ArticleDevelopmental biology2018
sox2 and sox3 cooperate to regulate otic/epibranchial placode induction in zebrafish.
Article in Developmental biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- Diverse SOX3 genetic variants and their associated phenotypic spectrum in human disease.Endocrine reviews · 2026Review
- Article
- Deletion of Pax1 scoliosis-associated regulatory elements leads to a female-biased tail abnormality.Cell reports · 2024Article
- ZebrafishZebrafish · 2023Article
- Comparative assessment of Fgf's diverse roles in inner ear development: A zebrafish perspective.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Review
- EditingInternational journal of molecular sciences · 2021Review
- Hcfc1a regulates neural precursor proliferation and asxl1 expression in the developing brain.BMC neuroscience · 2020Article
- Notch signalling regulates epibranchial placode patterning and segregation.Development (Cambridge, England) · 2020Article
- Loss-of-function of sox3 causes follicle development retardation and reduces fecundity in zebrafish.Protein & cell · 2019Article
- sox2 and sox3 Play unique roles in development of hair cells and neurons in the zebrafish inner ear.Developmental biology · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Expression of sox3 is one of the earliest markers of Fgf-dependent otic/epibranchial placode induction. We report here that sox2 is also expressed in the early otic/epibranchial placode in zebrafish. To address functions of sox2 and sox3, we generated knockouts and heat shock-inducible transgenes. Mutant analysis, and low-level misexpression, showed that sox2 and sox3 act redundantly to establish a full complement of otic/epibranchial cells. Disruption of pax8, another early regulator, caused similar placodal deficiencies to sox3 mutants or pax8-sox3 double mutants, suggesting that sox3 and pax8 operate in the same pathway. High-level misexpression of sox2 or sox3 during early stages cell-autonomously blocked placode induction, whereas misexpression several hours later could not reverse placodal differentiation. In an assay for ectopic placode-induction, we previously showed that misexpression of fgf8 induces a high level of ectopic sox3, but not pax8. Partial knockdown of sox3 significantly enhanced ectopic induction of pax8, whereas full knockdown of sox3 inhibited this process. Together these findings show that sox2 and sox3 are together required for proper otic induction, but the level of expression must be tightly regulated to avoid suppression of differentiation and maintenance of pluripotency.
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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.