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2013 March

Characterizing Fetal Craniofacial Gene Expression Changes in Response to Chronic Gestational Ethanol Exposure Using a Mouse Model of FAS.

A. Murat Maga, PhD, Acting Assistance Professor
Pediatrics
Center for Tissue and Cell Sciences, Seattle Children's Research Institute

Description: "Fetal alcohol spectrum disorders” or FASD are considered to be the leading preventable cause of mental retardation. Fetal alcohol syndrome (FAS) represents the most extreme, viable consequence of maternal alcohol consumption. The reasons for the highly variable outcomes are unknown. The uncertainty might be related to dose, time and duration of exposure as well as the influence of race, gender and maternal age. Although the CNS anomalies are the most well-studied, the facial appearance is the most recognizable and robust diagnostic feature of the FASD. Understanding the factors impacting on craniofacial form is an essential step to improve diagnosis and management of FASD, and will significantly aid the development of more effective educational programs pertaining to the adverse effects of maternal alcohol consumption on fetal and adult health.

Here I propose to use a new mouse model of moderate dose chronic ethanol exposure that produces FAS related measurable phenotypes in adults. My long-term goals are to (1) investigate the role of epigenetic programming in the presentation of alcohol-related malformations through detailed quantification of the craniofacial phenotype and (2) correlate genomic differences with these features to find epigenetically modified genes responsible for the phenotypic differences. This particular proposal will investigate the effect of chronic gestational ethanol exposure to the gene expression levels using microarray experiments and also look for modified genes that might be responsible for the phenotypic variation observed.

2013 October

No grants were funded in this cycle.