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Identification of Potential Partners in ENaC Assembly and Modulation
Author(s) -
Ramirez Erika L,
Ybanez Raquel V,
Booth Rachell E
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.699.7
Subject(s) - epithelial sodium channel , pseudohypoaldosteronism , microbiology and biotechnology , ion channel , chemistry , function (biology) , sodium , endocrinology , medicine , aldosterone , biology , biochemistry , receptor , organic chemistry
Epithelial sodium channels (ENaC) are voltage independent Na+ channels situated within the apical membrane of epithelia. Their function is especially critical in the distal portion of nephron where Na+ and water must be reabsorbed in order to maintain appropriate blood pressure levels. Anomalous ENaC activity can lead to disorders such as Liddle's syndrome, which is due to overactive ENaC resulting in hypertension, or pseudohypoaldosteronism type I, which is caused by decreased ENaC activity resulting in hypotension. Understanding assembly and modulation of ENaC are essential to understanding its physiological role. We have previously reported the development of a quickly screen for monitoring ENaC activity, which takes advantage of ENaC's ability to transport Na+ into yeast cells and cause growth inhibition (i.e salt sensitivity phenotype). These results can easily be visually compared by using a survival pronging dilution assay. In an effort to examine critical partners in ENaC assembly and modulation, we have screened a series of Saccaromyces Genome Deletion Project strains. We report the identification of four genes required for proper ENaC function in yeast: SUR4, ERV14, EMP24, and ERV25 as well as ULA, which showed significant reduction in growth suggesting an overly active ENaC or an increased stability of otherwise normal channels. Funding provided by Research Corporation and the Welch Foundation.