Open AccessTargeted disruption of metallothionein I and II genes increases sensitivity to cadmium.
Author(s) -
Brian A. Masters,
Edward J. Kelly,
Carol J. Quaife,
Ralph L. Brinster,
Richard D. Palmiter
Publication year - 1994
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.91.2.584
Subject(s) - metallothionein , cadmium , mutant , gene , in vivo , biology , embryonic stem cell , cadmium poisoning , toxicity , allele , microbiology and biotechnology , chemistry , genetics , organic chemistry
We inactivated the mouse metallothionein (MT)-I and MT-II genes in embryonic stem cells and generated mice homozygous for these mutant alleles. These mice were viable and reproduced normally when reared under normal laboratory conditions. They were, however, more susceptible to hepatic poisoning by cadmium. This proves that these widely expressed MTs are not essential for development but that they do protect against cadmium toxicity. These mice provide a means for testing other proposed functions of MT in vivo.