Transcriptional dynamics of delaminating neuroblasts in the mouse otic vesicle

An abundance of research has recently highlighted the susceptibility of cochleovestibular ganglion (CVG) neurons to noise damage and aging in the adult cochlea, resulting in hearing deficits. Furthering our understanding of the transcriptional cascades that contribute to CVG development may provide...

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Published in:Cell reports (Cambridge) Vol. 42; no. 6; p. 112545
Main Authors: Matern, Maggie S., Durruthy-Durruthy, Robert, Birol, Onur, Darmanis, Spyros, Scheibinger, Mirko, Groves, Andrew K., Heller, Stefan
Format: Journal Article
Language:English
Published: United States Elsevier Inc 27-06-2023
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Abstract An abundance of research has recently highlighted the susceptibility of cochleovestibular ganglion (CVG) neurons to noise damage and aging in the adult cochlea, resulting in hearing deficits. Furthering our understanding of the transcriptional cascades that contribute to CVG development may provide insight into how these cells can be regenerated to treat inner ear dysfunction. Here we perform a high-depth single-cell RNA sequencing analysis of the E10.5 otic vesicle and its surrounding tissues, including CVG precursor neuroblasts and emerging CVG neurons. Clustering and trajectory analysis of otic-lineage cells reveals otic markers and the changes in gene expression that occur from neuroblast delamination toward the development of the CVG. This dataset provides a valuable resource for further identifying the mechanisms associated with CVG development from neurosensory competent cells within the otic vesicle. [Display omitted] •scRNA-seq of micro-dissected otic vesicles identifies three otic populations at E10.5•Otic neuroblasts express early neuronal, EMT, and proliferation markers•Expression dynamics analysis suggests potential regulators of neuroblast delamination•Integration with published E9.5 and E11.5 data results in a comprehensive resource Matern et al. provide a validated resource of E10.5 otic vesicle, neuroblast, and early otic neuron single-cell profiles. The neuroblast stage is defined by early neuronal and proliferative genes. Integrating published otic-lineage data from bracketing time points indicates neuroblast delamination as a dynamic process.
AbstractList An abundance of research has recently highlighted the susceptibility of cochleovestibular ganglion (CVG) neurons to noise damage and aging in the adult cochlea, resulting in hearing deficits. Furthering our understanding of the transcriptional cascades that contribute to CVG development may provide insight into how these cells can be regenerated to treat inner ear dysfunction. Here we perform a high-depth single-cell RNA sequencing analysis of the E10.5 otic vesicle and its surrounding tissues, including CVG precursor neuroblasts and emerging CVG neurons. Clustering and trajectory analysis of otic-lineage cells reveals otic markers and the changes in gene expression that occur from neuroblast delamination toward the development of the CVG. This dataset provides a valuable resource for further identifying the mechanisms associated with CVG development from neurosensory competent cells within the otic vesicle. Matern et al. provide a validated resource of E10.5 otic vesicle, neuroblast, and early otic neuron single-cell profiles. The neuroblast stage is defined by early neuronal and proliferative genes. Integrating published otic-lineage data from bracketing time points indicates neuroblast delamination as a dynamic process.
An abundance of research has recently highlighted the susceptibility of cochleovestibular ganglion (CVG) neurons to noise damage and aging in the adult cochlea, resulting in hearing deficits. Furthering our understanding of the transcriptional cascades that contribute to CVG development may provide insight into how these cells can be regenerated to treat inner ear dysfunction. Here we perform a high-depth single-cell RNA sequencing analysis of the E10.5 otic vesicle and its surrounding tissues, including CVG precursor neuroblasts and emerging CVG neurons. Clustering and trajectory analysis of otic-lineage cells reveals otic markers and the changes in gene expression that occur from neuroblast delamination toward the development of the CVG. This dataset provides a valuable resource for further identifying the mechanisms associated with CVG development from neurosensory competent cells within the otic vesicle.
An abundance of research has recently highlighted the susceptibility of cochleovestibular ganglion (CVG) neurons to noise damage and aging in the adult cochlea, resulting in hearing deficits. Furthering our understanding of the transcriptional cascades that contribute to CVG development may provide insight into how these cells can be regenerated to treat inner ear dysfunction. Here we perform a high-depth single-cell RNA sequencing analysis of the E10.5 otic vesicle and its surrounding tissues, including CVG precursor neuroblasts and emerging CVG neurons. Clustering and trajectory analysis of otic-lineage cells reveals otic markers and the changes in gene expression that occur from neuroblast delamination toward the development of the CVG. This dataset provides a valuable resource for further identifying the mechanisms associated with CVG development from neurosensory competent cells within the otic vesicle. [Display omitted] •scRNA-seq of micro-dissected otic vesicles identifies three otic populations at E10.5•Otic neuroblasts express early neuronal, EMT, and proliferation markers•Expression dynamics analysis suggests potential regulators of neuroblast delamination•Integration with published E9.5 and E11.5 data results in a comprehensive resource Matern et al. provide a validated resource of E10.5 otic vesicle, neuroblast, and early otic neuron single-cell profiles. The neuroblast stage is defined by early neuronal and proliferative genes. Integrating published otic-lineage data from bracketing time points indicates neuroblast delamination as a dynamic process.
ArticleNumber 112545
Author Matern, Maggie S.
Birol, Onur
Groves, Andrew K.
Durruthy-Durruthy, Robert
Darmanis, Spyros
Heller, Stefan
Scheibinger, Mirko
AuthorAffiliation 4 Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA
3 Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA
5 School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA, USA
2 Institute for Stem Cell Biology & Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA
6 Departments of Bioengineering and Applied Physics and Howard Hughes Medical Institute, Stanford University, Stanford, CA, USA
1 Department of Otolaryngology Head and Neck Surgery, Stanford University School of Medicine, Stanford, CA, USA
7 Lead contact
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Issue 6
Keywords cochlea
scRNA-seq
otic vesicle
CP: Neuroscience
neurogenesis
otic neuroblasts
vestibular
cochleovestibular ganglion
otic placode
Language English
License This is an open access article under the CC BY-NC-ND license.
Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.
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AUTHOR CONTRIBUTIONS
Conceptualization, M.S.M., R.D., and S.H.; methodology, M.S.M., R.D., M.S., A.G., and O.B.; formal analysis, M.S.M. and R.D.; investigation, M.S.M., R.D., O.B., and M.S.; resources, M.S.M., R.D., O.B., S.D., and M.S.; writing – original draft, M.S.M., R.D., and S.H.; writing – review & editing, M.S.M., A.G., and S.H.; visualization, M.S.M., R.D., O.B., and M.S.; supervision, A.G. and S.H.; funding acquisition, M.S.M., A.G., and S.H.
ORCID 0000-0002-0490-4440
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Snippet An abundance of research has recently highlighted the susceptibility of cochleovestibular ganglion (CVG) neurons to noise damage and aging in the adult...
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StartPage 112545
SubjectTerms Animals
Cochlea
cochleovestibular ganglion
CP: Neuroscience
Gene Expression Regulation, Developmental
Mice
Neural Stem Cells - metabolism
neurogenesis
Neurons
otic neuroblasts
otic placode
otic vesicle
scRNA-seq
vestibular
Title Transcriptional dynamics of delaminating neuroblasts in the mouse otic vesicle
URI https://dx.doi.org/10.1016/j.celrep.2023.112545
https://www.ncbi.nlm.nih.gov/pubmed/37227818
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https://doaj.org/article/edfacdabfdac43b3824d419aad9a89a5
Volume 42
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