Premium
Generation of a conditional null allele for Dmp1 in mouse
Author(s) -
Feng Jian Q.,
Scott Greg,
Guo Dayong,
Jiang Baichun,
Harris Marie,
Ward Toni,
Ray Manas,
Bonewald Lynda F.,
Harris Stephen E.,
Mishina Yuji
Publication year - 2008
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.20370
Subject(s) - dmp1 , biology , hypophosphatemic rickets , null allele , phenotype , rickets , microbiology and biotechnology , genetics , gene , pathology , endocrinology , medicine , viral matrix protein , vitamin d and neurology
Abstract Dentin matrix protein1 (DMP1), highly conserved in humans and mice, is highly expressed in teeth, the skeleton, and to a lesser extent in nonskeletal tissues such as brain, kidney, and salivary gland. Pathologically, DMP1 is associated with several forms of cancers and with tumor‐induced osteomalacia. Conventional disruption of the murine Dmp1 gene results in defects in dentin in teeth and in the skeleton, including hypophosphatemic rickets, and abnormalities in phosphate homeostasis. Human DMP1 mutations are responsible for the condition known as autosomal recessive hypophosphatemic rickets. For better understanding of the roles of DMP1 in different tissues at different stages of development and in pathological conditions, we generated Dmp1 floxed mice in which loxP sites flank exon 6 that encodes for over 80% of DMP1 protein. We demonstrate that Cre‐mediated recombination using Sox2‐Cre, a Cre line expressed in epiblast during early embryogenesis, results in early deletion of the gene and protein. These homozygous Cre‐recombined null mice display an identical phenotype to conventional null mice. This animal model will be useful to reveal distinct roles of DMP1 in different tissues at different ages. genesis 46:87–91, 2008. © 2008 Wiley‐Liss, Inc.