scholarly journals Genetic study of lymphoma induction by AKR mink cell focus-inducing virus in AKR x NFS crosses.

1981 ◽  
Vol 154 (2) ◽  
pp. 450-457 ◽  
Author(s):  
M W Cloyd ◽  
J W Hartley ◽  
W P Rowe
Keyword(s):  
Virus Infection ◽  
Mouse Strain ◽  
Genetic Study ◽  
Strain Analysis ◽  
Subsequent Development ◽  
Additional Gene ◽  
Mink Cell ◽  
Akr Mice ◽  
Ecotropic Virus

The mink cell focus-inducing (MCF)-247 virus, originally isolated from an AKR thymoma, is lymphomagenic in AKR mice but not in the ecotropic virus-negative NFS mouse strain. Analysis of sensitivity to lymphoma-induction by AKR-247 MCF virus in genetic hybrids between these two strains showed that F1 mice inoculated as sucklings were uniformly sensitive, whereas those inoculated as weanlings were generally resistant. In NFS backcross mice inoculated as sucklings, inheritance and expression of endogenous ecotropic virus from AKR was an essential correlate of replication of MCF virus and subsequent development of lymphoma. However, one-third of the mice expressing ecotropic virus and replicating the inoculated MCF virus did not develop lymphoma. The results suggested that an additional gene that influenced development of lymphoma may be involved, and that mice inheriting both virus-inducing loci from AKR were more susceptible than those inheriting only one. These findings indicate that the causal role of ecotropic virus infection in spontaneous thymomagenesis in AKR mice involves not only the generation of leukemogenic MCF viruses but also the establishment of permissiveness for their growth.

scholarly journals Amplified env and gag products on AKR cells. Origin from different murine leukemia virus genomes.

1980 ◽  
Vol 151 (4) ◽  
pp. 975-979 ◽  
Author(s):  
J S Tung ◽  
E Fleissner
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Mouse Strains ◽  
Type Antigen ◽  
Mink Cell ◽  
Virus Expression ◽  
Virus Genomes ◽  
Akr Mice ◽  
Ecotropic Virus ◽  
Murine Leukemia

Thymocytes of AKR mice express two species of gp70, the envelope glycoprotein of murine leukemia virus (MuLV), encoded by the env gene. One is denoted Ec+ gp70 in reference to the type-antigen Ec and association with ecotropic virus. The other, Ec- gp70, resembles gp70 found also on thymocytes of mouse strains that are not overt producers of MuLV, and has no evident relation to ecotropic virus. Expression of Ec- gp70 type, but not of Ec+ gp70 type, is amplified with age on AKR thymocytes. In contrast, viral core polyproteins, encoded by the gag gene and simultaneously amplified with age, appear to be related to ecotropic virus. These observations imply selective amplification of products of env and gag genes from two sorts of provirus, a phenomenon which may be connected to the dual genetic origin of recombinant mink-cell-focus inducing viruses in AKR mice.

scholarly journals Effect of MuLV-related genes on plasmacytomagenesis in BALB/c mice.

1984 ◽  
Vol 160 (2) ◽  
pp. 435-440 ◽  
Author(s):  
M Potter ◽  
J W Hartley ◽  
J S Wax ◽  
D Gallahan
Keyword(s):  
Dna Hybridization ◽  
Partial Resistance ◽  
Gene Locus ◽  
Chromosome 17 ◽  
Linked Gene ◽  
Mink Cell ◽  
Resistance To Infection ◽  
Successive Generations ◽  
Ecotropic Virus

The role of spreading somatic cell infections with ecotropic MuLV viruses in the induction of plasmacytomas in BALB/cAN pi mice was determined by constructing congenic mice that lacked the gene locus Cv that codes for ecotropic virus. DBA/2 mice that lack Cv on chromosome (chr) 5 carry a closely linked gene Rmcfr that determines resistance to infection with mink cell focus-forming viruses (MCF). Rmcfr was retrogressively back-crossed onto BALB/c for six successive generations to produce N6 mice. N6 mice were mated to each other to produce BALB/c.DBA/2 Rmvfr/Rmcfr homozygotes. This stock of mice lacked Cv, as demonstrated by DNA hybridization and were as fully susceptible to developing plasmacytomas as the parental BALB/c. A second congenic stock BALB/c.DBA/2 Rmcfr/Rmcfr Fv-1n/Fv-1n was also developed, but the mice of this stock showed a reduced incidence of plasmacytomas, as did BALB/c.DBA/2 Fv-1n/Fv-1n mice. These findings indicated Fv-1 or a gene closely linked to it conferred partial resistance to plasmacytomagenesis. In constructing the BALB/c.DBA/2 Fv-1n/Fv-1n stock, a "control" congenic BALB/c.DBA/2 Fv-1b/Fv-1b was also developed at N6. Surprisingly, this stock carried the Qa2+ trait. These mice were also partially resistant to plasmacytomagenesis, suggesting a gene on chromosome 17 (the location of Qa2) or a gene located elsewhere that regulates Qa2 expression is linked to a gene controlling partial resistance to plasmacytoma development.

scholarly journals Lymphomagenicity of recombinant mink cell focus-inducing murine leukemia viruses.

1980 ◽  
Vol 151 (3) ◽  
pp. 542-552 ◽  
Author(s):  
M W Cloyd ◽  
J W Hartley ◽  
W P Rowe
Keyword(s):  
Mouse Strain ◽  
National Institutes Of Health ◽  
Accelerate Development ◽  
Mink Cell ◽  
Leukemia Viruses ◽  
Ecotropic Virus ◽  
Murine Leukemia

Recombinant mink cell focus-inducing (MCF) murine leukemic viruses, as well as ecotropic and xenotropic viruses, were tested for ability to accelerate or cause development of lymphoma in AKR and other strains of mice. Of the three classes of virus isolated from AKR, only the MCF viruses were able to accelerate development of AKR lymphoma. This fully supports the idea that the MCF viruses are the proximal cause of spontaneous AKR lymphoma. MCF lymphomagenicity was strain specific, however, in that AKR MCF viruses did not induce lymphomas in many murine strains; they were moderately lymphomagenic in C3H/Bi mice and in National Institutes of Health Swiss partially congenic for Akv-1 or Akv-2. In contrast, MCF viruses from nonthymic hematopoietic neoplasms of C3H/Fg, BALB/c, or mice partially congenic for ecotropic virus loci (Akv-1, Akv-2, Fgv-1, C58v-1, and C58v-2) were not able to accelerate or cause lymphomia in AKR or any other mouse strain tested, including some of the strains of origin. MCF lymphomagenicity correlated with thymic origin in the virus and with ability to replicate in the thymus.

THE ROLE OF SHAIKH NURIDDIN AND SHOKHMALIK IN THE POLITICAL PROCESSESTHAT TOOK PLACE IN THE FIRST DAYS AFTER THE DEATH OF AMIR TEMUR

2020 ◽  
Vol 11 (3) ◽  
pp. 47-54
Author(s):  
Laylo Begimkulova ◽  
Keyword(s):  
Subsequent Development ◽  
Primary Sources ◽  
The Political ◽  
Political Processes

In this article, the author, on the basis of historical primary sources, highlights the role and influence of the great emirs Shaikh Nuriddin and Shokhmalik on the political processes that took place after the death of Amir Temur and the subsequent development of events.

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