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 |
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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.
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•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. |
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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 |
AuthorAffiliation_xml | – name: 5 School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA, USA – name: 7 Lead contact – name: 3 Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA – name: 2 Institute for Stem Cell Biology & Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA – name: 4 Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA – name: 6 Departments of Bioengineering and Applied Physics and Howard Hughes Medical Institute, Stanford University, Stanford, CA, USA – name: 1 Department of Otolaryngology Head and Neck Surgery, Stanford University School of Medicine, Stanford, CA, USA |
Author_xml | – sequence: 1 givenname: Maggie S. surname: Matern fullname: Matern, Maggie S. organization: Department of Otolaryngology Head and Neck Surgery, Stanford University School of Medicine, Stanford, CA, USA – sequence: 2 givenname: Robert surname: Durruthy-Durruthy fullname: Durruthy-Durruthy, Robert organization: Department of Otolaryngology Head and Neck Surgery, Stanford University School of Medicine, Stanford, CA, USA – sequence: 3 givenname: Onur surname: Birol fullname: Birol, Onur organization: Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA – sequence: 4 givenname: Spyros surname: Darmanis fullname: Darmanis, Spyros organization: Departments of Bioengineering and Applied Physics and Howard Hughes Medical Institute, Stanford University, Stanford, CA, USA – sequence: 5 givenname: Mirko surname: Scheibinger fullname: Scheibinger, Mirko organization: Department of Otolaryngology Head and Neck Surgery, Stanford University School of Medicine, Stanford, CA, USA – sequence: 6 givenname: Andrew K. surname: Groves fullname: Groves, Andrew K. organization: Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA – sequence: 7 givenname: Stefan orcidid: 0000-0002-0490-4440 surname: Heller fullname: Heller, Stefan email: hellers@stanford.edu organization: Department of Otolaryngology Head and Neck Surgery, Stanford University School of Medicine, Stanford, CA, USA |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37227818$$D View this record in MEDLINE/PubMed |
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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. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 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. |
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