Chromosomal assignment and trans regulation of the tyrosine aminotransferase structural gene in hepatoma hybrid cells.

Peterson, Theresa C.; Killary, Ann M.; Fournier, R. E. K.

doi:10.1128/mcb.5.9.2491

Cited by 55 publications

(35 citation statements)

References 18 publications

(20 reference statements)

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“…Based on the recombinant inbred analysis, we initially analysed microcell hybrids containing mouse chromosomes 3 or 17 carried as Robertsonian translocations onto chromosome 8 [5,6]. Microcell hybrids containing mouse chromosome 8 alone were intended to serve as negative controls, as were the parental rat and hamster cell lines (table 1).…”

Section: Chromosomal Localization Of the Angiotensinogen Gene Using Hmentioning

confidence: 99%

“…This conclusion is reinforced by the fact that the monochromosom~ microcell hybrids 8D-1 and F(8)D were independently derived by positive selection for APRT activity carried on chromosome 8 [5,6]. Furthermore, the mouse angiotensinogen gene segregated condordantly with mouse chromosome 8 when the primary F(8)D and F(8)E cell lines Table 1 Chromosomal localization of the mouse angiotensinogen gene using microcell hybrids Cell line (8)E were derived by backselection for the APRT-phenotype in medium containing 2,6 diaminopurine [6] were backselected for the APRT-phenotype in medium containing 2,6 diaminopurine ( fig.3A and table 1). This chromosomal localization for angiotensinogen excludes linkage to the serine protease inhibitor locus on chromosome 12 [17],…”

Section: Chromosomal Localization Of the Angiotensinogen Gene Using Hmentioning

confidence: 99%

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The angiotensinogen gene is located on mouse chromosome 8

Clouston¹,

Fournier²,

Richards³

1989

FEBS Letters

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We have recently identified a c&acting genetic lesion affecting angiotensinogen gene expression in testis and salivary gland. Accordingly, the an~otensinogen gene was assigned to mouse chromosome 8 by screening a series of hybrid cell lines for retention of mouSe angiotensinogen sequences by genomic Southern analysis. In AKXD recombinant inbred mice, the angiotensinogen gene is 2.4+ 1.8 centiMorgan from Rn7S-&a 7S RNA gene located on chromosome 8 (Taylor, B.A., personal communication). However, the segregation of salivary and testicular angiotensinogen expression phenotypes into inbred mouse strains was not concordant with the known chromosome 8 proviruses Emv-2. Mtv-21, Xmv-I2or Xmv-26.

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Section: Chromosomal Localization Of the Angiotensinogen Gene Using Hmentioning

confidence: 99%

Section: Chromosomal Localization Of the Angiotensinogen Gene Using Hmentioning

confidence: 99%

The angiotensinogen gene is located on mouse chromosome 8

Clouston¹,

Fournier²,

Richards³

1989

FEBS Letters

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“…Mouse embryo fibroblast donor cells were prepared from C57BL/6J embryos or from translocation stocks with specific Robertsonian translocations (5,19). These parental lines were used to generate hybrid and microcell hybrid clones (Table 1) whose properties have been reported elsewhere (25,31,38 FTO-2B rat hepatoma recipients as described previously (25). TK+ microcell hybrids were selected in medium containing HAT plus 3 mM ouabain.…”

Section: Methodsmentioning

confidence: 99%

Tse-2: a trans-dominant extinguisher of albumin gene expression in hepatoma hybrid cells.

Chin¹,

Fournier²

1989

Mol. Cell. Biol.

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Serum albumin gene expression is generally extinguished in hepatoma x fibroblast hybrids. To define the genetic basis of this phenomenon, we screened a panel of hepatoma hybrids retaining different fibroblast chromosomes for albumin production by immunofluorescence. We report that albumin extinction in these clones was strictly correlated with the retention of mouse chromosome 1. Furthermore, albumin was systematically reexpressed in chromosome 1 segregants. These data define a tissue-specific extinguisher locus (Tse-2) that affects albumin gene expression in trans. Two other liver genes, those encoding liver alcohol dehydrogenase and liv-10, were coordinately extinguished with albumin in monochromosomal hybrids that specifically retained mouse chromosome 1.

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“…In microcell hybrids between fibroblasts and hepatoma cells, transactivation of the tyrosine aminotransferase (TAT) gene was observed (30). The fibroblast TAT gene was transactivated in microcell hybrids only when the fibroblast chromosome carrying the TSE-1 locus was not present.…”

mentioning

confidence: 97%

Pigment-cell-specific genes from fibroblasts are transactivated after chromosomal transfer into melanoma cells.

1994

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Human and mouse fibroblast chromosomes carrying tyrosinase or b-locus genes were introduced, by microcell hybridization, into pigmented Syrian hamster melanoma cells, and the microcell hybrids were tested for transactivation of the fibroblast tyrosinase and b-locus genes. By using species-specific PCR amplification to distinguish fibroblast and melanoma cDNAs, it was demonstrated that the previously silent fibroblast tyrosinase and b-locus genes were transactivated following chromosomal transfer into pigmented melanoma cells. However, transactivation of the mouse fibroblast tyrosinase gene was unstable in microcell hybrid subclones and possibly dependent on a second fibroblast locus that could have segregated in the subclones. This second locus was not necessary for transactivation of the fibroblast b-locus gene, thus demonstrating noncoordinate transactivation of fibroblast tyrosinase and b-locus genes. Transactivation of the fibroblast tyrosinase gene in microcell hybrids apparently is dependent on the absence of a putative fibroblast extinguisher locus for tyrosinase gene expression, which presumably is responsible for the extinction of pigmentation in hybrids between karyotypically complete fibroblasts and melanoma cells.The generation of distinct cell types in multicellular animals only recently has begun to be understood at the genetic and molecular levels. Much emphasis has been placed on factors regulating transcription and on the DNA sequences interacting with such factors. However, the control mechanisms determining which regulatory factors will be active and when they will be expressed are still largely unknown, as are the mechanisms which maintain the differentiated state. Studies on the molecular control of pigment cell differentiation are still at an early stage, since pigment-cell-specific genes were cloned more recently than genes associated with a number of other tissue types.Pigmentation in mammals results from the synthesis of melanin in melanocytes of the skin, hairbulbs, and pigmented epithelium of the eye. Pigmentation is a complex biochemical and genetic process, with, in the mouse, over 50 distinct genetic loci involved (41). The synthesis of melanin in melanocytes requires the enzyme tyrosinase, encoded by the mouse albino (c) locus. In addition, other enzymes which regulate the type of melanin synthesized have recently been identified (for a review see reference 19). Another locus encoding an enzyme related to tyrosinase is the mouse brown (b) locus, which encodes a pigment-cell-specific catalase (18).Tyrosinase cDNAs from both mice (46) and humans (25) have been cloned and sequenced. The cDNA clones map to the albino (c) locus on mouse chromosome 7 (28) and to human chromosome 11 (q14-21) (2). Evidence that these clones encode the authentic tyrosinase enzyme and that mutations therein are the cause of albinism has been provided by (i) synthesis of an enzyme with tyrosinase activity upon transfection of the mouse cDNA clone and expression in cultured cells (28), (ii) identification of m...

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Chromosomal assignment and trans regulation of the tyrosine aminotransferase structural gene in hepatoma hybrid cells.

Cited by 55 publications

References 18 publications

The angiotensinogen gene is located on mouse chromosome 8

The angiotensinogen gene is located on mouse chromosome 8

Tse-2: a trans-dominant extinguisher of albumin gene expression in hepatoma hybrid cells.

Pigment-cell-specific genes from fibroblasts are transactivated after chromosomal transfer into melanoma cells.

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