The goal of this pilot project is to determine if the observed differences in susceptibility to hyperthermia-induced neural tube defects are due to strain differences in heat shock protein synthesis and/or the duration of arrested normal protein synthesis during embryonic development. Demonstrating that heat shock proteins have a role in conferring resistance to a teratogen-induced neural tube defects would be of major significance, for it would imply that resistance to adverse environmental stress is under genetic control and is therefore amenable to genetic manipulation. As neural tube defects are a leading cause of mental deficiency in human populations, an understanding of the genetic and pathogenetic basis of these anomalies would be invaluable in broadening our appreciation for the molecular nature of these defects. This knowledge is a necessary prerequisite to any program designed for prenatal prevention.
| Finnell, R H; Bennett, G D; Karras, S B et al. (1988) Common hierarchies of susceptibility to the induction of neural tube defects in mouse embryos by valproic acid and its 4-propyl-4-pentenoic acid metabolite. Teratology 38:313-20 |
