• Prenatal Alcohol Exposure;
  • Neural Crest Apoptosis;
  • Craniofacial;
  • Genetics;
  • Chicken Embryo

Background: Ethanol-induced neural crest apoptosis likely contributes to the distinctive craniofacial phenotype that results from prenatal alcohol exposure. The mechanism responsible for this apoptosis is incompletely understood. A serendipitous change in poultry production flocks led to the discovery that, in chick, the embryo's genetic background modulates its susceptibility to ethanol-induced apoptosis.

Methods: We examined the level of ethanol-induced neural crest apoptosis in 11 chick layer strains or crosses, using acridine orange uptake.

Results: Holding the ethanol dose and exposure stage constant, strains were classified into very sensitive (Babcock ISA, HyLine W98, Babcock B300/Hampshire Red cross [BxHR]), moderately sensitive (Spafas, HyLine W36, Babcock B300), and nonresponsive (DeKalb White and Black, Shaver White and 2000, DeKalb White/Hampshire Red cross). Detailed examination of two susceptible strains (W98, BxHR) and a resistant strain (DeKalb White) revealed that the DeKalb's nonresponse was not caused by a shift in; timing of apoptosis, or to a lower alcohol exposure at either time of injection or time of death. Strains had identical stage distributions at the time of injection and at apoptosis; housing and diet were held constant.

Conclusions: Factors within the embryo and/or egg environment can affect the susceptibility to ethanol-induced apoptosis. These sensitive and resistant strains will be important tools to dissect the molecular mechanism of ethanol-induced apoptosis, and for understanding how these losses affect subsequent development.