Chromosomal mapping of the mink cell focus-inducing and xenotropic env gene family in the mouse.

Blatt, Cila; Mileham, K A; Haas, Martin; Nesbitt, Muriel N.; Harper, Mary‐Ellen; Simon, Melvin I.

doi:10.1073/pnas.80.20.6298

Cited by 91 publications

(34 citation statements)

References 32 publications

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“…Having established restriction fragment length polymorphisms between two inbred strain progenitors, one can compare the strain distribution pattern of the unmapped gene in a set of RI strains relative to well-characterized genomic markers. Restriction fragment length polymorphisms in RI strains have proved very useful in the mapping of a number of mouse genes and gene families (5,6,12,16). In the case of contrapsin, we were able to s particular gene(s) encoding contrapsin is withi predicted by the DNA analysis.…”

Section: Resultsmentioning

confidence: 99%

A genetic locus closely linked to a protease inhibitor gene complex controls the level of multiple RNA transcripts.

Hill¹,

Shaw²,

Barth³

et al. 1985

Mol. Cell. Biol.

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The two major protease inhibitors in mouse plasma are a1-protease inhibitor (a,-PI), putative inhibitor of neutrophil elastase, and contrapsin, an inhibitor in vitro of trypsinlike proteases. We have shown by nucleotide sequence analysis that these two inhibitors are related (R. E. Hill, P. H. Shaw, P. A. Boyd, H. Baumann, and N. D. Hastie, Nature (London) 311: [175][176][177] 1984). Here, we show that the contrapsin and al-PI genes are members of two different multigene families, each containing at least three genes in mice and rats. We established the chromosomal locations of these genes by analyzing the segregation of restriction fragment length polymorphisms in recombinant inbred mouse strains. These experiments show that the multiple genes in each family are clustered and that the two gene families are closely linked on chromosome 12. Thus the genes for contrapsin and al-PI are likely to have evolved by duplication of a common ancestral gene. The contrapsin multigene family codes for multiple mRNA transcripts in the liver. There is a genetic difference among inbred mouse strains in the regulation of two of these transcripts. In some inbred strains the transcripts are synthesized constitutively; in others they are induced by inflammation. We mapped in recombinant inbred strains the regulatory locus responsible for this genetic variation and found it is linked to the contrapsin multigene family, which suggests a cis-acting regulatory element. We also found that the contrapsin and the a,-PI multigene families have acquired very different regulatory responses since the time of the gene duplication event.The two major mouse plasma protease inhibitors are a1-proteinase inhibitor (a,-PI; also called otl-antitrypsin) and contrapsin, which together are responsible for most of the trypsinlike inhibitory activity of mice (27, 28). These two inhibitors are synthesized by hepatocytes, and secretion from this cell type is primarily responsible for their high levels in plasma (3,4,21). Mouse a,-PI is homologous to (14) and appears to be functionally equivalent to human a1-PI; in contrast, contrapsin activity appears to be novel to rodents (27). At the nucleotide sequence level, however, the contrapsin gene is closely related to that encoding human plasma al-antichymotrypsin (ao-achy) (14). In addition, contrapsin and ao-PI are related to each other (59% nucleotide homology) but to a lesser extent than with their counterparts in humans (14).These inhibitors have been placed into a larger superfamily of proteins (sharing 29 to 34% amino acid homology with each member) which includes other protease inhibitors such as antithrombin III (7) as well as proteins with no known inhibitory activity, including chicken ovalbumin (15) and rat angiotensinogen (10). It is not known whether these members evolved from a common ancestral gene or are related through a process of convergent evolution (19). Genetic analysis of the chromosomal location of related genes may provide insight into their mode of evolution. Because a,-PI and contraps...

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Section: Resultsmentioning

confidence: 99%

A genetic locus closely linked to a protease inhibitor gene complex controls the level of multiple RNA transcripts.

Hill¹,

Shaw²,

Barth³

et al. 1985

Mol. Cell. Biol.

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“…Comparison of these strain distribution patterns with those previously determined for other polymorphic loci in these strain sets showed linkage between the N-CAM gene restriction fragment length polymorphism and the Sep-i (apolipoprotein 1) and Lap-i (leucine aminopeptidase 1) loci on the proximal portion of chromosome 9 (6 recombinants among 63 strains and 9 recombinants among 40 strains, respectively). In the BXD strain set, linkage was found as well between N-CAM and Env-2 (2 recombinants among 24 strains typed) (31), and in the AKXD set, linkage was found between N-CAM and Thy-i (4 recombinants among 25 strains typed).…”

Section: Methodsmentioning

confidence: 86%

Chromosomal location of the gene encoding the neural cell adhesion molecule (N-CAM) in the mouse.

D’Eustachio¹,

Owens²,

Edelman³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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The gene encoding the neural cell adhesion molecule, N-CAM, has been localized on mouse chromosome 9. A BALB/cJ mouse genomic library prepared in lambda bacteriophage EMBL4 was screened by using a cDNA probe, pEC204, that corresponds to the coding region of the chicken N-CAM gene. Four weakly reactive and one strongly reactive recombinant phage were isolated. A region of the latter that was strongly homologous to pEC204 was subcloned to yield a new probe, pEC501. RNA transfer blots and nucleotide sequencing indicated that pEC501 encoded part of the mouse N-CAM gene. This probe defined a unique genetic locus, Ncam, associated with a restriction fragment length polymorphism that allowed the definition of two alleles. The locus could be provisionally assigned either to chromosome 9 or to chromosome 10 by correlating the presence or absence of mouse-specific DNA fragments reactive with the probe in a panel of somatic hybrid cell lines with the presence or absence of the various mouse chromosomes. Analysis of the inheritance of the Ncam-associated DNA polymorphism in recombinant inbred strains of mice revealed close linkage between Ncam and the Lap-1, Sep-1, and Thy-1 loci on chromosome 9. This result suggests an additional linkage between Ncam and the locus for the cerebellar mutation staggerer (sg). The Ncam locus provides an important reference point for mapping the genes for additional cell adhesion molecules as well as genes for other molecules involved in neural development and function.

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“…Precedent for the control of virus expression by flanking sequences comes from studies of Mov expression (Jaenisch et al, 1981) and from transfection studies (Cooper & Silverman, 1978;Copeland & Cooper, 1979). Recent studies using recombinant inbred strains of mice have placed a variety of endogenous viruses in the vicinity of lymphocyte differentiation antigens (Blatt et al, 1983;Meruelo et al, 1983). By molecularly cloning the integrated proviruses of BXV and BDV, both of which are expressed in differentiating B-cells, we expect the flanking sequences to contain interesting probes for studying the expression of genes important for B-cell development in addition to facilitating molecular studies on the control of the retrovirus sequences.…”

Section: Discussionmentioning

confidence: 99%

Proliferation and Differentiation Requirements for the Induction of Two Retroviral Loci during B-Cell Activation

Stoye

Moroni

1985

Journal of General Virology

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Chromosomal mapping of the mink cell focus-inducing and xenotropic env gene family in the mouse.

Cited by 91 publications

References 32 publications

A genetic locus closely linked to a protease inhibitor gene complex controls the level of multiple RNA transcripts.

A genetic locus closely linked to a protease inhibitor gene complex controls the level of multiple RNA transcripts.

Chromosomal location of the gene encoding the neural cell adhesion molecule (N-CAM) in the mouse.

Proliferation and Differentiation Requirements for the Induction of Two Retroviral Loci during B-Cell Activation

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