Targeting and Germ-Line Transmission of a Null Mutation at the Metallothionein I and II Loci in Mouse

We report the generation of transgenic mice deficient in the metallothionein MT-I and MT-II genes. The mutations were introduced into embryonic stem cells by homologous recombination. Chimeric mice resulting from the targeted embryonic stem cells transmitted the disrupted alleles through their germ...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1993-09, Vol.90 (17), p.8088-8092
Main Authors: Michalska, Anna E., K. H. Andy Choo
Format: Article
Language:English
Subjects:
Alleles
Animals
Base Sequence
Biological and medical sciences
Biotechnology
Blotting, Southern
Cadmium
Cell lines
Chimera
Crosses, Genetic
DNA - genetics
DNA - isolation & purification
DNA probes
Embryo, Mammalian
Female
Fetuses
Fundamental and applied biological sciences. Psychology
Genes
Genetic Carrier Screening
Genetic engineering
Genetic loci
Genetic mutation
Genetic technics
Homozygote
Male
Messenger RNA
Metallothionein - deficiency
Metallothionein - genetics
Methods. Procedures. Technologies
Mice
Mice - genetics
Mice, Inbred C57BL - genetics
Molecular Sequence Data
Mutation
Oligodeoxyribonucleotides
Polymerase chain reaction
Polymerase Chain Reaction - methods
Recombination, Genetic
Restriction Mapping
Rodents
Stem Cells - metabolism
Transgenic animals
Transgenic animals and transgenic plants
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Summary:We report the generation of transgenic mice deficient in the metallothionein MT-I and MT-II genes. The mutations were introduced into embryonic stem cells by homologous recombination. Chimeric mice resulting from the targeted embryonic stem cells transmitted the disrupted alleles through their germ line. Homozygous animals were born alive and appeared phenotypically normal and fertile. Absence of MT proteins was confirmed by direct measurement in liver extracts. Challenging the mutant animals with moderate levels of CdSO4indicated their greater susceptibility to cadmium toxicity than wild-type animals. These mice should provide a useful model to allow detailed study of the physiological roles of MT-I and MT-II.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.90.17.8088