| NTDs such as spina bifida present a significant public health problem. The broad goal of this thesis was to establish the efficacy of C. elegans as a model for neural tube defects, allowing the molecular mechanisms of cell migrations associated with neural tube closure to be examined in a simple system. Alternative food sources, genetic components, and environmental variables (ethanol and valproic acid) were investigated. Folate pathway mutants had increased embryonic lethality, as did embryos from hermaphrodites grown in the presence of valproic acid and ethanol, but the effect level was variable. The variable outcomes may be a result of the multi- factorial nature of neural tube defects and the involved covariates. Based on these experiments, the most promising candidate approaches for examining the usefulness of C. elegans as a model for NTDs are genetic components in the folate pathway and in utero ethanol exposure. |
