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Upregulation of the PPAR signaling pathway and accumulation of lipids are related to the morphological and structural transformation of the dragon-eye goldfish eye 被引量:9

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摘要 Goldfish comprise around 300 different strains with drastically altered and aesthetical morphologies making them suitable models for evolutionary developmental biology.The dragon-eye strain is characterized by protruding eyes(analogous to those of Chinese dragons).Although the strain has been selected for about 400 years,the mechanism of its eye development remains unclear.In this study,a stable dragon-eye goldfish strain with a clear genetic background was rapidly established and studied.We found that upregulation of the PPAR signaling pathway accompanied by an increase in lipid accumulation might trigger the morphological and structural transformation of the eye in dragon-eye goldfish.At the developmental stage of proptosis(eye protrusion),downregulation of the phototransduction pathway was consistent with the structural defects and myopia of the dragon-eye strain.With the impairment of retinal development,cytokine-induced inflammation was activated,especially after proptosis,similar to the pathologic symptoms of many human ocular diseases.In addition,differentially expressed transcription factors were significantly enriched in the PAX and homeobox families,two well-known transcription factor families involved in eye development.Therefore,our findings reveal the dynamic changes in key pathways during eye development in dragon-eye goldfish,and provide insights into the molecular mechanisms underlying drastically altered eyes in goldfish and human ocular disease.
出处 《Science China(Life Sciences)》 SCIE CAS CSCD 2021年第7期1031-1049,共19页 中国科学(生命科学英文版)
基金 supported by the Strategic Priority Research Program of Chinese Academy of Sciences(XDB31000000) the National Natural Science Foundation of China(31930111) the China Agriculture Research System(CARS-45-07) the Autonomous Project of the State Key Laboratory of Freshwater Ecology and Biotechnology(2019FBZ04) supported by the Wuhan Branch,Supercomputing Centre,Chinese Academy of Sciences,China。
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