Interplay between maternal Slc6a4 mutation and prenatal stress: a possible mechanism for autistic behavior development.

ABSTRACT: The low activity allele of the maternal polymorphism, 5HTTLPR, in the serotonin transporter, SLC6A4, coupled with prenatal stress is reported to increase the risk for children to develop autism spectrum disorder (ASD). Similarly, maternal Slc6a4 knock-out and prenatal stress in rodents results in offspring demonstrating ASD-like characteristics. The present study uses an integrative genomics approach to explore mechanistic changes in early brain development in mouse embryos exposed to this maternal gene-environment phenomenon. Restraint stress was applied to pregnant Slc6a4 ^+/+ and Slc6a4 ^+/- mice and post-stress embryonic brains were assessed for whole genome level profiling of methylome, transcriptome and miRNA using Next Generation Sequencing. Embryos of stressed S

SUBMITTER: Sjaarda CP 

PROVIDER: S-EPMC5562880 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature