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Gene expression profiling of the palate in Erk2 mutant mouse models

ABSTRACT: The overall goal of this project is to investigate the role of Erk2-mediated signaling in regulating the cellular metabolism of cranial neural crest (CNC) cells during palate development. Here, we conducted gene expression profiling of palate tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Erk2 gene. The latter mice exhibit micrognathia, tongue defects and cleft palate, which is among the most common congenital birth defects and observed in many syndromic conditions. To investigate the adverse effects of dysfunctional ERK signaling on the cellular metabolism of palatal mesenchyme during palatogenesis, we analyzed mice with a neural crest cell-specific conditional inactivation of Erk2 (Erk2fl/fl;Wnt1-Cre). We performed microarray analyses of primary mouse embryonic palatal mesenchymal cells of Erk2fl/fl;Wnt1-Cre mutant mice and Erk2fl/fl control mice, collected at embryonic day 13.5 (n=3 per genotype) and E14.5 (n=5 per genotype).

ORGANISM(S): Mus musculus

SUBMITTER: Richard Pelikan 

PROVIDER: E-GEOD-67087 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Disruption of the ERK/MAPK pathway in neural crest cells as a potential cause of Pierre Robin sequence.

Parada Carolina C   Han Dong D   Grimaldi Alexandre A   Sarrión Patricia P   Park Shery S SS   Pelikan Richard R   Sanchez-Lara Pedro A PA   Chai Yang Y  

Development (Cambridge, England) 20150922 21

Disrupted ERK1/2 signaling is associated with several developmental syndromes in humans. To understand the function of ERK2 (MAPK1) in the postmigratory neural crest populating the craniofacial region, we studied two mouse models: Wnt1-Cre;Erk2(fl/fl) and Osr2-Cre;Erk2(fl/fl). Wnt1-Cre;Erk2(fl/fl) mice exhibited cleft palate, malformed tongue, micrognathia and mandibular asymmetry. Cleft palate in these mice was associated with delay/failure of palatal shelf elevation caused by tongue malpositio  ...[more]

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