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Hypomorphic phenotype in mice with pituitary‐specific knockout of steroidogenic factor 1
Author(s) -
Zhao Liping,
Bakke Marit,
Krimkevich Yelena,
Cushman Lisa J.,
Parlow A. F.,
Camper Sally A.,
Parker Keith L.
Publication year - 2001
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/gene.1034
Subject(s) - cre recombinase , biology , transgene , allele , phenotype , recombinase , locus (genetics) , gene knockout , gene targeting , genetically modified mouse , endocrinology , hypogonadotropic hypogonadism , knockout mouse , anterior pituitary , genetics , steroidogenic factor 1 , medicine , gene , hormone , transcription factor , nuclear receptor , recombination
Summary: The bacteriophage Cre recombinase provides a powerful approach for tissue‐specific gene inactivation. Using a Cre transgene driven by the common alpha subunit of glycoprotein hormones (αGSU‐Cre), we have previously inactivated steroidogenic factor 1 (SF‐1) in the anterior pituitary, causing hypogonadotropic hypogonadism with sexual infantilism, sterility, and severe gonadal hypoplasia. We now explore the molecular mechanisms underlying a hypomorphic gonadal phenotype in mice carrying two floxed SF‐1 alleles (F/F) relative to mice carrying one recombined and one floxed allele (F/R). Because their Cre‐mediated disruption of the locus encoding SF‐1 was less efficient, αGSU‐Cre, F/F mice retained some gonadotropin‐expressing cells in the anterior pituitary, thereby stimulating some gonadal function. This novel in vivo model for exploring the effects of differing levels of gonadotropins on gonadal development highlights the need for careful genotype‐phenotype comparisons in studies using Cre recombinase to produce tissue‐specific knockouts. genesis 30:65–69, 2001. © 2001 Wiley‐Liss, Inc.