Sorting nexin 9 (SNX9) is not essential for development and auditory function in mice
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Chengcheng Liu1, Xiaoyan Zhai1, Haibo Du1, Yujie Cao1,3, Huiren Cao1, Yanfei Wang1, Xiao Yu2, Jiangang Gao1, Zhigang Xu1
1Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Jinan, Shandong 250100, P. R. China.
2Department of Physiology, Shandong University School of Medicine, Jinan, Shandong 250012, P. R. China
3Current Address: Cell Biology, Department of Biology, Faculty of Science, Utrecht University, CH Utrecht 3584, The Netherlands
Zhigang Xu, email: email@example.com
Keywords: SNX9, knockout mice, inner ear, hearing, hair cells
Received: April 07, 2016 Accepted: September 02, 2016 Published: September 15, 2016
Sorting nexins are a large family of evolutionarily conserved proteins that play fundamental roles in endocytosis, endosomal sorting and signaling. As an important member of sorting nexin family, sorting nexin 9 (SNX9) has been shown to participate in coordinating actin polymerization with membrane tubulation and vesicle formation. We previously showed that SNX9 is expressed in mouse auditory hair cells and might regulate actin polymerization in those cells. To further examine the physiological role of SNX9, we generated Snx9 knockout mice using homologous recombination method. Unexpectedly, Snx9 knockout mice have normal viability and fertility, and are morphologically and behaviorally indistinguishable from control mice. Further investigation revealed that the morphology and function of auditory hair cells are not affected by Snx9 inactivation, and Snx9 knockout mice have normal hearing threshold. In conclusion, our data revealed that Snx9-deficient mice do not show defects in development as well as auditory function, suggesting that SNX9 is not essential for mice development and hearing.
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