Submitted on December 24, 2007
Accepted on November 22, 2008
Conditional gene targeting of the ENaC subunit genes Scnn1b and Scnn1g
Anne-Marie Merillat1, Roch-Philippe Charles1, Andree Porret2, Marc Maillard3, Bernard C Rossier1, Friedrich Beermann4, and Edith Hummler1*
1 Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland
2 Transgenic Animal Facility, University of Lausanne, Lausanne, Switzerland
3 CHUV, Service de Nephrologie, Lausanne, Switzerland
4 ISREC, EPFL Lausanne, Epalinges, Switzerland
* To whom correspondence should be addressed. E-mail: Edith.Hummler{at}unil.ch.
Epithelial sodium channels (ENaC) are members of the degenerin/ENaC superfamily of non-voltage-gated, highly amiloride-sensitive cation channels that are composed of three subunits (
-, 
- and 
-ENaC). Since complete gene inactivation of the - and -ENaC subunit genes (Scnn1b and Scnn1g) leads to early postnatal death, we generated conditional alleles and obtained mice harboring floxed and null alleles for both gene loci. Using quantitative RT-PCR analysis, we showed that the introduction of the loxP sites did not interfere with the mRNA transcript expression level of the Scnn1b and Scnn1g gene locus, respectively. Upon regular and salt-deficient diet, both - and -ENaC floxed mice showed no difference in their mRNA transcript expression levels, plasma electrolytes and aldosterone concentrations as well as weight changes when compared to control animals. These mice can now be utilized to dissect the role of ENaC function in classical and non-classical target organs/tissues.
