ArticleDevelopmental biology2023
Tbx2 and Tbx3 regulate cell fate progression of the otic vesicle for inner ear development.
Article in Developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- The Roles of Tbx2 in Cochlear Development and Auditory Function.Neuroscience bulletin · 2026Article
- Reduced dosage of Kmt2d modifies Tbx1 haploinsufficiency toward phenotypes of 22q11.2DS.JCI insight · 2026Article
- Transcriptomic profiling of inner ear hair cell spontaneous regeneration reveals the key role of dlx5a.Nature communications · 2026Article
- Synergistic SHH activation and BMP inhibition remodel progenitor niche for enhanced hair cell generation.Science China. Life sciences · 2026Article
- Harmony in the Molecular Orchestra of Hearing: Developmental Mechanisms from the Ear to the Brain.Annual review of neuroscience · 2024Review
- Advance and Application of Single-cell Transcriptomics in Auditory Research.Neuroscience bulletin · 2024Review
- Revisiting the Potency of Tbx2 Expression in Transforming Outer Hair Cells into Inner Hair Cells at Multiple Ages In Vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Single-cell transcriptomics uncovers a non-autonomous Tbx1-dependent genetic program controlling cardiac neural crest cell development.Nature communications · 2023Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
The morphogenesis of the otic vesicle (OV) to form inner ear organs serves as an excellent model system to understand cell fate acquisition on a single cell level. Tbx2 and Tbx3 (Tbx2/3) encode closely related T-box transcription factors that are expressed widely in the mammalian OV. Inactivation of both genes in the OV (Tbx2/3cKO) results in failed morphogenesis into inner ear organs. To understand the basis of these defects, single cell RNA-sequencing (scRNA-seq) was performed on the OV lineage, in controls versus Tbx2/3cKO embryos. We identified a multipotent population termed otic progenitors in controls that are marked by expression of the known otic placode markers Eya1, Sox2, and Sox3 as well as new markers Fgf18, Cxcl12, and Pou3f3. The otic progenitor population was increased three-fold in Tbx2/3cKO embryos, concomitant with dysregulation of genes in these cells as well as reduced progression to more differentiated states of prosensory and nonsensory cells. An ectopic neural population of cells was detected in the posterior OV of Tbx2/3cKO embryos but had reduced maturation to delaminated neural cells. As all three cell fates were affected in Tbx2/3cKO embryos, we suggest that Tbx2/3 promotes progression of multipotent otic progenitors to more differentiated cell types in the OV.
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