Identification of fetal alcohol-affected children: Alterations in imprinted gene expression and methylation as biomarkers of neurobehavioral and growth impairment.

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In the U.S. maternal alcohol use during pregnancy remains an important problem with approximately 10% of women consuming alcohol and 3% reporting binge drinking [1]. Fetal alcohol spectrum disorders (FASD) are the most common preventable cause of birth defects and neurodevelopmental disorders [2]. This problem is accentuated in heavily exposed populations like the Cape Coloured in South Africa, which has one of highest prevalence of FASD in the world [3]. Given the important consequences to child development of this prevalent exposure, it is imperative to identify early-life biomarkers that help identify children with FASD as early as possible so they can receive prompt targeted interventions [4]. This is the aim of the parent R01 study “Identification of fetal alcohol-affected children: Alterations in imprinted gene expression and methylation as biomarkers of neurobehavioral and growth impairment” (PI Dr. Carter). In Aim 1, the parent study will characterize imprinted gene expression biomarkers in blood and placental tissues from children prenatally exposed to alcohol and controls from the Cape Town longitudinal Cohort Study using RNA-seq. However, placental RNA-seq data to be generated from the parent study are composed of a mix of gene profiles from distinct cell- subtypes within a heterogenous tissue and to date there are no studies addressing this. The aim of the research in this supplement is to leverage recent placenta single-cell RNA-seq to construct a panel of cell-type specific gene makers to disentangle bulk placenta RNAs-seq data from the parent study and assess alcohol-related cell-type specific effects in these data.