PUBLICATION
sox2 and sox3 play unique roles in development of hair cells and neurons in the zebrafish inner ear
- Authors
- Gou, Y., Vemaraju, S., Sweet, E.M., Kwon, H.J., Riley, B.B.
- ID
- ZDB-PUB-180123-5
- Date
- 2018
- Source
- Developmental Biology 435(1): 73-83 (Journal)
- Registered Authors
- Kwon, Hye-Joo, Riley, Bruce, Sweet, Elly, Vemaraju, Shruti
- Keywords
- SoxB1, otic placode, sensory epithelia, statoacoustic ganglion
- MeSH Terms
-
- Animals
- Fibroblast Growth Factors/genetics
- Fibroblast Growth Factors/metabolism
- Gene Expression Regulation, Developmental/physiology*
- Hair Cells, Auditory, Inner/cytology
- Hair Cells, Auditory, Inner/metabolism*
- Neurogenesis/physiology*
- PAX2 Transcription Factor/genetics
- PAX2 Transcription Factor/metabolism
- Receptors, Notch/genetics
- Receptors, Notch/metabolism
- SOX Transcription Factors/biosynthesis*
- SOX Transcription Factors/genetics
- Zebrafish/embryology*
- Zebrafish Proteins/biosynthesis*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 29355523 Full text @ Dev. Biol.
Citation
Gou, Y., Vemaraju, S., Sweet, E.M., Kwon, H.J., Riley, B.B. (2018) sox2 and sox3 play unique roles in development of hair cells and neurons in the zebrafish inner ear. Developmental Biology. 435(1):73-83.
Abstract
Formation of neural and sensory progenitors in the inner ear requires Sox2 in mammals, and in other species is thought to rely on both Sox2 and Sox3. How Sox2 and/or Sox3 promote different fates is poorly understood. Our mutant analysis in zebrafish showed that sox2 is uniquely required for sensory development while sox3 is uniquely required for neurogenesis. Moderate misexpression of sox2 during placodal stages led to development of otic vesicles with expanded sensory and reduced neurogenic domains. However, high-level misexpression of sox2 or sox3 expanded both sensory and neurogenic domains to fill the medial and lateral halves of the otic vesicle, respectively. Disruption of medial factor pax2a eliminated the ability of sox2/3 misexpression to expand sensory but not neurogenic domains. Additionally, mild misexpression of fgf8 during placodal development was sufficient to specifically expand the zone of prosensory competence. Later, cross-repression between atoh1a and neurog1 helps maintain the sensory-neural boundary, but unlike mouse this does not require Notch activity. Together, these data show that sox2 and sox3 exhibit intrinsic differences in promoting sensory vs. neural competence, but at high levels these factors can mimic each other to enhance both states. Regional cofactors like pax2a and fgf8 also modify sox2/3 functions.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping