한빛사논문
- 조회1,555
서울대학교
Abstract
Gyu-Sang Hong,1,4 Byeongjun Lee,1,4 Jungwon Wee,1 Hyeyeon Chun,2 Hyungsup Kim,2 Jooyoung Jung,2 Joo Young Cha,2 Tae-Ryong Riew,3 Gyu Hyun Kim,3 In-Beom Kim,3 and Uhtaek Oh1,2,*
1Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Gyunggy 16229, Korea
2Sensory Research Center, CRI, College of Pharmacy, Seoul National University, Seoul 08826, Korea
3Department of Anatomy, Catholic Neuroscience Institute, College of Medicine, Catholic University, Seoul 06591, Korea
4Co-first author
*Correspondence : Uhtaek Oh
Summary
Touch sensation or proprioception requires the transduction of mechanical stimuli into electrical signals by mechanoreceptors in the periphery. These mechanoreceptors are equipped with various transducer channels. Although Piezo1 and 2 are mechanically activated (MA) channels with rapid inactivation, MA molecules with other inactivation kinetics have not been identified. Here we report that heterologously expressed Tentonin3 (TTN3)/TMEM150C is activated by mechanical stimuli with distinctly slow inactivation kinetics. Genetic ablation of Ttn3/Tmem150c markedly reduced slowly adapting neurons in dorsal-root ganglion neurons. The MA TTN3 currents were inhibited by known blockers of mechanosensitive ion channels. Moreover, TTN3 was localized in muscle spindle afferents. Ttn3-deficient mice exhibited the loss of coordinated movements and abnormal gait. Thus, TTN3 appears to be a component of a mechanosensitive channel with a slow inactivation rate and contributes to motor coordination. Identification of this gene advances our understanding of the various types of mechanosensations, including proprioception.
논문정보
- Research article
- 2016년 07월 (BRIC 등록일 2016-06-22)
- 국내 연구진
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