Investigating the Contribution of the Imprinted Gene Asb4 to Parental Care
TL;DR
It is proposed that Asb4 supports normal activation of MPOA Gal+ neurons required for parental care and activity of MPOA Gal+ neurons in brain‐specific maternal Asb4 knockout mice and hypothesis knockout animals will demonstrate a deficient behavioural phenotype in one or more parental behavioural characteristics.
Abstract
Genomic imprinting is a form of epigenetic regulation that leads to expression from one parental allele only and, in animals, is unique to mammals. Imprinted gene expression is predominant in the brain and their roles in neural processes are becoming more appreciated. Recent analyses have indicated an enrichment of imprinted gene expression in the ‘parental hub’ circuitry. Specifically, imprinted genes were over‐represented in the transcriptomic profile of galanin positive (Gal+) neurons in the medial preoptic area (MPOA) of the hypothalamus. One of those imprinted genes showing enriched expression in Gal+ neurons was the maternally expressed Asb4. Here, we propose that Asb4 supports normal activation of MPOA Gal+ neurons required for parental care. We aim to demonstrate abnormal parental behaviours—such as decreased pup retrieval and impaired nest building—and activity of MPOA Gal+ neurons in brain‐specific maternal Asb4 knockout mice and hypothesis knockout animals will demonstrate a deficient behavioural phenotype in one or more parental behavioural characteristics.