Priority Research Paper|Volume 12, Issue 19|pp 18804—18821

The slc4a2b gene is required for hair cell development in zebrafish

Fuping Qian¹, Xin Wang², Zhenhua Yin², Gangcai Xie³, Huijun Yuan⁴, Dong Liu², Renjie Chai^1,^2,^5,⁶

¹MOE Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Jiangsu Province High-Tech Key Laboratory for Bio-Medical Research, Southeast University, Nanjing 210096, China
²School of Life Sciences, Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226019, China
³Medical School, Nantong University, Nantong 226019, China
⁴Medical Genetics Center, Southwest Hospital, Army Medical University, Chongqing 400038, China
⁵Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China
⁶Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, Beijing 100069, China

* Equal contribution

Received: May 19, 2020Accepted: July 6, 2020Published: October 12, 2020

Copyright: © 2020 Qian et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Hair cells (HCs) function as important sensory receptors that can detect movement in their immediate environment. HCs in the inner ear can sense acoustic signals, while in aquatic vertebrates HCs can also detect movements, vibrations, and pressure gradients in the surrounding water. Many genes are responsible for the development of HCs, and developmental defects in HCs can lead to hearing loss and other sensory dysfunctions. Here, we found that the solute carrier family 4, member 2b (slc4a2b) gene, which is a member of the anion-exchange family, is expressed in the otic vesicles and lateral line neuromasts in developing zebrafish embryos. An in silico analysis showed that the slc4a2b is evolutionarily conserved, and we found that loss of function of slc4a2b resulted in a decreased number of HCs in zebrafish neuromasts due to increased HC apoptosis. Taken together, we conclude that slc4a2b plays a critical role in the development of HCs in zebrafish.