PMID- 21558422 OWN - NLM STAT- MEDLINE DCOM- 20120210 LR - 20191210 IS - 1531-2267 (Electronic) IS - 1094-8341 (Linking) VI - 43 IP - 13 DP - 2011 Jul 14 TI - Evolution of the epithelial sodium channel and the sodium pump as limiting factors of aldosterone action on sodium transport. PG - 844-54 LID - 10.1152/physiolgenomics.00002.2011 [doi] AB - Despite large changes in salt intake, the mammalian kidney is able to maintain the extracellular sodium concentration and osmolarity within very narrow margins, thereby controlling blood volume and blood pressure. In the aldosterone-sensitive distal nephron (ASDN), aldosterone tightly controls the activities of epithelial sodium channel (ENaC) and Na,K-ATPase, the two limiting factors in establishing transepithelial sodium transport. It has been proposed that the ENaC/degenerin gene family is restricted to Metazoans, whereas the alpha- and beta-subunits of Na,K-ATPase have homologous genes in prokaryotes. This raises the question of the emergence of osmolarity control. By exploring recent genomic data of diverse organisms, we found that: 1) ENaC/degenerin exists in all of the Metazoans screened, including nonbilaterians and, by extension, was already present in ancestors of Metazoa; 2) ENaC/degenerin is also present in Naegleria gruberi, an eukaryotic microbe, consistent with either a vertical inheritance from the last common ancestor of Eukaryotes or a lateral transfer between Naegleria and Metazoan ancestors; and 3) The Na,K-ATPase beta-subunit is restricted to Holozoa, the taxon that includes animals and their closest single-cell relatives. Since the beta-subunit of Na,K-ATPase plays a key role in targeting the alpha-subunit to the plasma membrane and has an additional function in the formation of cell junctions, we propose that the emergence of Na,K-ATPase, together with ENaC/degenerin, is linked to the development of multicellularity in the Metazoan kingdom. The establishment of multicellularity and the associated extracellular compartment ("internal milieu") precedes the emergence of other key elements of the aldosterone signaling pathway. FAU - Studer, Romain A AU - Studer RA AD - Department of Ecology and Evolution, Biophore, Lausanne, Switzerland. romain.studer@unil.ch FAU - Person, Emilie AU - Person E FAU - Robinson-Rechavi, Marc AU - Robinson-Rechavi M FAU - Rossier, Bernard C AU - Rossier BC LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20110510 PL - United States TA - Physiol Genomics JT - Physiological genomics JID - 9815683 RN - 0 (ASIC2 protein, human) RN - 0 (Acid Sensing Ion Channels) RN - 0 (Degenerin Sodium Channels) RN - 0 (Epithelial Sodium Channels) RN - 0 (Membrane Proteins) RN - 0 (Nerve Tissue Proteins) RN - 0 (Phosphoproteins) RN - 135541-82-1 (phospholemman) RN - 4964P6T9RB (Aldosterone) RN - 9NEZ333N27 (Sodium) RN - EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase) SB - IM MH - Acid Sensing Ion Channels MH - Aldosterone/*metabolism MH - Animals MH - Degenerin Sodium Channels MH - Epithelial Sodium Channels/*genetics MH - *Evolution, Molecular MH - Humans MH - Ion Transport/drug effects MH - Membrane Proteins/genetics MH - Nerve Tissue Proteins/genetics MH - Phosphoproteins/genetics MH - Phylogeny MH - Sodium/*metabolism MH - Sodium-Potassium-Exchanging ATPase/*genetics EDAT- 2011/05/12 06:00 MHDA- 2012/02/11 06:00 CRDT- 2011/05/12 06:00 PHST- 2011/05/12 06:00 [entrez] PHST- 2011/05/12 06:00 [pubmed] PHST- 2012/02/11 06:00 [medline] AID - physiolgenomics.00002.2011 [pii] AID - 10.1152/physiolgenomics.00002.2011 [doi] PST - ppublish SO - Physiol Genomics. 2011 Jul 14;43(13):844-54. doi: 10.1152/physiolgenomics.00002.2011. Epub 2011 May 10.