Deletion of Kcnj16 in Mice Does Not Alter Auditory Function

Jun Lv; Xiaolong Fu; Yige Li; Guodong Hong; Peipei Li; Jing Lin; Youfang Xun; Lucheng Fang; Weibin Weng; Rongyu Yue; Geng-Lin Li; Bing Guan; He Li; Yideng Huang; Renjie Chai

doi:10.3389/fcell.2021.630361

Deletion of Kcnj16 in Mice Does Not Alter Auditory Function

Front Cell Dev Biol. 2021 Feb 22:9:630361. doi: 10.3389/fcell.2021.630361. eCollection 2021.

Authors

Jun Lv¹, Xiaolong Fu², Yige Li², Guodong Hong², Peipei Li³, Jing Lin⁴, Youfang Xun^{5

6}, Lucheng Fang¹, Weibin Weng¹, Rongyu Yue⁷, Geng-Lin Li⁸, Bing Guan⁶, He Li¹, Yideng Huang^{1

9}, Renjie Chai^{1

2

10

11}

Affiliations

¹ Department of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
² State Key Laboratory of Bioelectronics, School of Life Sciences and Technology, Jiangsu Province High-Tech Key Laboratory for Bio-Medical Research, Southeast University, Nanjing, China.
³ School of Life Sciences and Key Laboratory of the Ministry of Education for Experimental Teratology, Shandong University, Jinan, China.
⁴ Waksman Institute, Rutgers, The State University of New Jersey, Piscataway, NJ, United States.
⁵ Department of Otolaryngology, Head and Neck Surgery, Xiangya School of Medicine, Central South University, Changsha, China.
⁶ Department of Otolaryngology, Head and Neck Surgery, Clinical Medical College of Yangzhou University, Yangzhou, China.
⁷ Department of Otolaryngology-Head and Neck Surgery, Provincial Hospital Affiliated to Shandong University, Jinan, China.
⁸ Department of Otorhinolaryngology and ENT Institute, Eye and ENT Hospital, Fudan University, Shanghai, China.
⁹ Department of Otolaryngology-Head and Neck Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, China.
¹⁰ Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China.
¹¹ Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China.

Abstract

Endolymphatic potential (EP) is the main driving force behind the sensory transduction of hearing, and K⁺ is the main charge carrier. Kir5.1 is a K⁺ transporter that plays a significant role in maintaining EP homeostasis, but the expression pattern and role of Kir5.1 (which is encoded by the Kcnj16 gene) in the mouse auditory system has remained unclear. In this study, we found that Kir5.1 was expressed in the mouse cochlea. We checked the inner ear morphology and measured auditory function in Kcnj16 ^-/- mice and found that loss of Kcnj16 did not appear to affect the development of hair cells. There was no significant difference in auditory function between Kcnj16 ^-/- mice and wild-type littermates, although the expression of Kcnma1, Kcnq4, and Kcne1 were significantly decreased in the Kcnj16 ^-/- mice. Additionally, no significant differences were found in the number or distribution of ribbon synapses between the Kcnj16 ^-/- and wild-type mice. In summary, our results suggest that the Kcnj16 gene is not essential for auditory function in mice.

Keywords: Kir5.1; cochlea; endolymphatic potential; hair cell; hearing loss.