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Biomedical subjects

C Foubert

Publications and source records attributed to C Foubert.

16 recordsLinked to original sources

Assignment to chromosome 12 of the gene coding for the human cell surface antigen CD9(p24) using the monoclonal antibody ALB6.

An analysis of 20 independent man-mouse and man-hamster hybrids has shown that the gene coding for the cell-surface protein CD9(p24), a differentiation antigen recognized by the monoclonal antibody ALB6, is located on chromosome 12. A positive correlation was shown between CD9(p24) and chromosome 12 and all other chromosomes were excluded. In addition a synteny was observed between CD9(p24) and LDH-B, a well known marker of chromosome 12 (out of 27 hybrids, 15 were LDH-B+ ALB6+ and 12 were LDH-B-ALB6-). Expression of the antigen in hybrid CH-35K issued from parental fibroblasts possessing a balanced reciprocal translocation 46,X,Y,t(X,12)(q23,q12) indicated that the gene for CD9(p24) is probably localized on 12q12----pter. Monoclonal antibodies ALB6, Ba2 and 602/29 recognize the same protein of molecular weight 21 to 24 KD controlled by a gene located on chromosome 12. It is known that Ba2 and 602/29 recognize two different epitopes but the existence of a third epitope recognized by ALB6 remains to be shown.

Animals

The beta chorionic gonadotropin-beta luteinizing gene cluster maps to human chromosome 19.

We used a cloned human cDNA probe homologous to the placenta chorionic gonadotropin beta subunit (CGB) and to the pituitary luteinizing hormone beta subunit (LHB) and Southern blotting techniques to analyse DNA from a series of rodent X human somatic cell hybrids for the presence of specific gonadotropin beta subunit related sequences. Our results provide evidence for the assignment and linkage of the eight genes (or pseudogenes) coding for the beta subunit of these glycoprotein hormones to chromosome 19. Moreover, we observed a strict concordance between the permissivity of mouse X man hybrid cells to enteroviruses (which is linked to the presence of specific cell receptors encoded by human chromosome 19) and the presence of CGB and LHB related sequences, thus confirming the localization of the structural genes for the beta subunits on chromosome 19.

Animals

Assignment of the human gene for delta aminolevulinate dehydrase to chromosome 9 by somatic cell hybridization and specific enzyme immunoassay.

A non-competitive enzyme immunoassay specific for delta aminolevulinate dehydrase has been devised and applied to rodent-human hybrid cell lines. Two different conditions have been used, one specific for the human enzyme and the other indicative of both rodent and human enzymes. The ratio of the values obtained under the two conditions was used to discriminate between positive and negative clones. By this method the gene for ALA dehydrase has been assigned to chromosome 9.

Animals

[Localization of the LDHA-GST3-ESA4 synthetic group on human chromosome 11. Analyses of the classic man-rodent hybrids and of a new type (not adhering to the wall)].

Analysis of different human tissues showed that glutathione S-transferase (GST) of fibroblasts and leucocytes is GST3, an enzyme found in liver extracts by Board (1981). Consequently, the GST localized on human chromosome 11 by Silberstein and Shows (1981, 1982) is GST3. Analysis of tissue extracts showed a new GST band, very intense in muscle extracts and very weak or absent in other tissues, and called GSTM. Analysis of man-rodent hydrids showed synteny between LDHA, GST3, ESA4 and localization of this synteny group on chromosome 11. Analysis of discordant percentages and discordant types between markers favored the following assignments: LDHA on 11p12, GST3 on 11q13 leads to 11qter, ESA on 11q13 leads to 11q22. The present study suggests assignment of GST3 to 11q13 leads to 11q22. Different types of man-rodent hybrids are useful for human gene mapping. A new type hybrid, as used here (nonadhering to glass or plastic surfaces), appears useful because of rapid proliferation and growth in suspension, the latter feature facilitating culture and harvesting.

Animals

Human type I procollagen genes are located on different chromosomes.

A recombinant plasmid containing sequences complementary to human pro-alpha l(I) collagen mRNA was used for the chromosomal assignment of the pro-alpha l(I) collagen gene. Restriction endonuclease analysis of DNA from mouse-human and Chinese hamster-human somatic cell hybrids revealed cosegregation with human chromosome 17. Hybrids containing derivative chromosomes with a t(2;17)(q14;q21) translocation showed cosegregation of the pro-alpha l(I) gene with the segment 17q21 leads to qter. In situ hybridization on human metaphasic chromosomes confirmed this conclusion.

Amino Acid Sequence

Assignment of the human pro alpha 2(I) collagen structural gene (COLIA2) to chromosome 7 by molecular hybridization.

A cDNA for the pro alpha 2 chain of human type I collagen has been recently cloned and amplified. We have used this specific probe to identify the human chromosome carrying the pro alpha 2(I) collagen gene. The DNA from 17 independent human/hamster and human/mouse somatic cell hybrids was digested by Eco RI and the restriction pattern analyzed in Southern blot experiments, using the 32P-labeled cDNA as a hybridization probe. The gene coding for the pro alpha 2 collagen subunit could be unambiguously assigned to human chromosome 7. All the other chromosomes, including chromosome 17, were excluded.

Animals

Regional localization of the genes for human HEXB. PGK, GALA. HPRT, G6PD by somatic cell hybridization.

Twenty independent man-mouse (Cl1D,LA/TK-, HPRT-) and man-hamster (CH,HPRT-) hybrids using female human cells with balanced reciprocal translocation XX,t(X;5)(q21;q11) were analyzed for human genes localized on chromosome 5 (HEXB), on chromosome X (PGK, GALA, HPRT, G6PD) and for the different chromosomes in relation with the balanced reciprocal translocation (chr.5, chr.5q-, chr.Xq+, chr.X). The different results obtained indicate that the genes for human markers HEXB, PGK are on Xq+, and that the genes for human markers GALA, G6PD are on 5q-. These data implicate finally the following localizations: HEXB on 5q11 leads to 5qter; PGK on Xq21 leads to Xpter; GALA, HPRT, G6PD on Xq21 leads to Xqter.

Animals

[Genetic and epigenetic control of adenosine deaminase expression. Analysis of human and man-mouse hybrid cells (author's transl)].

Analysis of human-rodent hybrids showed the following: the assignment of the ADA1 structural gene to chromosome 20; the identification in hybrids of a new ADA, referred to as ADAx, with a migration more rapidly anodal than ADAd and less rapidly anodal than ADA1 (product of allele 1 or 2); ADAx and d are formed by ADA1 and ADCP (an adenosine deaminase complexing protein). ADCP synthesis is controlled, at least, by a gene (ADCP2) localized on chromosome 2, probably in the IDH1 region; the combined action of another gene (ADCP1), assigned by other authors to chromosome 6, could be neither proved nor disproved, if this gene exists, it must be on 6p or in the 6qter region; the presence of chromosomes 20, 2, and 6 does not constitute a sufficient condition for the formation of ADAx and d, in either the hybrids or the human strains or lines: other factors intervene in its formation, i.e., an interaction between the culture medium, the human parental strain or line, and the rodent parental line.

Adenosine Deaminase

[Assignment of the creatine kinase BB gene to chromosome 14 by man-rodent cell hybridization (author's transl)].

The value of man-rodent hybrids for detecting creatine kinase BB (CKBB) was greatly increased by the use of an agar technique, in extended incubation (20 hours) with a concentrated solution of creatine as substrate (8 mg/ml instead of 1 mg/ml as usual). The selection of a man-rodent hybrid without discordant between chr. 14 and nucleoside phosphorylase (NP) (a marker of this chromosome) contributed efficiently to the detection of the positive correlation between CKBB and chr. 14/NP. Among 22 independent hybrids, the following were observed : 8 NP + CKBB+, 3 NP + CKBB(+), 11 NP-CKBB- and 6 chr. 14 + CKBB+, 2 chr. 14 + CKBB(+), 11 chr. 14 CKBB-, 2 chr. 14/CKBB+ and 1 chr. 14/CKBB(+). The presence of the chromosome was noted + or - according to its presence in more or less than 30% of the cells. These results show that the gene for CKBB is located on chr. 14 and that the presence of this single chr. 14 is sufficient for the expression of human CKBB in man-rodent hybrids. Discordant results reported by others (Povey et al., 1979) may be due to the weakness of the human CKBB detection in man-rodent hybrids or to the bad conservation of this enzyme.

Animals