A cytoskeleton structure revealed by super-resolution fluorescence imaging in inner ear hair cells

Qi, Jieyu; Liu, Yan; Chu, Cenfeng; Chen, Xin; Zhu, Weijie; Shu, Yilai; He, Shuai; Chai, Renjie; Zhong, Guisheng

doi:10.1038/s41421-018-0076-4

Cited by 65 publications

(58 citation statements)

References 10 publications

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“…In the mammal's inner ear, hair cells and spiral ganglion neurons are critical for hearing ability; hair cells convert the mechanical sound waves into neural signals, and spiral ganglion neuron transmits these signals to the auditory cortex for hearing [40][41][42]. In the mammal's inner ear, hair cells and spiral ganglion neurons are vulnerable for multiple damages, including gene mutation, noise, different ototoxic drugs, inflammation, or aging [43][44][45][46][47] while the mammals only have very limited hair cell and spiral ganglion neuron regeneration ability; most of the damaged hair cells and spiral ganglion neurons cannot be spontaneously regenerate [48][49][50][51][52][53][54][55].…”

Section: Discussionmentioning

confidence: 99%

Differences in Clinical Characteristics and Brain Activity between Patients with Low- and High-Frequency Tinnitus

Zhang

Huang

et al. 2020

Neural Plasticity

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This study was aimed at delineating and comparing differences in clinical characteristics and brain activity between patients with low- and high-frequency tinnitus (LFT and HFT, respectively) using high-density electroencephalography (EEG). This study enrolled 3217 patients with subjective tinnitus who were divided into LFT (frequency<4000 Hz) and HFT (≥4000 Hz) groups. Data regarding medical history, Tinnitus Handicap Inventory, tinnitus matching, and hearing threshold were collected from all patients. Twenty tinnitus patients and 20 volunteers were subjected to 256-channel EEG, and neurophysiological differences were evaluated using standardized low-resolution brain electromagnetic tomography (sLORETA) source-localized EEG recordings. Significant differences in sex (p<0.001), age (p=0.022), laterality (p<0.001), intensity (p<0.001), tinnitus type (p<0.001), persistent tinnitus (p=0.04), average threshold (p<0.001), and hearing loss (p=0.028) were observed between LFT and HFT groups. The tinnitus pitch only appeared to be correlated with the threshold of the worst hearing loss in the HFT group. Compared with the controls, the LFT group exhibited increased gamma power (p<0.05), predominantly in the posterior cingulate cortex (PCC, BA31), whereas the HFT group had significantly decreased alpha1 power (p<0.05) in the angular gyrus (BA39) and auditory association cortex (BA22). Higher gamma linear connectivity between right BA39 and right BA41 was observed in the HFT group relative to controls (t=3.637, p=0.027). Significant changes associated with increased gamma in the LFT group and decreased alpha1 in the HFT group indicate that tinnitus pitch is crucial for matching between the tinnitus and control groups. Differences of band frequency energy in brain activity levels may contribute to the clinical characteristics and internal tinnitus “spectrum” differences.

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Section: Discussionmentioning

confidence: 99%

Differences in Clinical Characteristics and Brain Activity between Patients with Low- and High-Frequency Tinnitus

Zhang

Huang

et al. 2020

Neural Plasticity

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“…However, these processes do not only depend on the properties of the motors and their assemblies, but also on the structural organization of the actin cytoskeleton. In the future, our approach should be complemented by imaging and modelling of the actin cytoskeleton using super-resolution microscopy (Martinez et al, 2020;Qi et al, 2019;Shelden et al, 2016;Wassie et al, 2019). In a next step, our insights into the distinct cellular roles of the different NM II isoforms should be transferred to the tissue context, e.g.…”

Section: Discussionmentioning

confidence: 99%

Distinct roles of nonmuscle myosin II isoforms for establishing tension and elasticity during cell morphodynamics

Weißenbruch

Grewe

Hippler

et al. 2020

Preprint

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Nonmuscle myosin II (NM II) is an integral part of essential cellular processes, including adhesion and migration. Mammalian cells express up to three isoforms termed NM IIA, B, and C. We used U2OS cells to create CRISPR/Cas9-based knockouts of all three isoforms and analyzed the phenotypes on homogeneous and micropatterned substrates. We find that NM IIA is essential to build up cellular tension during initial stages of force generation, while NM IIB is necessary to elastically stabilize NM IIA-generated tension. The knockout of NM IIC has no detectable effects. A scale-bridging mathematical model explains our observations by relating actin fiber stability to the molecular rates of the myosin crossbridge cycle. We also find that NM IIA initiates and guides co-assembly of NM IIB into heterotypic minifilaments. We finally use mathematical modeling to explain the different exchange dynamics of NM IIA and B in minifilaments, as measured in FRAP experiments.

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“…The cause of hearing loss is extremely heterogeneous, and in many regions of the world, deaf people tend to marry with each other to form rather complex deaf families [33][34][35][36][37][38][39][40]. In one such family, we identified two separate genetic causes of hearing loss in distinct affected members, including the recessive c.235delC (p.L79Cfs * 3) mutation in GJB2 (III-2) and the dominant c.481C>T (p.R161C) mutation in SOX10 (II-1, III-1, and IV-1).…”

Section: Discussionmentioning

confidence: 99%

Targeted Next-Generation Sequencing Identifies Separate Causes of Hearing Loss in One Deaf Family and Variable Clinical Manifestations for the p.R161C Mutation inSOX10

Lin

2020

Neural Plasticity

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Hearing loss is the most common sensory deficit in humans. Identifying the genetic cause and genotype-phenotype correlation of hearing loss is sometimes challenging due to extensive clinical and genetic heterogeneity. In this study, we applied targeted next-generation sequencing (NGS) to resolve the genetic etiology of hearing loss in a Chinese Han family with multiple affected family members. Targeted sequencing of 415 deafness-related genes identified the heterozygous c.481C>T (p.R161C) mutation in SOX10 and the homozygous c.235delC (p.L79Cfs∗3) mutation in GJB2 as separate pathogenic mutations in distinct affected family members. The SOX10 c.481C>T (p.R161C) mutation has been previously reported in a Caucasian patient with Kallmann syndrome that features congenital hypogonadotropic hypogonadism with anosmia. In contrast, family members carrying the same p.R161C mutation in this study had variable Waardenburg syndrome-associated phenotypes (hearing loss and/or hair hypopigmentation) without olfactory or reproductive anomalies. Our results highlight the importance of applying comprehensive diagnostic approaches such as NGS in molecular diagnosis of hearing loss and show that the p.R161C mutation in SOX10 may be associated with a wide range of variable clinical manifestations.

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A cytoskeleton structure revealed by super-resolution fluorescence imaging in inner ear hair cells

Cited by 65 publications

References 10 publications

Differences in Clinical Characteristics and Brain Activity between Patients with Low- and High-Frequency Tinnitus

Differences in Clinical Characteristics and Brain Activity between Patients with Low- and High-Frequency Tinnitus

Distinct roles of nonmuscle myosin II isoforms for establishing tension and elasticity during cell morphodynamics

Targeted Next-Generation Sequencing Identifies Separate Causes of Hearing Loss in One Deaf Family and Variable Clinical Manifestations for the p.R161C Mutation inSOX10

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