain 3' untranslated region
mutations upstream of the PPT were incompatible with or severely
impaired viral replication. To distinguish defects in plus-strand
priming from other replication defects and to assess the relative use
of mutant and wild-type PPTs, we examined plus-strand priming from an
ectopic, secondary PPT inserted in U3. The results demonstrated that
the analyzed mutations within the PPT primarily affected plus-strand
priming whereas mutations upstream of the PPT appeared to affect both plus-strand priming and other stages of viral replication.
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Effects of 3' Untranslated Region Mutations on Plus-Strand
Priming during Moloney Murine Leukemia Virus Replication
*
Corresponding author. Mailing address: Department of
Microbiology and Immunology and Comprehensive Cancer Center, University of Michigan Medical School, 6620 Medical Sciences Bldg. II, Ann Arbor,
MI 48109-0620. Phone: (734) 936-6466. Fax: (734) 764-3562. E-mail:
ateles{at}umich.edu.
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