ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2010
Long-term consequences of Sox9 depletion on inner ear development.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- SOX9 and SOX10 control fluid homeostasis in the inner ear for hearing through independent and cooperative mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Loss of Mst1/2 activity promotes non-mitotic hair cell generation in the neonatal organ of Corti.NPJ Regenerative medicine · 2022Article
- Sox8 remodels the cranial ectoderm to generate the ear.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Exome sequencing of families from Ghana reveals known and candidate hearing impairment genes.Communications biology · 2022Article
- Otic Neurogenesis inFrontiers in neuroanatomy · 2021Article
- Six1 proteins with human branchio-oto-renal mutations differentially affect cranial gene expression and otic development.Disease models & mechanisms · 2020Article
- Six1 and Irx1 have reciprocal interactions during cranial placode and otic vesicle formation.Developmental biology · 2019Article
- Pa2G4 is a novel Six1 co-factor that is required for neural crest and otic development.Developmental biology · 2017Article
- Dissecting the molecular basis of organ of Corti development: Where are we now?Hearing research · 2011Review
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
The transcription factor Sox9 has been implicated in inner ear formation in several species. To investigate the long-term consequences of Sox9 depletion on inner ear development we analyzed the inner ear architecture of Sox9-depleted Xenopus tadpoles generated by injection of increasing amounts of Sox9 morpholino antisense oligonucleotides. We found that Sox9-depletion resulted in major defects in the development of vestibular structures, semicircular canals and utricle, while the ventrally located saccule was less severely affected in these embryos. Consistent with this phenotype, we observed a specific loss of the dorsal expression of Wnt3a expression in the otic vesicle of Sox9 morphants, associated with an increase in cell death and a reduction in cell proliferation in the region of the presumptive otic epithelium. We propose that, in addition to its early role in placode specification, Sox9 is also required for the maintenance of progenitors in the otic epithelium.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.