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J Levilliers

Publications and source records attributed to J Levilliers.

50 records · Page 3Linked to original sources
PubMed1987

An abnormal terminal X-Y interchange accounts for most but not all cases of human XX maleness.

To determine if human XX maleness results from an abnormal chromosomal X-Y interchange, we studied the inheritance of the paternal pseudoautosomal region in nine patients. Those six patients in whom Y-specific DNA was found (Y(+)) inherited the entire pseudoautosomal region from the paternal Y chromosome and lost that of the paternal X chromosome. Moreover, in three Y(+) cases, we observed the deletion of a paternal Xp locus tightly linked to the pseudoautosomal region. These results definitively show that an abnormal and terminal X-Y interchange during paternal meiosis causes Y(+)XX maleness. In contrast, no abnormal X-Y interchange was observed in any of the three Y(-) cases analyzed, suggesting that maleness can occur in the absence of any Y-specific DNA.

Alleles↗
PubMed1987

Normal and abnormal interchanges between the human X and Y chromosomes.

A single obligatory recombination event takes place at male meiosis in the tips of the X- and Y-chromosome short arms (i.e. the pseudoautosomal region). The crossover point is at variable locations and thus allows recombination mapping of the pseudoautosomal loci along a gradient of sex linkage. Recombination at male meiosis in the terminal regions of the short arms of the X and Y chromosomes is 10- to 20-fold higher than between the same regions of the X chromosomes during female meiosis. The human pseudoautosomal region is rich in highly polymorphic loci associated with minisatellites. However, these minisatellites are unrelated to those resembling the bacterial Chi sequence and which possibly represent recombination hotspots. The high recombination activity of the pseudoautosomal region at male meiosis sometimes results in unequal crossover which can generate various sex-reversal syndromes.

Base Sequence↗
PubMed1986

Tissue-specific expression of the rat albumin gene: genetic control of its extinction in microcell hybrids.

Numerous studies of cell hybrids have indicated that somatic cells produce negative regulators (extinguishers) that prevent the expression of functions foreign to their own differentiation. Here, we report genetic evidence of such control. In microcell hybrids between well-differentiated rat hepatoma cells and microcells of mouse fibroblast L cells, the extinction of albumin synthesis is directly related to the presence of a single specific chromosome of the mouse fibroblast parent. The expression of several other hepatic functions is not affected. Transfection of these hybrids with a recombinant plasmid, containing a tissue-specific control element of the upstream region of the rat albumin gene linked to coding sequences of the chloramphenicol acetyltransferase gene, reveals that extinction acts on or via this cis-control element.

Albumins↗
PubMed1983

Differentiation is not restored in hybrids between independent variants of a rat hepatoma.

Crosses have been undertaken between cells of three independent clones of dedifferentiated rat hepatoma variants to investigate whether "complementation" leading to restoration of the original differentiation would occur. Hybrids were examined between ten days and two months after fusion for the presence of intracellular albumin and for their ability to proliferate in glucose-free medium where survival requires activity of the liver-specific gluconeogenic enzymes. In none of the three possible crosses involving the three variants was evidence of reexpression of hepatic functions obtained.

Animals↗
PubMed1982

Undermethylation at the 5' end of the albumin gene is necessary but not sufficient for albumin production by rat hepatoma cells in culture.

We have measured methylation of the albumin gene in clones of rat hepatoma cells that vary quantitatively in their rates of synthesis of albumin and in variant and hybrid cells that produce no albumin. Although the albumin gene is undermethylated for its entire length in rat liver, only the 5' end is ever undermethylated in hepatoma cells. Moreover, undermethylation of the 5' end of the gene appears to be necessary for stable expression of the albumin gene in hepatoma cells. Since undermethylation of this region is found in some variant cells that fail to produce albumin, it is not a sufficient condition for albumin gene expression. Despite the excellent correlation between undermethylation of the 5' end of the albumin gene and its stable expression, the results argue against the possibility that the methylated state of such genes during development determines whether they will or will not be expressed.

Albumins↗