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2. Functional complementation of ataxia-telangiectasia group D (AT-D) cells by microcell-mediated chromosome transfer and mapping of the AT-D locus to the region 11q22-23.

Author

Lambert, C, Schultz, RA, Smith, M, Wagner-McPherson, C, McDaniel, LD, Donlon, T, Stanbridge, EJ, and Friedberg, EC

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Neurodegenerative, Ataxia Telangiectasia, Brain Disorders, Rare Diseases, Human Genome, Neurosciences, 2.1 Biological and endogenous factors, Chromosome Mapping, Chromosomes, Human, Pair 11, DNA Damage, DNA Repair, Genetic Complementation Test, Humans, Hybrid Cells, In Vitro Techniques, Karyotyping, Nucleic Acid Hybridization, Phenotype, GENE TRANSFER, HEREDITARY DISEASES, IONIZING RADIATION, CELL CYCLE, DNA SYNTHESIS, Cell cycle, DNA synthesis, Gene transfer, Hereditary diseases, Ionizing radiation, animal cell, article, ataxia telangiectasia, chromosome 11q, chromosome 18, gene mapping, gene transfer, human, human cell, hybrid cell, mouse, nonhuman, priority journal, Human, In Vitro, Support, Non-U.S. Gov't, Support, U.S. Gov't, Non-P.H.S., Support, U.S. Gov't, P.H.S., Animalia, Ataxia, Ataxia telangiectasia
Abstract

The hereditary human disease ataxia-telangiectasia (AT) is characterized by phenotypic complexity at the cellular level. We show that multiple mutant phenotypes of immortalized AT cells from genetic complementation group D (AT-D) are corrected after the introduction of a single human chromosome from a human-mouse hybrid line by microcell-mediated chromosome transfer. This chromosome is cytogenetically abnormal. It consists primarily of human chromosome 18, but it carries translocated material from the region 11q22-23, where one or more AT genes have been previously mapped by linkage analysis. A cytogenetically normal human chromosome 18 does not complement AT-D cells after microcell-mediated transfer, whereas a normal human chromosome 11 does. We conclude that the AT-D gene is located on chromosome 11q22-23.

Published
1991

3. Functional complementation of ataxia-telangiectasia group D (AT-D) cells by microcell-mediated chromosome transfer and mapping of the AT-D locus to the region 11q22-23.

Author

Lambert, C, Schultz, RA, Smith, M, Wagner-McPherson, C, McDaniel, LD, Donlon, T, Stanbridge, EJ, and Friedberg, EC

Subjects
Hybrid Cells, Chromosomes, Human, Pair 11, Humans, Ataxia Telangiectasia, DNA Damage, Chromosome Mapping, Genetic Complementation Test, Karyotyping, Nucleic Acid Hybridization, DNA Repair, Phenotype, In Vitro Techniques, GENE TRANSFER, HEREDITARY DISEASES, IONIZING RADIATION, CELL CYCLE, DNA SYNTHESIS, Chromosomes, Human, Pair 11, Cell cycle, DNA synthesis, Gene transfer, Hereditary diseases, Ionizing radiation, animal cell, article, ataxia telangiectasia, chromosome 11q, chromosome 18, gene mapping, gene transfer, human, human cell, hybrid cell, mouse, nonhuman, priority journal, In Vitro, Support, Non-U.S. Gov't, U.S. Gov't, Non-P.H.S., P.H.S., Animalia, Ataxia, Ataxia telangiectasia, Support, Non-U.S. Gov't, Support, U.S. Gov't, Non-P.H.S., Support, U.S. Gov't, P.H.S.
Abstract

The hereditary human disease ataxia-telangiectasia (AT) is characterized by phenotypic complexity at the cellular level. We show that multiple mutant phenotypes of immortalized AT cells from genetic complementation group D (AT-D) are corrected after the introduction of a single human chromosome from a human-mouse hybrid line by microcell-mediated chromosome transfer. This chromosome is cytogenetically abnormal. It consists primarily of human chromosome 18, but it carries translocated material from the region 11q22-23, where one or more AT genes have been previously mapped by linkage analysis. A cytogenetically normal human chromosome 18 does not complement AT-D cells after microcell-mediated transfer, whereas a normal human chromosome 11 does. We conclude that the AT-D gene is located on chromosome 11q22-23.

Published
1991

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