Collectively, our data suggests that EtOH exposure causes viability loss and apoptosis in neural progenitors and immature neurons with a limited impact on fully differentiated mature neuron cultures, suggesting a possible mechanism by which prenatal alcohol exposure exerts detrimental deficits in the brain. In addition, selective missplicing of Mcl-1 is associated with neural progenitor cell death and might be the underlying mechanism of increased sensitivity of progenitors to the toxic effects of EtOH. Altogether, these results suggest that EtOH-mediated missplicing of Mcl-1 pre-mRNA may contribute to FASD phenotype due to the depletion of neural progenitors in the developing fetal brain.
