Molecular Evolution of Aralkylamine N-Acetyltransferase in Fish: A Genomic Survey

International Journal of Molecular Sciences

Jia Li³  Xinxin You²  Chao Bian²  Hui Yu³  Steven L. Coon¹  Qiong Shi³ 

[1] Molecular Genomics Laboratory, National Institutes of Health, Bethesda, MD 20892, USAShenzhen Key Lab of Marine Genomics, Guangdong Provincial Key Lab of Molecular Breeding in Marine Economic Animals, BGI, Shenzhen 518083, China;BGI Education Center, University of Chinese Academy of Sciences, Shenzhen 518083, China;

关键词: aralkylamine N-acetyltransferase;    phylogenetic analysis;    synteny;    molecular evolution;    Whole-Genome Duplication (WGD);    gene loss;   

DOI  :  10.3390/ijms17010051

来源: mdpi

【 摘 要 】

All living organisms synchronize biological functions with environmental changes; melatonin plays a vital role in regulating daily and seasonal variations. Due to rhythmic activity of the timezyme aralkylamine N-acetyltransferase (AANAT), the blood level of melatonin increases at night and decreases during daytime. Whereas other vertebrates have a single form of AANAT, bony fishes possess various isoforms of aanat genes, though the reasons are still unclear. Here, we have taken advantage of multiple unpublished teleost aanat sequences to explore and expand our understanding of the molecular evolution of aanat in fish. Our results confirm that two rounds of whole-genome duplication (WGD) led to the existence of three fish isoforms of aanat, i.e., aanat1a, aanat1b, and aanat2; in addition, gene loss led to the absence of some forms from certain special fish species. Furthermore, we suggest the different roles of two aanat1s in amphibious mudskippers, and speculate that the loss of aanat1a, may be related to terrestrial vision change. Several important sites of AANAT proteins and regulatory elements of aanat genes were analyzed for structural comparison and functional forecasting, respectively, which provides insights into the molecular evolution of the differences between AANAT1 and AANAT2.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.