PUBLICATION
Prolactin controls branchial clcn2c but not atp1a1a.2 in zebrafish Danio rerio
- Authors
- Breves, J.P.
- ID
- ZDB-PUB-181028-7
- Date
- 2018
- Source
- Journal of Fish Biology 94(1): 168-172 (Journal)
- Registered Authors
- Keywords
- Cl- channel, Na+-K+-ATPase, gill, ionocyte, prolactin, zebrafish
- MeSH Terms
-
- Animals
- Chloride Channels/genetics
- Chloride Channels/metabolism*
- Chlorine/metabolism
- Fresh Water/chemistry
- Gene Expression Regulation/drug effects
- Gills/metabolism
- Homeostasis
- Prolactin/pharmacology*
- Protein Transport
- RNA, Messenger/metabolism
- Sodium Chloride Symporters/metabolism
- Sodium-Potassium-Exchanging ATPase/metabolism
- Zebrafish/metabolism*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 30367725 Full text @ J. Fish Biol.
Citation
Breves, J.P. (2018) Prolactin controls branchial clcn2c but not atp1a1a.2 in zebrafish Danio rerio. Journal of Fish Biology. 94(1):168-172.
Abstract
This study examined the branchial epithelium of stenohaline zebrafish Danio rerio, Na+ -Cl- cotransporter-like 2 (Slc12a10.2)-expressing ionocytes [Na+ -Cl- cotransporter (Ncc)-cells], which mediate the active uptake of ions from freshwater environments. The study assessed whether the pituitary hormone prolactin (Prl) stimulates the expression of messenger (m)RNAs encoding a Clc Cl- channel family member (clcn2c) and a Na+ -K+ -ATPase α1 subunit (atp1a1a.2) expressed in Ncc-cells. Branchial clcn2c, but not atp1a1a.2 levels, were sensitive to Prl both in vitro and in vivo. These observations suggest that Prl contributes to maintaining systemic Cl- balance via the regulation of clcn2c. This article is protected by copyright. All rights reserved.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping