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Tamoxifen‐inducible Cre‐mediated recombination in adipocytes
Author(s) -
Sassmann Antonia,
Offermanns Stefan,
Wettschureck Nina
Publication year - 2010
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.20665
Subject(s) - adipose tissue , white adipose tissue , biology , transgene , tamoxifen , adipocyte , adiponectin , adipokine , cre lox recombination , cre recombinase , genetically modified mouse , microbiology and biotechnology , gene , endocrinology , genetics , leptin , insulin , cancer , insulin resistance , breast cancer , obesity
To generate a mouse line which allows inducible, Cre/loxP‐dependent recombination in adipocytes, we used RedE/RedT‐mediated recombineering to insert the CreER T2 ‐transgene, which encodes a fusion protein of Cre and a mutated tamoxifen‐responsive estrogen receptor, into the start codon of the adipocyte‐specific Adipoq gene. Adipoq encodes adiponectin, an adipokine specifically expressed in differentiated adipocytes. Tamoxifen treatment induced almost complete recombination in white adipose tissue of the Adipoq CreER T2 mouse line (97%–99%), while no recombination was seen in vehicle‐treated animals. Recombination in brown adipose tissue was about 15%, whereas other organs and tissues did not undergo recombination. In addition, mice expressing CreER T2 in adipocytes did not show any alterations of metabolic functions like glucose tolerance, lipolysis, or energy expenditure compared to control mice. Therefore the Adipoq CreER T2 mouse line will be a valuable tool for studying the consequences of a temporally controlled deletion of floxed genes in white adipose tissue. genesis 48:618–625, 2010. © 2010 Wiley‐Liss, Inc.