Literature DB >> 10438850

Selection of reversions and suppressors of a mutation in the CBF binding site of a lymphomagenic retrovirus.

M J Martiney1, K Rulli, R Beaty, L S Levy, J Lenz.   

Abstract

The retrovirus SL3 induces T-cell lymphomas in mice. The transcriptional enhancer in the long terminal repeat (LTR) of SL3 contains two 72-bp repeats. Each repeat contains a binding site for the transcription factor CBF (also called AML1). The CBF binding sites are called core elements. SAA is a mutant that is identical to SL3 except for the presence of a single-base-pair substitution in each of the two core elements. This mutation significantly attenuates viral lymphomagenicity. Most lymphomas that occur in SAA-infected mice contain proviruses with reversions or second-site suppressor mutations within the core element. We examined the selective pressures that might account for the predominance of the reversions and suppressor mutations in tumor proviruses by analyzing when proviruses with altered core sequences became abundant during the course of lymphomagenesis. Altered core sequences were easily detected in thymus DNAs by 4 to 6 weeks after SAA infection of mice, well before lymphomas were grossly evident. This result is consistent with the hypothesis that viruses with the core sequence alterations emerged because they replicated more effectively in mice than SAA. The number of 72-bp tandem, repeats in the viral LTR was found to vary, presumably as a consequence of reverse transcriptase slippage during polymerization. Proviruses with two repeats predominated in the thymuses of SAA- and SL3-infected mice before lymphomas developed, although LTRs with one or three repeats were also present. This suggested that two was the optimal number of 72-bp repeats for viral replication. However, in lymphomas, proviruses with three or four repeats usually predominated. This suggested that a late step in the process of lymphomagenesis led to the abundance of proviruses with additional repeats. We hypothesize that proviruses with additional 72-bp repeats endowed the cells containing them with a selective growth advantage.

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Year:  1999        PMID: 10438850      PMCID: PMC104287     

Source DB:  PubMed          Journal:  J Virol        ISSN: 0022-538X            Impact factor:   5.103


  28 in total

1.  R region sequences in the long terminal repeat of a murine retrovirus specifically increase expression of unspliced RNAs.

Authors:  A M Trubetskoy; S A Okenquist; J Lenz
Journal:  J Virol       Date:  1999-04       Impact factor: 5.103

Review 2.  Structure, replication, and recombination of retrovirus genomes: some unifying hypotheses.

Authors:  J M Coffin
Journal:  J Gen Virol       Date:  1979-01       Impact factor: 3.891

3.  Binding of SL3-3 enhancer factor 1 transcriptional activators to viral and chromosomal enhancer sequences.

Authors:  A Thornell; B Hallberg; T Grundström
Journal:  J Virol       Date:  1991-01       Impact factor: 5.103

4.  Differential protein binding in lymphocytes to a sequence in the enhancer of the mouse retrovirus SL3-3.

Authors:  A Thornell; B Hallberg; T Grundström
Journal:  Mol Cell Biol       Date:  1988-04       Impact factor: 4.272

5.  An SL3-3 murine leukemia virus enhancer variant more pathogenic than the wild type obtained by assisted molecular evolution in vivo.

Authors:  S Ethelberg; A B Sørensen; J Schmidt; A Luz; F S Pedersen
Journal:  J Virol       Date:  1997-12       Impact factor: 5.103

6.  Isolation of cDNA clones encoding T cell-specific membrane-associated proteins.

Authors:  S M Hedrick; D I Cohen; E A Nielsen; M M Davis
Journal:  Nature       Date:  1984 Mar 8-14       Impact factor: 49.962

7.  Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3.

Authors:  A Nieves; L S Levy; J Lenz
Journal:  J Virol       Date:  1997-02       Impact factor: 5.103

8.  Suppressor mutations within the core binding factor (CBF/AML1) binding site of a T-cell lymphomagenic retrovirus.

Authors:  M J Martiney; L S Levy; J Lenz
Journal:  J Virol       Date:  1999-03       Impact factor: 5.103

9.  Thymic dendritic cells are primary targets for the oncogenic virus SL3-3.

Authors:  C H Uittenbogaart; W Law; P J Leenen; G Bristol; W van Ewijk; E F Hays
Journal:  J Virol       Date:  1998-12       Impact factor: 5.103

10.  Endogenous murine leukemia proviral long terminal repeats contain a unique 190-base-pair insert.

Authors:  A S Khan; M A Martin
Journal:  Proc Natl Acad Sci U S A       Date:  1983-05       Impact factor: 11.205

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  13 in total

1.  Disruption of hematopoiesis and thymopoiesis in the early premalignant stages of infection with SL3-3 murine leukemia virus.

Authors:  Karen Rulli; Jack Lenz; Laura S Levy
Journal:  J Virol       Date:  2002-03       Impact factor: 5.103

2.  Comparison of replication-competent molecular clones of porcine endogenous retrovirus class A and class B derived from pig and human cells.

Authors:  U Krach; N Fischer; F Czauderna; R R Tönjes
Journal:  J Virol       Date:  2001-06       Impact factor: 5.103

3.  ALY is a common coactivator of RUNX1 and c-Myb on the type B leukemogenic virus enhancer.

Authors:  Jennifer A Mertz; Ryuji Kobayashi; Jaquelin P Dudley
Journal:  J Virol       Date:  2007-01-17       Impact factor: 5.103

4.  The number of a U3 repeat box acting as an enhancer in long terminal repeats of polytropic replication-competent porcine endogenous retroviruses dynamically fluctuates during serial virus passages in human cells.

Authors:  G Scheef; N Fischer; U Krach; R R Tönjes
Journal:  J Virol       Date:  2001-08       Impact factor: 5.103

5.  Control of pathogenicity and disease specificity of a T-lymphomagenic gammaretrovirus by E-box motifs but not by an overlapping glucocorticoid response element.

Authors:  Ditte Ejegod; Karina Dalsgaard Sørensen; Ilona Mossbrugger; Leticia Quintanilla-Martinez; Jörg Schmidt; Finn Skou Pedersen
Journal:  J Virol       Date:  2008-10-22       Impact factor: 5.103

6.  Ikaros, a lymphoid-cell-specific transcription factor, contributes to the leukemogenic phenotype of a mink cell focus-inducing murine leukemia virus.

Authors:  Nancy L DiFronzo; Cheuk T Leung; Mark K Mammel; Katia Georgopoulos; Barbara J Taylor; Quynh N Pham
Journal:  J Virol       Date:  2002-01       Impact factor: 5.103

7.  Duplication of U3 sequences in the long terminal repeat of mink cell focus-inducing viruses generates redundancies of transcription factor binding sites important for the induction of thymomas.

Authors:  Nancy L DiFronzo; Marisa Frieder; Scott A Loiler; Quynh N Pham; Christie A Holland
Journal:  J Virol       Date:  2003-03       Impact factor: 5.103

8.  Selection for c-myc integration sites in polyclonal T-cell lymphomas.

Authors:  Dana R Broussard; Jennifer A Mertz; M Lozano; Jaquelin P Dudley
Journal:  J Virol       Date:  2002-03       Impact factor: 5.103

9.  Type B leukemogenic virus has a T-cell-specific enhancer that binds AML-1.

Authors:  J A Mertz; F Mustafa; S Meyers; J P Dudley
Journal:  J Virol       Date:  2001-03       Impact factor: 5.103

10.  Relative age of proviral porcine endogenous retrovirus sequences in Sus scrofa based on the molecular clock hypothesis.

Authors:  Ralf R Tönjes; Marcus Niebert
Journal:  J Virol       Date:  2003-11       Impact factor: 5.103

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