Document Type
Article
Publication Date
9-1-2024
Original Citation
Young C,
Burt E,
Munnamalai V.
A cochlear progenitor pool influences patterning of the mammalian sensory epithelium via MYBL2. Development. 2024;151(17):dev202635.
Keywords
JMG, Animals, Cochlea, Mice, Epithelium, Cell Proliferation, Stem Cells, Jagged-1 Protein, Gene Expression Regulation, Developmental, Wnt Signaling Pathway, Body Patterning, Trans-Activators, Hair Cells, Auditory, Inner, Cell Cycle Proteins
JAX Source
Development. 2024;151(17):dev202635.
ISSN
1477-9129
PMID
39254648
DOI
https://doi.org/10.1242/dev.202635
Grant
This work was supported by the National Institutes of Health (R21DC016376 to V.M.) and the University of Maine T32 fellowship (National Institute of General Medical Sciences, GM132006 to C.A.Y.). Open access funding provided by The Jackson Laboratory.
Abstract
During embryonic development, Wnt signaling influences both proliferation and sensory formation in the cochlea. How this dual nature of Wnt signaling is coordinated is unknown. In this study, we define a novel role for a Wnt-regulated gene, Mybl2, which was already known to be important for proliferation, in determining the size and patterning of the sensory epithelium in the murine cochlea. Using a quantitative spatial analysis approach and analyzing Mybl2 loss-of-function, we show that Mybl2 promoted proliferation in the inner sulcus domain but limited the size of the sensory domain by influencing their adjoining boundary position via Jag1 regulation during development. Mybl2 loss-of-function simultaneously decreased proliferation in the inner sulcus and increased the size of the sensory domain, resulting in a wider sensory epithelium with ectopic inner hair cell formation during late embryonic stages. These data suggest that progenitor cells in the inner sulcus determine boundary formation and pattern the sensory epithelium via MYBL2.
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.