My current research interest centers around the teretogenic effects of alcohol exposure on fetal development. Alcohol exposure is know to effect embryo development beginning as early as neurulation (end of the first trimester) and causes developmental alterations to the cranio-facial midline, brain, limbs, heart, otic and ocular formation and are suggested to be attributed in part to proliferation, migration and differentiation of neural crest stem cells. Previous studies for fetal alcohol spectrum disorders (FASD) suggest early developmental miscues attributed to cell losses and reduced proliferation of stem cells and shows that major contributors include mis-regulation of cell cycle, DNA synthesis, and apoptosis, all likely linked to growth retardation and altered organ morphogenesis characteristic of FASD. However, there is little evidence on the mechanistic changes in these cellular events and how this may affect organ development. Our resent results, using whole embryo cultures exposed to ethanol, shows cell losses and reduced proliferation in several areas of the E10 mouse embryo. More recent studies, using neural crest derived stem cells, suggest alterations in cell cycle progression or checkpoint control that may be the driving force behind growth abnormalities and reduced cell numbers. These alterations coincide with reduced proliferation; change in G1-S phase cell cycle regulatory proteins attributed to an accelerated G1 phase, and alterations in DNA content. We suggest that understanding the aberrant cell cycle mechanism(s) creating altered proliferation and cell loss is paramount for directing treatment for FASD.
