scholarly journals Genetic mapping of a cellular DNA region involved in induction of thymic lymphomas (Mlvi-1) to mouse chromosome 15.

1985 ◽  
Vol 5 (4) ◽  
pp. 894-897 ◽  
Author(s):  
C A Kozak ◽  
P G Strauss ◽  
P N Tsichlis
Keyword(s):  
Mouse Chromosome ◽  
Genetic Locus ◽  
Leukemia Virus ◽  
Moloney Murine Leukemia Virus ◽  
Chromosome 15 ◽  
Dna Integration ◽  
Common Domain ◽  
Cellular Oncogenes ◽  
Cellular Dna ◽  
Mouse Somatic Cell

Mlvi-1 defines a genetic locus representing a common domain for proviral DNA integration in Moloney murine leukemia virus-induced rat thymic lymphomas. Cellular sequences homologous to Mlvi-1 are present in mouse DNA, and we have used hamster-mouse somatic cell hybrids to chromosomally map Mlvi-1 in the mouse genome. Results demonstrated that Mlvi-1 maps to mouse chromosome 15 and that it is distinct from the Mlvi-2 integration region and from the cellular oncogenes c-myc and c-sis, which also map to this chromosome. Therefore, Mlvi-1 may contain novel sequences involved in the establishment and maintenance of virus-induced murine tumors, many of which contain abnormalities of chromosome 15.

Genetic mapping of a cellular DNA region involved in induction of thymic lymphomas (Mlvi-1) to mouse chromosome 15

1985 ◽  
Vol 5 (4) ◽  
pp. 894-897
Author(s):  
C A Kozak ◽  
P G Strauss ◽  
P N Tsichlis
Keyword(s):  
Mouse Chromosome ◽  
Genetic Locus ◽  
Leukemia Virus ◽  
Moloney Murine Leukemia Virus ◽  
Chromosome 15 ◽  
Dna Integration ◽  
Common Domain ◽  
Cellular Oncogenes ◽  
Cellular Dna ◽  
Mouse Somatic Cell

Mlvi-1 defines a genetic locus representing a common domain for proviral DNA integration in Moloney murine leukemia virus-induced rat thymic lymphomas. Cellular sequences homologous to Mlvi-1 are present in mouse DNA, and we have used hamster-mouse somatic cell hybrids to chromosomally map Mlvi-1 in the mouse genome. Results demonstrated that Mlvi-1 maps to mouse chromosome 15 and that it is distinct from the Mlvi-2 integration region and from the cellular oncogenes c-myc and c-sis, which also map to this chromosome. Therefore, Mlvi-1 may contain novel sequences involved in the establishment and maintenance of virus-induced murine tumors, many of which contain abnormalities of chromosome 15.

scholarly journals Cellular DNA region involved in induction of thymic lymphomas (Mlvi-2) maps to mouse chromosome 15.

1984 ◽  
Vol 4 (5) ◽  
pp. 997-1000 ◽  
Author(s):  
P N Tsichlis ◽  
P G Strauss ◽  
C A Kozak
Keyword(s):  
Mouse Chromosome ◽  
Leukemia Virus ◽  
Moloney Murine Leukemia Virus ◽  
Chromosome 15 ◽  
Repeated Dna ◽  
Dna Integration ◽  
Cellular Dna ◽  
Chromosomal Map ◽  
Map Location ◽  
Mouse Somatic Cell

Two cellular DNA regions representing common domains for proviral DNA integration ( Mlvi -1 and Mlvi -2) have been identified in Moloney murine leukemia virus-induced rat thymic lymphomas. Cellular sequences which were free of repeated DNA derived from a clone that defines the Mlvi -2 integration domain (lambda Cl228 ) were found to be highly conserved in a variety of vertebrate species that we examined, including mice, hamsters, cats, and humans. In this study, we identified the chromosomal map location of the Mlvi -2 homologous sequences in mice by using hamster-mouse somatic cell hybrids. The results show that Mlvi -2 is present on mouse chromosome 15 but is unrelated to the c-myc and c-sis proto-oncogenes, which map on the same chromosome. Since aberrations on chromosome 15 have been observed reproducibly in mouse thymomas, our data suggest that Mlvi -2 may define a novel sequence involved in the induction or progression of murine thymic lymphomas.

Cellular DNA region involved in induction of thymic lymphomas (Mlvi-2) maps to mouse chromosome 15

1984 ◽  
Vol 4 (5) ◽  
pp. 997-1000
Author(s):  
P N Tsichlis ◽  
P G Strauss ◽  
C A Kozak
Keyword(s):  
Mouse Chromosome ◽  
Leukemia Virus ◽  
Moloney Murine Leukemia Virus ◽  
Chromosome 15 ◽  
Repeated Dna ◽  
Dna Integration ◽  
Cellular Dna ◽  
Chromosomal Map ◽  
Map Location ◽  
Mouse Somatic Cell

Two cellular DNA regions representing common domains for proviral DNA integration ( Mlvi -1 and Mlvi -2) have been identified in Moloney murine leukemia virus-induced rat thymic lymphomas. Cellular sequences which were free of repeated DNA derived from a clone that defines the Mlvi -2 integration domain (lambda Cl228 ) were found to be highly conserved in a variety of vertebrate species that we examined, including mice, hamsters, cats, and humans. In this study, we identified the chromosomal map location of the Mlvi -2 homologous sequences in mice by using hamster-mouse somatic cell hybrids. The results show that Mlvi -2 is present on mouse chromosome 15 but is unrelated to the c-myc and c-sis proto-oncogenes, which map on the same chromosome. Since aberrations on chromosome 15 have been observed reproducibly in mouse thymomas, our data suggest that Mlvi -2 may define a novel sequence involved in the induction or progression of murine thymic lymphomas.

scholarly journals Genetic Analysis of Gv1, a Gene Controlling Transcription of Endogenous Murine Polytropic Proviruses

1999 ◽  
Vol 73 (10) ◽  
pp. 8227-8234 ◽  
Author(s):  
Peter L. Oliver ◽  
Jonathan P. Stoye
Keyword(s):  
Genetic Analysis ◽  
Mouse Chromosome ◽  
Murine Leukemia Virus ◽  
Genetic Locus ◽  
Leukemia Virus ◽  
Protection Assay ◽  
Chromosome 13 ◽  
Nuclease Protection Assay ◽  
Genetic Techniques ◽  
Murine Leukemia

ABSTRACT Gv1 is a genetic locus that coordinately regulates the expression of multiple murine leukemia virus-related endogenous proviral sequences. A quantitative nuclease protection assay for typingGv1 inheritance has been developed. Use of this assay demonstrates that Gv1 controls transcription of polytropic but not of modified polytropic endogenous proviruses. A combination of genetic techniques were used to map Gv1; these analyses demonstrate that Gv1 lies approximately 37 centimorgans from the centromeric end of mouse chromosome 13.

Fidelity of two retroviral reverse transcriptases during DNA-dependent DNA synthesis in vitro

1989 ◽  
Vol 9 (2) ◽  
pp. 469-476
Author(s):  
J D Roberts ◽  
B D Preston ◽  
L A Johnston ◽  
A Soni ◽  
L A Loeb ◽  
...  
Keyword(s):  
Dna Synthesis ◽  
Leukemia Virus ◽  
Dna Polymerases ◽  
Moloney Murine Leukemia Virus ◽  
Avian Myeloblastosis Virus ◽  
Single Base ◽  
Reverse Transcriptases ◽  
Template Strand ◽  
Cellular Dna

We determined the fidelity of avian myeloblastosis virus and Moloney murine leukemia virus reverse transcriptases (RTs) during DNA synthesis in vitro using the M13mp2 lacZ alpha gene as a mutational target. Both RTs commit an error approximately once for every 30,000 nucleotides polymerized. DNA sequence analysis of mutants generated in a forward mutation assay capable of detecting many types of errors demonstrated that avian myeloblastosis virus RT produced a variety of different mutations. The majority (58%) were single-base substitutions; all of which resulted from the misincorporation of either dAMP or dGMP. Minus-one frameshifts were also common, composing about 30% of the mutations. In addition to single-base events, eight mutants contained sequence changes involving from 2 to 59 bases. The frequency of these mutants suggests that, at least during DNA synthesis in vitro, RTs also commit errors by mechanisms other than classical base miscoding and misalignment. We examined the ability of RTs to synthesize DNA from a mismatched primer terminus at a sequence where the mismatched base was complementary to the next base in the template. Unlike cellular DNA polymerases which polymerize from the mismatched template-primer, RTs preferred to polymerize from a rearranged template-primer containing a matched terminal base pair and an unpaired base in the template strand. The unusual preference for this substrate suggests that the interactions between RTs and the template-primer are different from those of cellular DNA polymerases. The overall error rate of RT in vitro is sufficient to account for the estimated mutation rate of these viruses.

scholarly journals Fidelity of two retroviral reverse transcriptases during DNA-dependent DNA synthesis in vitro.

1989 ◽  
Vol 9 (2) ◽  
pp. 469-476 ◽  
Author(s):  
J D Roberts ◽  
B D Preston ◽  
L A Johnston ◽  
A Soni ◽  
L A Loeb ◽  
...  
Keyword(s):  
Dna Synthesis ◽  
Leukemia Virus ◽  
Dna Polymerases ◽  
Moloney Murine Leukemia Virus ◽  
Avian Myeloblastosis Virus ◽  
Single Base ◽  
Reverse Transcriptases ◽  
Template Strand ◽  
Cellular Dna

We determined the fidelity of avian myeloblastosis virus and Moloney murine leukemia virus reverse transcriptases (RTs) during DNA synthesis in vitro using the M13mp2 lacZ alpha gene as a mutational target. Both RTs commit an error approximately once for every 30,000 nucleotides polymerized. DNA sequence analysis of mutants generated in a forward mutation assay capable of detecting many types of errors demonstrated that avian myeloblastosis virus RT produced a variety of different mutations. The majority (58%) were single-base substitutions; all of which resulted from the misincorporation of either dAMP or dGMP. Minus-one frameshifts were also common, composing about 30% of the mutations. In addition to single-base events, eight mutants contained sequence changes involving from 2 to 59 bases. The frequency of these mutants suggests that, at least during DNA synthesis in vitro, RTs also commit errors by mechanisms other than classical base miscoding and misalignment. We examined the ability of RTs to synthesize DNA from a mismatched primer terminus at a sequence where the mismatched base was complementary to the next base in the template. Unlike cellular DNA polymerases which polymerize from the mismatched template-primer, RTs preferred to polymerize from a rearranged template-primer containing a matched terminal base pair and an unpaired base in the template strand. The unusual preference for this substrate suggests that the interactions between RTs and the template-primer are different from those of cellular DNA polymerases. The overall error rate of RT in vitro is sufficient to account for the estimated mutation rate of these viruses.

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