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| 2009/06/18 |
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Zebrafish beta-adrenergic receptor mRNA expression and control of pigmentation.
Zebrafish β-adrenergic receptor mRNA expression and control of pigmentation
Zhipeng Wang a, Yuhei Nishimura a,b,c, Yasuhito Shimada a,b,c, Noriko Umemoto a, Minoru Hirano a,
Liqing Zang a, Takehiko Oka a, Chikara Sakamoto a, Junya Kuroyanagi a, Toshio Tanaka a,b,c,⁎
a Department of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine, Tsu, Mie, Japan
b Department of Bioinformatics, Mie University Life Science Research Center, Tsu, Mie, Japan
c Department of Medical Chemogenomics, Mie University Venture Business Laboratory, Tsu, Mie, Japan
Article history:
Received 29 January 2009
Received in revised form 12 June 2009
Accepted 15 June 2009
Available online 18 June 2009
Abstract
Beta adrenergic receptors (beta-ARs) are members of the G-protein-coupled receptor superfamily and mediate various physiological processes in many species. The expression patterns and functions of beta-ARs in zebrafish are, however, largely unknown. We have identified zebrafish beta-AR orthologs, which we have designated as adrb1, adrb2a, adrb2b, adrb3a and adrb3b. adrb1 was found to be expressed in the heart and brain. Expression of adrb2a predominated in the brain and skin, whereas adrb2b was found to be highly expressed in muscle, pancreas and liver. Both adrb3a and adrb3b were exclusively expressed in blood. Knock-down of these beta-ARs by morpholino oligonucleotides revealed a functional importance of adrb2a in pigmentation. Expression of atp5a1 and atp5b, genes that encode subunits of F1F0-ATPase, which is known to be involved in pigmentation, was significantly increased by knock-down of adrb2a. Our data suggest that adrb2a may regulate pigmentation, partly by modulating F1F0-ATPase.
PMID: 19540320 [PubMed - indexed for MEDLINE]
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