In addition to transcription, alternative pre-mRNA splicing is a key cellular process whereby utilization of potential splice sites of the pre-mRNA in various combinations by spliceosome under the regulation of alternative splicing factors makes a significant contribution to proteomic diversity by leading to expression of various isoforms of the proteins with distinct functions17,18. Recent studies suggest that alternative pre-mRNA splicing of genes may contribute to the development of alcohol-induced disorders19–23. However, little is known regarding the potential impact of alcohol on alternative splicing of genes during the fetal development and its involvement in the development of fetal alcohol spectrum disorder (FASD). We have recently shown that EtOH exposure of fetal neurons suppresses expression levels of serine/arginine rich splicing factor 1 (SRSF1) and causes missplicing of myeloid cell leukemia 1 (Mcl-1) by favoring the Mcl-1S splicing over Mcl-1L24. Several studies suggested that while the longer gene product Mcl-1L enhances cell survival by inhibiting apoptosis in response to various stress conditions in different cell types, the alternatively spliced shorter gene product Mcl-1S may promote apoptosis25,26. Hence, the possibility arises that alternative splicing
