2014), heritability for 100 diverse phenotypes in a heterogeneous stock of mice, again with genotyped parents, was estimated based on genomewide genetic similarity, and partitioned into variance components representing PoE and non-PoE. 2008), quantitative trait loci (QTL) for growth were mapped in an advanced intercross of mice, in which offspring and their parents were genotyped: a significant fraction of the phenotypic variance attributable to QTL was due to PoE. More is understood about PoE in mice their phenotypic impact, as assessed in controlled reciprocal crosses and in populations of mice in which the parental origin of alleles can be determined, suggests PoE can be considerable. In humans, disruption of specific imprinted genes cause developmental syndromes ( Ishida and Moore 2013), and while the genome-wide impact of parent-of-origin effects (PoE) on human complex traits-as distinct from these syndromes-is less clear, a handful of examples are known for example PoE at the imprinted DLK1-MEG3 locus associates with type I diabetes ( Wallace et al. The identities of these genes and the parental origin of the silenced allele depend on the species, tissue and developmental stage, with a core set of imprinted genes common to most species. 2013), i.e., mono-allelically expressed in a parent-of-origin specific manner. In placental mammals, around 100 transcriptional units are imprinted ( Morison et al. Parental genotypes do not necessarily make equal contributions to the phenotypes of their offspring ( Barlow 1995). Multiparent Advanced Generation Inter-Cross (MAGIC), MultiParental Populations, MPP Our study is the first to assess genetic parent-of-origin effects in rats, and confirm earlier findings in mice that such effects influence coping and impulsive behavior, and suggest these effects might be significant in other mammals, including humans. We observed parent-of-origin effects on F1 rat anxiety/coping-related behavior in the Elevated Zero Maze test. To confirm these findings on coping behavior, and to eliminate the possibility that the parent of origin effects are due to confounding with shared environment, we performed a reciprocal F1 cross between the behaviorally divergent RHA and RLA rat strains. Among the phenotypes with the most enhanced parent-of-origin heritability were 10 coping style behaviors, with average 3.2 fold heritability enrichment. Parent-of-origin-like heritability was on average 2.7fold larger than classical additive heritability.
We use this theory to investigate the effects on heritability of the parental origin of alleles in 798 outbred heterogeneous stock rats across 199 complex traits. We develop theory, based on earlier work, to partition heritability into a component due to a combination of parent of origin, maternal, paternal and shared environment, and another component that estimates classical additive genetic variance. In this study we investigate the effects of parent of origin on complex traits in the laboratory rat, with a focus on coping style behavior in stressful situations.
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