Please use this identifier to cite or link to this item: https://doi.org/10.7554/eLife.45418.001
Title: Neural Crest-Specific Deletion of Rbfox2 in Mice Leads to Craniofacial Abnormalities Including Cleft Palate.
Authors: DASAN MARY CIBI 
MIA MD MASUM 
SHAMINI D/O GUNA SHEKERAN 
Yun LS
SANDIREDDY REDDEMMA 
Gupta P
MONALISA HOTA 
SUN LEI 
SUJOY GHOSH 
Singh Manvendra Kumar 
Issue Date: 26-Jun-2019
Publisher: eLife Sciences Publications Ltd
Citation: DASAN MARY CIBI, MIA MD MASUM, SHAMINI D/O GUNA SHEKERAN, Yun LS, SANDIREDDY REDDEMMA, Gupta P, MONALISA HOTA, SUN LEI, SUJOY GHOSH, Singh Manvendra Kumar (2019-06-26). Neural Crest-Specific Deletion of Rbfox2 in Mice Leads to Craniofacial Abnormalities Including Cleft Palate.. eLife 8 : e45418. ScholarBank@NUS Repository. https://doi.org/10.7554/eLife.45418.001
Abstract: Alternative splicing (AS) creates proteomic diversity from a limited size genome by generating numerous transcripts from a single protein-coding gene. Tissue-specific regulators of AS are essential components of the gene regulatory network, required for normal cellular function, tissue patterning, and embryonic development. However, their cell-autonomous function in neural crest development has not been explored. Here, we demonstrate that splicing factor Rbfox2 is expressed in the neural crest cells (NCCs), and deletion of Rbfox2 in NCCs leads to cleft palate and defects in craniofacial bone development. RNA-Seq analysis revealed that Rbfox2 regulates splicing and expression of numerous genes essential for neural crest/craniofacial development. We demonstrate that Rbfox2-TGF-β-Tak1 signaling axis is deregulated by Rbfox2 deletion. Furthermore, restoration of TGF-β signaling by Tak1 overexpression can rescue the proliferation defect seen in Rbfox2 mutants. We also identified a positive feedback loop in which TGF-β signaling promotes expression of Rbfox2 in NCCs.
Source Title: eLife
URI: https://scholarbank.nus.edu.sg/handle/10635/168453
ISSN: 2050-084X
DOI: 10.7554/eLife.45418.001
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