The science of genetics is undergoing a paradigm shift. Recent discoveries, including the activity of retrotransposons, the extent of copy number variations, somatic and chromosomal mosaicism, and the nature of the epigenome as a regulator of DNA expressivity, are challenging a series of dogmas concerning the nature of the genome and the relationship between genotype and phenotype. According to three widely held dogmas, DNA is the unchanging template of heredity, is identical in all the cells and tissues of the body, (...) and is the sole agent of inheritance. Rather than being an unchanging template, DNA appears subject to a good deal of environmentally induced change. Instead of identical DNA in all the cells of the body, somatic mosaicism appears to be the normal human condition. And DNA can no longer be considered the sole agent of inheritance. We now know that the epigenome, which regulates gene expressivity, can be inherited via the germline. These developments are particularly significant for behavior genetics for at least three reasons: First, epigenetic regulation, DNA variability, and somatic mosaicism appear to be particularly prevalent in the human brain and probably are involved in much of human behavior; second, they have important implications for the validity of heritability and gene association studies, the methodologies that largely define the discipline of behavior genetics; and third, they appear to play a critical role in development during the perinatal period and, in particular, in enabling phenotypic plasticity in offspring. I examine one of the central claims to emerge from the use of heritability studies in the behavioral sciences, the principle of minimal shared maternal effects, in light of the growing awareness that the maternal perinatal environment is a critical venue for the exercise of adaptive phenotypic plasticity. This consideration has important implications for both developmental and evolutionary biology. (shrink)

In discussing the relationship between genetically influenced differences and educational attainment (EA), Burt employs the concept of downward causation. I note the similarities between Burt's concept of downward causation and the sociogenomics concept of vertical pleiotropy and argue that her discussion of downward causation introduces an unnecessary normative component. The core problem concerns not the appropriateness of phenotypes that influence EA but mistaken assumptions about which phenotypes are being predicted.

My response is divided into four sections: (1) is devoted to a potpourri of commentaries that are essentially in agreement with the substance of my target article (with one exception); in (2) I address, in response to one of the commentaries, several issues relating to the use of candidate gene association studies in behavior genetics (in particular those proposing a specific G×E interaction); in (3) I provide a detailed response to several defenses of the twin study methodology; and in (4) (...) I conclude with several reflections on that methodology and the conception of human nature it has fostered. (shrink)