Abstract
Mice with a termination codon mutation in exon 2 of the cystic fibrosis (CF) gene were generated using homologous recombination in embryonic stem cells. Animals homozygous for the mutant allele display a severe intestinal phenotype similar to that previously reported for CF mutant mice. The null nature of this allele was demonstrated by the absence of detectable wild-type mRNA, by the absence of detectable CFTR in the serous gland collecting ducts of salivary tissues, and by the lack of cAMP-mediated short-circuit current responses in colonic epithelium of mutant animals.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Animals
-
Base Sequence
-
Chlorides / metabolism
-
Cystic Fibrosis / genetics*
-
Cystic Fibrosis / pathology
-
Cystic Fibrosis Transmembrane Conductance Regulator / genetics*
-
DNA
-
Exons*
-
Immunohistochemistry
-
Intestinal Mucosa / metabolism
-
Ion Transport
-
Mice
-
Mice, Mutant Strains
-
Molecular Sequence Data
-
Mutation*
-
Phenotype
-
RNA, Messenger / genetics
-
RNA, Messenger / metabolism
-
Salivary Glands / metabolism
-
Terminator Regions, Genetic / genetics*
Substances
-
Chlorides
-
RNA, Messenger
-
Cystic Fibrosis Transmembrane Conductance Regulator
-
DNA