Population Genomics Reveal Recent Speciation and Rapid Evolutionary Adaptation in Polar Bears

• Main Authors: Liu, Shiping, Lorenzen, Eline D, Fumagalli, Matteo, Li, Bo, Harris, Kelley, Xiong, Zijun, Zhou, Long, Korneliussen, Thorfinn Sand, Somel, Mehmet, Babbitt, Courtney, Wray, Greg, Li, Jianwen, He, Weiming, Wang, Zhuo, Fu, Wenjing, Xiang, Xueyan, Morgan, Claire C, Doherty, Aoife, O’Connell, Mary J, McInerney, James O, Born, Erik W, Dalén, Love, Dietz, Rune, Orlando, Ludovic, Sonne, Christian, Zhang, Guojie, Nielsen, Rasmus, Willerslev, Eske, Wang, Jun
• Format: Article in Journal/Newspaper
• Language: unknown
• Published: eScholarship, University of California 2014
• Subjects: Biological Sciences; Genetics; Heart Disease; Cardiovascular; Human Genome; Atherosclerosis; Adaptation; Physiological; Adipose Tissue; Animals; Apolipoproteins B; Arctic Regions; Biological Evolution; Fatty Acids; Gene Flow; Population; Genome; Ursidae; Medical and Health Sciences; Developmental Biology; Biomedical and clinical sciences; Arctic; brown bear; polar bear
• Online Access: https://escholarship.org/uc/item/4fj7t28j

Polar bears are uniquely adapted to life in the High Arctic and have undergone drastic physiological changes in response to Arctic climates and a hyper-lipid diet of primarily marine mammal prey. We analyzed 89 complete genomes of polar bear and brown bear using population genomic modeling and show that the species diverged only 479-343 thousand years BP. We find that genes on the polar bear lineage have been under stronger positive selection than in brown bears; nine of the top 16 genes under strong positive selection are associated with cardiomyopathy and vascular disease, implying important reorganization of the cardiovascular system. One of the genes showing the strongest evidence of selection, APOB, encodes the primary lipoprotein component of low-density lipoprotein (LDL); functional mutations in APOB may explain how polar bears are able to cope with life-long elevated LDL levels that are associated with high risk of heart disease in humans.