Premium
Neural crest cell deficiency of c‐myc causes skull and hearing defects
Author(s) -
Wei Ke,
Chen Jiyuan,
Akrami Kevan,
Galbraith Gary C.,
Lopez Ivan A.,
Chen Fabian
Publication year - 2007
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.20304
Subject(s) - neural crest , craniofacial , biology , skull , cranial neural crest , embryonic stem cell , mutant , hearing loss , microbiology and biotechnology , anatomy , embryo , gene , genetics , medicine , audiology
The proto‐oncogene c‐myc has a central role in multiple processes important for embryonic development, including cell proliferation, growth, apoptosis, and differentiation. We have investigated the role of c‐myc in neural crest by using Wnt1‐Cre ‐mediated deletion of a conditional mutation of the c‐myc gene. c‐myc deficiency in neural crest resulted in viable adult mice that have defects in coat color, skull frontal bone, and middle ear ossicle development. Physiological hearing studies demonstrated a significant hearing deficit in the mutant mice. In this report, we focus on the craniofacial and hearing defects. To further examine neural crest cells affected by c‐myc deficiency, we fate mapped Wnt1‐Cre expressing neural crest cells using the ROSA26 Cre reporter transgene. The phenotype obtained demonstrates the critical role that c‐myc has in neural crest during craniofacial development as well as in providing a model for examining human congenital skull defects and deafness. genesis 45:382–390, 2007. Published 2007 Wiley‐Liss, Inc.