This is the web page for a course in Behavior Genetics offered through the Psychology Department at the University of Missouri--Columbia. During the semester I (Mike Miller) will add to the information given below. I will make an announcement in class and/or by e-mail if anything critically important is added.
Printing Issues: Some of the handouts are in large .gif
files that are a little large for the browser window and often do not print
well from a web browser. You can handle these by downloading the
.gif files (using File-Save As) and printing it out from an image viewer
like ACDsee which
is freely available for download.
Week 1, Class 1 (Tuesday, 8/22). I explained what I mean
by "Behavior Genetics" (BG for short). Our book suggests that BG
stands alone at the intersection of biological sciences and behavioral
sciences. I would add that neuroscience is a part of that intersection.
We can be sure that BG forms the intersection of psychology and genetics.
I gave an example of how observations of familial aggregation in schizophrenia
have led to research implicating genetic influences on this mental disorder.
I then talked about the different fields of genetics and how they relate
to behavior genetics. Here is a
handout that I also used as an overhead for the discussion of subdisciplines
of genetics.
Week 1, Class 2 (Thursday, 8/24). We began coverage of basic Mendelian genetics and we looked at several examples of genetic diseases and how they are transmitted. We took a look at Mendel's original experiments and his original paper (translated into English). We discussed the implications of Mendel's findings for the distribution of a trait in a population--a recessive disease doesn't occur in 1/4 of the members of a population. The distribution depends on gene frequency. We discussed the Hardy-Weinberg law which shows the relation of gene frequencies to genotype frequencies when mating occurs at random with respect to a gene. We then applied the Hardy-Weinberg equations to figure out how often people carry the gene for cystic fibrosis (a recessive Mendelian disorder) given the rate at which people are affected (about 1 in 1600).
Week 2, Class 3 (Tuesday, 8/29). We talked first about Mendel's laws. The first law was discussed in the previous class--heterozygous parents (hybrids) are equally likely to transmit either of their two genes (A or a). Mendel's second law, that segregation of one gene pair is independent of segregation of every other gene pair (also called "independent assortment"), was a mistake! Mendel happened to study traits in peas that showed independent assortment--like wrinkled and yellow characteristics of seeds--but many traits do not show independent assortment. This is because when genes are near each other on the same chromosomes they tend to stick together when gametes are formed. We discussed achondroplasia (a type of dwarfism) very briefly--it is autosomal and dominant, but parents are often unaffected, and it is found in 2/3 of the offspring of two affected parents (instead of the usual 3/4), but why?? We then started watching a Nova documentary (PBS, 1989) about Huntington's Disease and the search for the single gene that causes it. We'll continue with this video on Thursday.
Week 2, Class 4 (Thursday, 8/31). We looked at rules for pedigree drawing. I relied on a paper by Bennett et al. (1995, American Journal of Human Genetics). The figures from Bennet et al.'s paper are here: Figure 1, Figure 2, Figure 3, Figure 4, Figure 5, Figure A1. (Try downloading ACDsee to view and print these figures, and any other figures that don't print to a single page from your web browser.) The first five figures show rules for how pedigrees should be drawn, the last figure (Figure 1A) shows a pedigree that should be thought of as an April-Fool's joke--it uses every possible type of symbol--but it also illustrates how all the symbols are used. Then we took a look at a pedigree diagram of an extended family where many members were affected with Nail-patella Syndrome (diagram taken from Suzuki et al., 1989, An introduction to genetic analysis, 4th Edition, page 115). Is it a dominant or a recessive condition? The same diagram showed the ABO blood group genotypes (alleles IA, IB and i) for all of the family members. Did the ABO genes seem to go along with the disease at all? That is, were ABO genes and the Nail-patella disease gene cotransmitted? Were they assorting dependently in contrast to Mendel's (often false) second law? If so, what does that mean? We then watched the rest of the PBS Nova video on Huntington's Disease. The video showed how Jim Gusella was able to determine the location of the Huntington's gene by showing cotransmission of a genetic marker with the disease gene. Gusella and colleagues reported their finding that the Huntington's gene was on chromosome 4 in the journal Nature in November 1983. If you're interested, the whole history of this gene-hunting research is catalogued here. The gene wasn't identified until 1993 when a large team of scientists reported their findings in Cell. The video tape also taught us about how different people respond in very different ways to the challenge of having a parent with Huntington's disease. Most people in that situation have not wanted genetic testing to see if they have the gene. The video showed genetics counseling of a woman whose parent had Huntington's disease. Genetics counselors can offer emotional support, but their main role is to provide information about genetic diseases, genetic testing, and assessment of risk. They must be able to explain complex ideas to everyday people who have limited knowledge of genetics and probability.
Week 3, Class 5 (Tuesday, 9/5). I went over the use of karyotyping in clinical genetics. We looked at a normal human karyotype (picture of chromosomes from a single cell). We discussed the sex chromosomes and how they determine whether we are male or female. Sex chromosome aneuploidies (abnormal numbers of sex chromosomes) were discussed briefly. We learned that the presence of the Y chromosome makes a person male--having more X chromosomes causes Klinefelter's syndrome when the Y chromosome is present but doesn't cause the person to be female. We also talked about imprinting and anticipation in Huntington's disease. In imprinting, the effect of a gene is different when it is inherited from the father than when it is inherited from the mother. In Huntington's disease (HD) it was always known that inheriting the HD gene from the father caused an earlier age of onset in the affected offspring. This is an imprinting effect. It was also known that in successive generations of a family, onset of HD symptoms appeared at a progressively earlier age. This is an anticipation effect. We learned that a single discovery back in 1993-1994 solved they mystery of both of these effects for HD. The gene that causes HD has a triplet repeat (CAG) in it. The longer the repeat sequence, the earlier the age of onset of disease symptoms. The length of the repeat sequence tends to increase in successive generations (causing the anticipation effect) and it increases more when transmitted from an affected father than when transmitted from an affected mother (causing the imprinting effect). Amazing stuff! So for HD, it is mutation of the gene sequence that causes the imprinting and anticipation effects.
Week 3, Class 6 (Thursday, 9/7). We formed groups of two students per group and used coin tosses to simulate sampling of parents alleles at five loci from a population in Hardy-Weinberg equilibrium (and in linkage equilibrium). We then used the coins again to simulate Mendelian segregation at the five loci (on different chromosomes so that they segregated independently) to produce genotypes for two offspring. We then applied an additive-genetic model where every "upper case allele" (a head in the coin toss) was worth a point and every "lower case allele" (a tail in the coin toss) was worth zero points. In the additive model, we simply add up the number of upper case alleles. For example, the genotype AaBBCcDDEe would have a phenotype score of seven because seven of the alleles were upper case. We call the upper case alleles increasing alleles because they increase the phenotype score. This model is totally genetically deterministic. We observed that the parents are uncorrelated (and independent) in their scores, but the siblings had a correlation of 0.5. Why are parents uncorrelated, but their children are correlated?
Week 4, Class 7 (Tuesday, 9/12). Started on the basics of molecular genetics. Watched an old PBS Nova show called Decoding the Book of Life.
Week 4, Class 8 (Thursday, 9/14).
Week 5, Class 9 (Tuesday, 9/19).
Week 5, Class 10 (Thursday, 9/21). Exam #1 to be given on this date.
Week 6, Class 12 (Tuesday, 9/26). Went over the exam. Then we got into a discussion of conceptual issues in the "Nature-Nurture Debate". We discussed behaviorism, radical environmentalism, radical hereditarianism, self-control and agency and free will. We went over the basic philosophical ideas of Pavlov, Watson and Skinner--three different approaches to 'behaviorism'. We then went on to discuss "genetic determinism"--the notion that our genes, not our minds or our environments, determine our behavior. Some radical hereditarians and eugenecists seemed to hold to this view. We discussed the radical environmentalism of Trofim Lysenko and the effects of "Lysenkoism" in Stalinist Russia. We then discussed some "genetic diseases" and the effects of environment on those diseases--phenylketonuria, favism, and acrodermatitis enteropathica. We then discussed the notion of "heritability" and what we mean by that term.
Week 6, Class 13 (Thursday, 9/28).
Week 7, Class 14 (Tuesday, 10/3).
Week 7, Class 15 (Thursday, 10/5).
Week 8, Class 16 (Tuesday, 10/10).
Week 8, Class 17 (Thursday, 10/12).
Week 9, Class 18 (Tuesday, 10/17).
Week 9, Class 19 (Thursday, 10/19).
Week 10, Class 20 (Tuesday, 10/24).
Week 10, Class 21 (Thursday, 10/26). Exam #2 to be given on this date.
Week 11, Class 22 (Tuesday, 10/31).
Week 11, Class 23 (Thursday, 11/2).
Week 12, Class 24 (Tuesday, 11/7).
Week 12, Class 25 (Thursday, 11/9).
Week 13, Class 26 (Tuesday, 11/14).
Week 13, Class 27 (Thursday, 11/16).
Week 15, Class 28 (Tuesday, 11/28).
Week 15, Class 29 (Thursday, 11/30).
Week 16, Class 30 (Tuesday, 12/5).
Week 16, Class 2 (Thursday, 12/7). The term paper is due
on this date.
