Affiliation:
1. Molecular Oncology, Swiss Institute for Experimental Cancer Research, National Center of Competence in Research, 1066 Epalinges
2. Institute of Pathology, University of Lausanne, 1005 Lausanne, Switzerland
Abstract
ABSTRACT
The tyrosinase family comprises three members, tyrosinase (
Tyr
), tyrosinase-related protein 1 (
Tyrp1
), and dopachrome tautomerase (
Dct
). Null mutations and deletions at the
Tyr
and
Tyrp1
loci are known and phenotypically affect coat color due to the absence of enzyme or intracellular mislocalization. At the
Dct
locus, three mutations are known that lead to pigmentation phenotype. However, these mutations are not null mutations, and we therefore set out to generate a null allele at the
Dct
gene locus by removing exon 1 of the mouse
Dct
gene. Mice deficient in
Dct
[
Dct
tm1(Cre)Bee
] lack
Dct
mRNA and dopachrome tautomerase protein. They are viable and do not show any abnormalities in
Dct
-expressing sites such as skin, retinal pigment epithelium, or brain. However, the mice show a diluted coat color phenotype, which is due to reduced melanin content in hair. Primary melanocytes from
Dct
knockout mice are viable in culture and show a normal distribution of tyrosinase and tyrosinase-related protein 1. In comparison to the knockout, the
slaty
mutation (
Dct
slt
/Dct
slt
) has less melanin and affects growth of primary melanocytes severely. In summary, we have generated a knockout of the
Dct
gene in mice with effects restricted to pigment production and coat color.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
109 articles.
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