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A novel vasopressin‐induced transcript promotes MAP kinase activation and ENaC downregulation
Author(s) -
Nicod Marie,
Michlig Stéphanie,
Flahaut Marjorie,
Salinas Miguel,
Jaeger Nicole Fowler,
Horisberger JeanDaniel,
Rossier Bernard C.,
Firsov Dmitri
Publication year - 2002
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/cdf509
Subject(s) - biology , renal sodium reabsorption , epithelial sodium channel , xenopus , downregulation and upregulation , aquaporin 2 , vasopressin , microbiology and biotechnology , oocyte , reabsorption , gene expression , endocrinology , medicine , gene , kidney , sodium , biochemistry , chemistry , embryo , mechanical engineering , organic chemistry , water channel , engineering , inlet
In the principal cell of the renal collecting duct, vasopressin regulates the expression of a gene network responsible for sodium and water reabsorption through the regulation of the water channel and the epithelial sodium channel (ENaC). We have recently identified a novel v asopressin‐ i nduced t ranscript (VIT32) that encodes for a 142 amino acid v asopressin‐ i nduced p rotein (VIP32), which has no homology with any protein of known function. The Xenopus oocyte expression system revealed two functions: (i) when injected alone, VIT32 cRNA rapidly induces oocyte meiotic maturation through the activation of the maturation promoting factor, the amphibian homolog of the universal M phase trigger Cdc2/cyclin; and (ii) when co‐injected with the ENaC, VIT32 cRNA selectively downregulates channel activity, but not channel cell surface expression. In the kidney principal cell, VIP32 may be involved in the downregulation of transepithelial sodium transport observed within a few hours after vasopressin treatment. VIP32 belongs to a novel gene family ubiquitously expressed in oocyte and somatic cells that may be involved in G to M transition and cell cycling.