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Behavioural genetics

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For the journal, see Behavior Genetics (journal).

Behavioural genetics, also commonly referred to as behaviour genetics, is the field of study that examines the role of genetic and environmental influences on behaviour, with subspecialties focused on human behavioural genetics and animal behaviour genetics. Behavioural genetics is a field that uses genetic methodologies to understand the nature and origins of individual differences in behavior. Often associated with the "nature versus nurture" debate, behavioural genetics is highly interdisciplinary, involving contributions from biology, neuroscience, genetics, epigenetics, ethology, psychology, and statistics. Behavioural geneticists study the inheritance of behavioural traits. In humans, this information is often gathered through the use of genetic association studies or family studies including the twin study or adoption study. In animal studies, breeding, transgenesis, and gene knockout techniques are common. Psychiatric genetics, epigenetic research on behaviour, and genetic research in neuroscience are related subfields within behavioral genetics.

History

Galton in his later years

Sir Francis Galton, a nineteenth-century intellectual, is recognized as one of the first behavioural geneticists. Galton, a cousin of Charles Darwin, studied the heritability of human ability, focusing on mental characteristics as well as eminence among close relatives in the English upper-class. In 1869, Galton published his results in Hereditary Genius.[1] In his work, Galton "introduced multivariate analysis and paved the way towards modern Bayesian statistics" that are used throughout the sciences—launching what has been dubbed the "Statistical Enlightenment".[2] Galton is often credited as the pioneer of eugenics.

In 1951, Calvin S. Hall in his seminal book chapter on behavioural genetics introduced the term "psychogenetics",[3] which enjoyed some limited popularity in the 1960s and 1970s.[4][5] However, it eventually disappeared from usage in favour of "behaviour genetics".

Behaviour genetics, per se, gained recognition as a research discipline with the publication in 1960 of the textbook Behavior Genetics by John L. Fuller and William Robert (Bob) Thompson (then Chair of the Department of Psychology at Queen's University, Canada).[6] Nowadays, it is widely accepted that most behaviours in animals and humans are under some degree of genetic influence.[7]

Underscoring the role of evolution in behavioural genetics, Theodosius Dobzhansky was elected the first president of the Behavior Genetics Association in 1972; the BGA bestows the Dobzhansky Award on researchers for their outstanding contributions to the field. In the early 1970s, Lee Ehrman, a doctoral student of Dobzhansky, wrote seminal papers describing the relationship between genotype frequency and mating success in Drosophila,[8][9][10] lending impetus to the pursuit of genetic studies of behaviour in other animals. Studies on hygienic behaviour in honey bees were also carried out early in the history of the field.[11][12] The social behaviour of honey bees has also been studied and recent work has focussed on the gene involved in the foraging behaviour of Drosophila; this essentially allowed for deriving a relationship between gene expression and behaviour, where the gene regulating foraging behaviour in Drosophila also regulated social behaviour in bees.[13]

Methods

The primary goal of behavioural genetics is to establish causal relationships between genes, environment and behaviour. Traditionally, different methods were used in human and animal experiments. In animal research selection experiments have often been employed. For example, laboratory house mice have been bred for open-field behaviour,[14] thermoregulatory nesting,[15] and voluntary wheel-running behaviour.[16] A range of methods in these designs are covered on those pages.

Twin and family studies

Main article: Twin studies

In human behavioural genetics, early research designs used special variations on family designs (also known as pedigree designs), including twin studies and adoption studies. Quantitative genetic modeling of individuals with known genetic relationships (e.g., parent-child, dizygotic and monozygotic twins) allows one to estimate to what extent genes and environment contribute to phenotypic differences among individuals.

Measured genetic variants

The Human Genome Project has allowed scientists to directly measure the sequence of human DNA nucleotides. Once measured, genetic polymorphisms can be tested for association with a behavioral phenotype, such as psychiatric disorder, cognitive ability, etc.

Candidate genes

One popular approach has been to test for association candidate genes with behavioural phenotypes, where the candidate gene is selected based on some a priori theory about biological mechanisms involved in the genesis of a behavioural trait or phenotype. In general, such studies have proven difficult to broadly replicate[17] and there has been concern raised that the false positive rate in this type of research is high[18][19].

Genome-wide association studies

In genome-wide association studies, researchers test the relationship of millions of genetic polymorphisms with behavioural phenotypes across the genome. This approach to genetic association studies is largely atheoretical, and typically not guided by a particular biological hypothesis about phenotype etiology. Genetic association findings for behavioral traits and psychiatric disorders have been found to be highly polygenic (involving many small genetic effects).[20][21][22][23][24]

SNP heritability and co-heritability

Recently, researchers have begun to use similarity between classically unrelated people at their measured single nucleotide polymorphisms (SNPs) to estimate genetic variation or covariation that is tagged by SNPs[25][26]. To do this, researchers find the average genetic correlation across all SNPs between all individuals in a (typically large) sample, and use Haseman-Elston regression or restricted maximum likelihood to estimate the genetic variation that is tagged by SNPs. The proportion of phenotypic variation that is tagged by SNPs is called "SNP heritability." Intuitively, SNP heritability increases to the degree that phenotypic similarity is predicted by genetic similarity at measured SNPs, and is expected to be lower than the true narrow-sense heritability to the degree that measured SNPs fail to predict (typically rare) causal variants. The value of this method is that it is an independent way to estimate heritability that does not require the same assumptions as those in twin and family studies, and that it gives insight into the allelic frequency spectrum of the causal variants underlying trait variation.

Notable behavioural geneticists

Main category: Behavior geneticists

Notable behavioural geneticists include Dorret Boomsma, Thomas Bouchard, Wim Crusio (the founding editor of the journal Genes, Brain and Behavior), John DeFries, Theodosius Dobzhansky, Lindon Eaves, David Fulker, Irving Gottesman, John K. Hewitt, Jerry Hirsch, Kenneth Kendler, John C. Loehlin, Nick Martin, Matt McGue, Gerald McClearn, Robert Plomin, Theodore Reich (a pioneer in psychiatric genetics), Hans van Abeelen, and Steven G. Vandenberg (the founding editor of the journal Behavior Genetics).

Journals

Behavioural geneticists are active in a variety of scientific disciplines including biology, medicine, pharmacology, psychiatry, and psychology; thus, behavioural-genetic research is published in a variety of scientific journals, including Nature and Science. Journals that specifically publish research in behavioural genetics include Behavior Genetics, Molecular Psychiatry, Psychiatric Genetics, Twin Research and Human Genetics, Genes, Brain and Behavior, "Nature Genetics", and the Journal of Neurogenetics.

Societies

There exist several learned societies in the broader area of behavioural genetics:

See also

References

  1. ^ Hereditary Genius: An Inquiry into Its Laws and Consequences. London: MacMillan and Co. 1869.
  2. ^ Stigler SM (July 2010). "Darwin, Galton and the Statistical Enlightenment". Journal of the Royal Statistical Society, Series A. 173 (3): 469–482. doi:10.1111/j.1467-985X.2010.00643.x.
  3. ^ Hall CS (1951). "The genetics of behavior". In Stevens SS (ed.). Handbook of Experimental Psychology. New York: John Wiley and Sons. pp. 304–329.
  4. ^ Grigorenko EL; Ravich-Shcherbo I (1997). "Russian psychogenetics". In Grigorenko EL (ed.). Psychology of Russia: Past, Present, Future. Commack, NY: Nova Science. pp. 83–124.
  5. ^ Broadhurst PL (July 1969). "Psychogenetics of emotionality in the rat". Annals of the New York Academy of Sciences. 159 (3): 806–24. Bibcode:1969NYASA.159..806B. doi:10.1111/j.1749-6632.1969.tb12980.x. PMID 5260300.
  6. ^ Fuller JL; Thompson WR (1960). Behavior Genetics. New York: John Wiley and Sons.
  7. ^ Plomin, Robert (1989). "Behavioral Genetics". Journal of Nervous and Mental Disease. 177 (10): 645. doi:10.1097/00005053-198910000-00020.
  8. ^ Ehrman L (1966). "Mating success and genotype frequency in Drosophila". Animal Behaviour. 14 (2): 332–9. doi:10.1016/S0003-3472(66)80093-3. PMID 5956600.
  9. ^ Ehrman L (February 1970). "Simulation of the mating advantage in mating of rare Drosophila males". Science. 167 (3919): 905–6. Bibcode:1970Sci...167..905E. doi:10.1126/science.167.3919.905. PMID 5410860.
  10. ^ Ehrman L (February 1970). "The mating advantage of rare males in Drosophila". Proc. Natl. Acad. Sci. U.S.A. 65 (2): 345–8. Bibcode:1970PNAS...65..345E. doi:10.1073/pnas.65.2.345. PMC 282908. PMID 5263769.
  11. ^ Rothenbuhler WC (May 1964). "Behavior genetics of nest cleaning in honey bees. IV. Responses of F1 and backcross generations to disease-killed brood". Am. Zool. 4 (2): 111–123. doi:10.1093/icb/4.2.111. PMID 14172721.
  12. ^ Rothenbuhler WC (1958). "Genetics and breeding of the honey bee". Annual Review of Entomology. 3: 161–180. doi:10.1146/annurev.en.03.010158.001113.
  13. ^ Christians JK (June 2005). "Behavioural genetics". BioEssays. 27 (6): 664–666. doi:10.1002/bies.20247. PMID 15892115.
  14. ^ DeFries JC; Hegmann JP; Halcomb RA (1974). "Response to 20 generations of selection for open-field activity in mice". Behavior. 11 (4): 481–485. doi:10.1016/s0091-6773(74)90800-1.
  15. ^ Lynch CB (1980). "Response to divergent selection for nesting behavior in Mus musculus". Genetics. 96 (3): 757–765. PMC 1214374. PMID 7196362.
  16. ^ Swallow JG; Carter PA; Garland T, Jr. (1998). "Artificial selection for increased wheel-running behavior in house mice" (PDF). Behavior Genetics. 28 (3): 227–237. doi:10.1023/A:1021479331779. PMID 9670598.
  17. ^ Farrel MS, Werge T, Sklar P, Owen MJ, Ophoff RA, O'Donovan MC, Corvin A, Cichon S, Sullivan PF (2015). "Evaluating historical candidate genes for schizophrenia". Molecular Psychiatry. 20: 555–562. doi:10.1038/mp.2015.16.
  18. ^ Colhoun, Helen M; McKeigue, Paul M; Smith, George Davey (2003). "Problems of reporting genetic associations with complex outcomes". The Lancet. 361 (9360): 865–872. doi:10.1016/S0140-6736(03)12715-8. ISSN 0140-6736.
  19. ^ Duncan, Laramie E.; Keller, Matthew C. (2011). "A Critical Review of the First 10 Years of Candidate Gene-by-Environment Interaction Research in Psychiatry". American Journal of Psychiatry. 168 (10): 1041–1049. doi:10.1176/appi.ajp.2011.11020191. ISSN 0002-953X.
  20. ^ Visscher PM, Brown MA, McCarthy MI, Yang J (2012). "Five years of GWAS discovery". American Journal of Human Genetics. 90: 7–24. doi:10.1016/j.ajhg.2011.11.029.
  21. ^ Schizophrenia Working Group of the Psychiatric Genomics Consortium (2014). "Biological insights from 108 schizophrenia-associated genetic loci". Nature. 511: 421–427. doi:10.1038/nature13595.
  22. ^ Lee SH, DeCandia TR, Ripke S, Yang J, Schizophrenia Psychiatric Genome-Wide Association Study Consortium (PGC-SCZ), International Schizophrenia Consortium (ISC), Molecular Genetics of Schizophrenia Collaboration (MGS), Sullivan PF, Goddard ME, Keller MC, Visscher PM, Wray NR (2012). "Estimating the proportion of variation in susceptibility to schizophrenia captured by common SNPs". Nature Genetics. 44 (3): 247–250. doi:10.1038/ng.1108.
  23. ^ Sullivan PF, Daly MJ, ODonovan M (2012). "Genetic architectures of psychiatric disorders: the emerging picture and its implications". Nature Reviews Genetics. 13: 537–551. doi:10.1038/nrg3240.
  24. ^ Genetics of Personality Consortium (2015). "Meta-analysis of genome-wide association studies for neuroticism, and the polygenic association with major depressive disorder". JAMA Psychiatry. 72: 642–650. doi:10.1001/jamapsychiatry.2015.0554.
  25. ^ Yang, Jian; Benyamin, Beben; McEvoy, Brian P; Gordon, Scott; Henders, Anjali K; Nyholt, Dale R; Madden, Pamela A; Heath, Andrew C; Martin, Nicholas G; Montgomery, Grant W; Goddard, Michael E; Visscher, Peter M (2010). "Common SNPs explain a large proportion of the heritability for human height". Nature Genetics. 42 (7): 565–569. doi:10.1038/ng.608. ISSN 1061-4036.
  26. ^ Yang, Jian; Lee, S. Hong; Goddard, Michael E.; Visscher, Peter M. (2011). "GCTA: A Tool for Genome-wide Complex Trait Analysis". The American Journal of Human Genetics. 88 (1): 76–82. doi:10.1016/j.ajhg.2010.11.011. ISSN 0002-9297.

Further reading

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