All association analyses, at the level of individual SNPs or gene loci, were performed under different assumed modes of inheritance of effect – dominant, recessive or codominant – associated with alleles.
Furthermore, theoretical work has established that imperfect diagnostics and incomplete or variable exposure produce a downward bias in estimates of heritability and of SNP (single nucleotide polymorphism) effects, and affect inferences about modes of inheritance of SNP effects for disease resistance [ 1, 5].
Data on the inheritance-of-stress effect have been accumulating and some mechanistic insights, such as epigenetic regulation, have also been suggested.
In this respect, the narrowness of this shelf cannot be accounted for by the inheritance of shearing effects.
This model does not preclude the possibility of polygenic inheritance of combined effects of multiple low penetrance susceptibility alleles segregating dominantly.
It is therefore not unlikely that the observed mode consists of polygenic inheritance of combined effects of multiple low penetrance susceptibility alleles segregating dominantly.
We used two logistic regression models to specifically test for dominant versus recessive inheritance of the effects of the T allele.
Although early studies showed transgenerational inheritance of EDC effects elicited by high doses of single chemicals, more recent studies showed that high doses of a variety of chemicals (fungicides, pesticide mixture, plastic mixture, dioxin, and a hydrocarbon mixture) could also elicit transgenerational effects (Manikkam et al. 2012; Nilsson et al. 2012).
We selected Drosophila to search for evidence of transgenerational epigenetic inheritance of environmental effect following exposure of adult males.
This review summarizes the current data on the inheritance of stress effect and possible mechanisms involved in this process.
