GENEWATCH
 
IN OUR DNA?
By Stuart Newman
 

Behaviors are innate or environmentally induced novel or habitual actions by humans or other organisms that, at a minimum, involve interactions between the nervous system and other organs. A gene specifies the sequence of subunits of a single RNA or protein molecule. How is it possible for specific behaviors to be associated with particular genes? Can anything significant be learned from such associations?

One persistent view, increasingly discredited in recent years, is that genes collectively provide a blueprint or software program for the generation of all organismal characters—anatomical structures, but also behaviors—and variant genes are lines of code of alternative programs. So, for example, two recent reports in the journal Nature Genetics described evidence that variations within any of 11 DNA regions in the human genome have a strong association with schizophrenia, bipolar disorder, or both.1 One of the studies’ authors was quoted as stating, “Our findings are a significant advance in our knowledge of the underlying causes of psychosis—especially in relation to the development and function of the brain.”2

The expectation that such genetic associations will provide insight into how the brain generates normal or abnormal behaviors is directly connected to belief in the notion of a genetic program. No one would assert that learning the chemical composition of a piece of tile from a medieval mosaic represents a significant advance in understanding the meaning of the art work. But when it comes to living organisms which operate individually and socially on multiple spatial and temporal scales and have assumed their present forms and behavior patterns over billions of years, genetically reductionist explanations can unfortunately still be advanced without evoking derision.

The acceptance of this bizarre way of thinking, which is even more prevalent in the scientific and medical professions than in lay society, derives from a particular theory of evolution that has prevailed over the past century. Referred to as the Modern Synthesis, it links Darwin’s idea of natural selection as the generator of all inherited traits to the notion that genes and their variants are the only significant determinants passed from one generation to the next. All standard features of an organism, e.g., the five fingers of the human hand or the propensity of humans to live in social groups, are consequently considered adaptations. By this argument, pathological behaviors that are endemic to many societies, like racism and rape, are likely to be adaptations as well (or sometimes negative but understandable misappropriation of adaptive behaviors).3,4 And now that a “genetic basis” is claimed to have been discerned for psychosis, it is all but certain that some evolutionary psychologist is laboring to uncover its benefits on the prehistoric savannah.

Fortunately, a new concept of evolution is now taking hold. In various subdisciplines like “evolutionary developmental biology”5 and “ecological developmental biology”6 there is increasing receptivity to the idea of a loose, nonprogrammatic relation between the phenotype (particularly the behavioral phenotype) and the genotype. This includes an openness to the notion that the external environment may influence the development of inherently plastic living systems,7 not in arbitrary ways, but in ways constrained by the forming systems’ inherent modes of action.8

The “Baldwin effect,” the name given to a concept put forward by the psychologist J. Mark Baldwin in the Post-Darwinian period of intellectual ferment before the Modern Synthesis consolidated its grip, in a paper titled “A New Factor in Evolution,”9 has gained renewed prominence. This is a “phenotype first” scenario in which a character or trait change occurring in an organism as a result of its interaction with its environment becomes assimilated (often by Darwinian selection) into its developmental repertoire. The descendent organisms are then born with the novel phenotype rather than having to acquire it each generation.

In this emerging theoretical framework not every persistent phenotype is an adaptation, organisms with novel anatomies or behaviors need not sink or swim in pre-existing niches but can construct new ways of life compatible with their new biology,10 and genes often play catch-up, consolidating behavioral or other phenotypic changes after the fact.11 This has permitted conceptual accommodation of older, puzzling findings and has energized previously proscribed research programs.

Genetics, since it deals with an intrinsic set of determinants of all living systems, is far from being sidelined in the new approach, but genes must now take their place alongside other key factors. A set of studies in Siberia, beginning in the 1950s, on farmed foxes, for example, showed that docile, human-friendly behavior could be propagated from parent to offspring, along with a suite of morphological attributes (shortened snouts, floppy ears, patchy coat color) seen in other, unrelated, independently domesticated animals, by a selective breeding protocol that acted not on gene frequency but on the level of stress hormones in the gestational environment.12 A more recent study demonstrated the passing on of grooming behavior from mother to daughter mice by the effects on the offspring’s biology of the behavior itself.13 In both studies an effect on DNA was one of the steps in trait transmission, but the DNA was not irreversibly changed, nor was it the first or unique event in the behavior modification.

Sexual dimorphism is one of the best known examples of the above-mentioned plasticity, and of the fact that an animal embryo can potentially follow alternative routes of development. In humans, this decision, with both anatomical and behavioral consequences, is specified by genes. Males differ from females by having an entire chromosome, the Y, with a set of genes which are absent in the female genome; with two X chromosomes a biological female takes form. Only one of these male-specific genes, SRY, is needed for development of a male body and male gender identity, however.14 If, as in XX male (de la Chapelle) syndrome, SRY winds up on the X chromosomes and no Y is present, the resulting anatomical and behavioral characteristics are still typically within the standard male range.

From the above it would seem that SRY is the gene for maleness. Indeed, its production sets the male developmental pathway in motion in most mammals, including marsupials. But some rodents, such as spiny rats, just use extra copies of the CBX2 gene, which is also present in females, to perform the same function15 So maleness can be generated without a specific gene for it, perhaps just needing more of some gene. But even this notion is refuted if we cast our zoological comparisons a little wider. In some birds and fish, and in many reptiles, particularly turtles, sex determination is controlled by the egg incubation temperature. That is, with respect to prospective sexual phenotype the genotype of the embryo is a matter of indifference. If it develops at a low temperature it will become a male, and if at a high temperature, a female. (Or vice versa, for some turtle species; or, in the case of other turtle species, female if high or low and male in between.)16

So for behaviors, reproductive and otherwise, and even for characters as deeply dimorphic as sexual anatomy, specific genes make a difference, or other genes make the same difference, or the difference is made by the social or physical environment acting on the organism during development—including, of course, the expression of many of its other genes. This reality consigns to the realm of tea-leaf reading any notion that we can infer the underlying cause of a behavior solely from its correlation to some gene variants.

 

Stuart A. Newman, PhD, is Professor of Cell Biology and Anatomy at New York Medical College. He was a founding member of the Council for Responsible Genetics.


Endnotes

1. Ripke, S., Sanders, A. R., Kendler, K. S., Levinson, D. F., Sklar, P., Holmans, P. A., Lin, D. Y. et al., 2011. Genome-wide association study identifies five new schizophrenia loci. Nat Genet. 43, 969-76; Sklar, P., Ripke, S., Scott, L. J., Andreassen, O. A., Cichon, S., Craddock, N., Edenberg, H. J., Nurnberger, J. I. et al. 2011. Large-scale genome-wide association analysis of bipolar disorder identifies a new susceptibility locus near ODZ4. Nat Genet. 43, 977-83.

2. http://www.healthcanal.com/genetics-birth-defects/22589-Researchers-most-powerful-genetic-studies-psychosis-date.html

3. Sidanius, J., Pratto, F., 1999. Social dominance: an intergroup theory of social hierarchy and oppression. Cambridge University Press, Cambridge, UK ; New York.

4. Thornhill, R., Palmer, C., 2000. A natural history of rape: biological bases of sexual coercion. MIT Press, Cambridge, Mass

5. Müller, G. B., 2007. Evo-devo: extending the evolutionary synthesis. Nat Rev Genet. 8, 943-9.

6. Gilbert, S. F., Epel, D., 2009. Ecological developmental biology: integrating epigenetics, medicine, and evolution. Sinauer, Sunderland, Mass., U.S.A.

7. West-Eberhard, M. J., 2003. Developmental plasticity and evolution. Oxford University Press, Oxford; New York.

8. Newman, S. A., Bhat, R., 2009. Dynamical patterning modules: a “pattern language” for development and evolution of multicellular form. Int J Dev Biol. 53, 693-705.

9. Baldwin, J. M., 1896. A new factor in evolution. The American Naturalist. 30, 441-451, 536-553.

10. Odling-Smee, F. J., Laland, K. N., Feldman, M. W., 2003. Niche construction: the neglected process in evolution. Princeton University Press, Princeton, N.J.

11. Palmer, A. R., 2004. Symmetry breaking and the evolution of development. Science. 306, 828-33.

12. Trut, L., Oskina, I., Kharlamova, A., 2009. Animal evolution during domestication: the domesticated fox as a model. Bioessays. 31, 349-60.

13. Weaver, I. C., Cervoni, N., Champagne, F. A., D’Alessio, A. C., Sharma, S., Seckl, J. R., Dymov, S., Szyf, M., Meaney, M. J., 2004. Epigenetic programming by maternal behavior. Nat Neurosci. 7, 847-54. 

14. Kashimada, K., Koopman, P., 2011. Sry: the master switch in mammalian sex determination. Development. 137, 3921-30.

15. Kuroiwa, A., Handa, S., Nishiyama, C., Chiba, E., Yamada, F., Abe, S., Matsuda, Y., 2011. Additional copies of CBX2 in the genomes of males of mammals lacking SRY, the Amami spiny rat (Tokudaia osimensis) and the Tokunoshima spiny rat (Tokudaia tokunoshimensis). Chromosome Res. 19, 635-44.

16. Graves, J. A. M., 2008. Weird animal genomes and the evolution of vertebrate sex and sex chromosomes. Ann rev genetics. 42, 565-86.


 
 
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