Behavioral Genetics Sixth Edition Test Bank

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TEST BANKto accompanyRobert PlominJohn C. DeFriesValerie S. KnopikJenae M. NeiderhiserBEHAVIORAL GENETICSSixth EditionChristina HewittUniversity of Colorado BoulderWORTH PUBLISHERSTest Bankby Christina Hewittto accompany

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Robert Plomin,John C. Defries, Valerie S. Knopik and Jenae M. NeiderhiserBehavioral Genetics,Sixth Edition© 2013 by Worth PublishersAll rights reserved.The contents, or parts thereof, may be reproduced for use withBehavioral Genetics,Sixth Edition by Robert Plomin, John C. Defries, Valerie S. Knopik and Jenae M. Neiderhiser,but may not be reproduced in any form for any other purposes withoutprior written permission of the publisher.ISBN-10: 1-4641-4199-1ISBN-13: 978-1-4641-4199-7First PrintingWorth Publishers41 Madison AvenueNew York, NY 10010www.worthpublishers.comContentsCHAPTER 1OverviewCHAPTER 2Mendel’s Laws of HeredityCHAPTER 3Beyond Mendel’s LawsCHAPTER 4DNA: The Basis of HeredityCHAPTER 5Animal Models in Behavioral Genetics

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CHAPTER 6Nature, Nurture, and Human BehaviorCHAPTER 7Estimating Genetic and Environmental InfluencesCHAPTER 8The Interplay between Genes and EnvironmentCHAPTER 9Identifying GenesCHAPTER 10Pathways between Genes and BehaviorCHAPTER 11Cognitive DisabilitiesCHAPTER 12General Cognitive AbilityCHAPTER 13Specific Cognitive AbilitiesCHAPTER 14SchizophreniaCHAPTER 15Other Adult PsychopathologyCHAPTER 16Developmental PsychopathologyCHAPTER 17Personality And Personality DisordersCHAPTER 18Substance Use DisordersCHAPTER 19Health Psychology and AgingCHAPTER 20Evolution and BehaviorCHAPTER 21The Future of Behavioral Genetics

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CHAPTER1OverviewVOCABULARYMatch the phrases to the terms below. Each term may be used once, more than once, or not at all.Phrases1.)A self-replicating, DNA containing structure found in the nucleus of a cell2.)The basic unit of heredity3.)One of the variant forms of a gene4.)A test used to discover if a fetus carries a genetic abnormality5.)The complete DNA sequence of an individual6.)The molecule that encodes genetic information7.)The proportion of total variation in phenotype that is due to genetic variationTermsalleleamniocentesischromosomeclonecorrelationDNAfragile Xgenegenomeheritabilitymultivariate genetic analysisAns:1.)chromosome2.)gene3.)allele4.)amniocentesis5.)genome6.)DNA7.)heritabilityLevel:MTopic:OverviewPages:15 and GlossaryTRUE / FALSE1.One of the most important changes in the behavioral sciences in the past 30 years is the recognition that genesinfluence almost all behaviorsAns:TrueLevel:EPage:1Topic:Overview2.If genes influence a behavior, we would expect identical twins to be more similar for that behavior than

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non-identical (fraternal) twins.Ans:TrueLevel:MPage:1Topic:Overview3.Among the childhood psychopathologies, autism and ADHD are the most genetically influenced.Ans:TrueLevel:EPage:1Topic:Overview4.Antisocial behavior in adolescence is highly heritable.Ans:FalseLevel:MPage:1Topic:Overview5.Genes only influence disordered behavior.Ans:FalseLevel:EPage:1Topic:Overview6.Weight is almost as influenced by genes as height.Ans:TrueLevel:EPage:2Topic:Overview7.Personality and cognitive ability vary from person to person in large part due to genetic differences betweenpeople.Ans:TrueLevel:DPage:2Topic:Overview8.Many cases of early-onset Alzheimer disease are caused by single genes.Ans:TrueLevel:EPage:2Topic:Overview9.No cure for Alzheimer disease has been discovered, so it is worthless that single-gene causes for the diseasehave been identified.Ans:FalseLevel:DPage:2Topic:Overview10.Late-onset Alzheimer’s disease is not influenced by genetics.

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Ans:FalseLevel:MPage:2Topic:Overview11.It is possible to get a genetic test for a gene-variant that influences risk for late-onset Alzheimer disease.Ans:TrueLevel:DPage:2Topic:Overview12.Down syndrome is caused by a problem in a single gene.Ans:FalseLevel:MPage:2Topic:Overview13.Gene influence on cognitive ability decreasesover the course of a lifetime.Ans:FalseLevel:EPage:3Topic:Overview14.Cognitive ability in adulthood is not nearly as influenced by genes as is height.Ans:FalseLevel:MPage:3Topic:Overview15.The family environment is the most important cause of similarities in behavior among family members.Ans:FalseLevel:MPage:3Topic:Overview16.The environment is not an important cause of individual differences in behavior.Ans:FalseLevel:MPage:3Topic:OverviewPROBLEMS1.Parents who play chess with their children have children who do better in school. Does this mean that playingchess is an environmental cause for better academic achievement?Ans:Not necessarily. A correlation does not prove causation. It might be that parents and children who like toplay chess together do so because they share similar genetic constitutions and this constitution makes thechildren do better in school.Level:MTopic:overview

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Pages:3, 52.Explain the statement, “To some extent,people create their own experiences for genetic reasons.”Ans:Since many environmental measures used in behavioral sciences show genetic influences, it is likely thatthese environmental outcomes (like parenting, childhood accidents, life events, social activities, etc.) comeabout in part because of the genetic constitution of the person, acting through characteristics like personalityand cognitive style.Level:DTopic:overviewPages:3, 5

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CHAPTER 2Mendel’s Laws of HeredityVOCABULARYMatch the phrases to the terms below. Each term may be used once, more than once, or not at all.Phrases1.)An alternative form of a gene at a locus2.)Describes an allele that needs two copies to bepresent to produce its phenotype3.)An example of a disorder caused by a dominant allele4.)Describes an allele that produces a particular phenotype even when only one copy is present5.)The genetic constitution of an individual, or the combination of alleles at a particular locus6.)An example of a disorder caused by a recessive allele7.)Cell division during which crossing-over occurs8.)Type of cell division that occurs in ovaries and testes, producing gametes9.)A basic unit of inheritance, found on a chromosome10.)Said to be present for genes close together on a chromosomeTermsalleleamino acidchromatidchromosomedominantgametegenegenotypeHuntington diseaselinkagelocusmeiosispedigreephenotypephenylalaninephenylketonuria (PKU)proteinrecessiverecombinationAns:1.)allele2.)recessive3.)Huntington disease4.)dominant5.)genotype6.)phenylketonuria7.)meiosis8.)meiosis9.)gene10.)linkageLevel:ETopic:Mendel’s Laws of Inheritance

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Pages:619PROBLEMS1.The albino phenotype is an inherited trait that has behavioral consequences in mice. In the offspring of twocarrier mice, the Mendelian phenotypic ratio of 3 normal to 1 albino is observed. How many genes does thissuggest albinism is controlled by?Ans:oneLevel:MTopic:Mendel’s First Law of HeredityPages:8102.The behavioralWaltzer phenotypein mice is characterized by head shaking, rapid circling, and irritability(van Abeelen and van der Kroon, 1967). True-breeding mice are mice that have two similar alleles at theWaltzer locus.True-breeding Waltzer males and females, when mated, produce offspring all with the Waltzer phenotype.True-breeding Waltzer females and non-Waltzer males produce all normal offspring. Second generation (F2)results from mating the offspring from a cross between true-breeding Waltzer and non-Waltzer mice areshown below:Normal (non-Waltzer) mice124Waltzer mice48TOTAL172a. Do you think the allele for theWaltzer phenotype is dominant or recessive?Ans:recessiveLevel:ETopic:Mendel’s First Law of HeredityPages:710b. Give your reason why.Ans:Waltzer mice crossed with normal mice produce all normal offspring, and it looks like the ratio ofphenotypes in crosses between these offspring (i.e., F2 mice) give normal to Waltzer in the ratio 3:1, asexpected from Mendel’s First Law.Level:ETopic:Mendel’s First Law of HeredityPages:10c. Perform a chi-square test to determine if the results given above are consistent with your hypothesis.Ans:Hypothesis: If Waltzer is caused by a recessive allele, expect 3:1 normal to Waltzer in F2 generation.Chi-square formula2=(obsexp)2/expTestObsExpO-E(O-E)2(O-E)2/E1241295250.19448435250.581= 0.775 =21df~32% probabilityConclusion: Retain hypothesis; the probability of getting such observed numbers is high.

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Level:DTopic:Mendel’s First Law of HeredityPages:893.The figure below shows a small portion of aHuntington disease pedigree:a. Using H as the symbol for the Huntington allele and h as the normal allele, give the genotypes at theHuntington locus for each of the four children (A,B,C,D)Ans:A = Hh B = hh C = hh D = HhLevel:MTopic:Huntington diseasePages:1011b. If child B marries an affected man, what is the probability that their first child would develop Huntingtondisease?Ans:0.5 (or 50%)Level:MTopic:Huntington diseasePages:1011c. If their first child is unaffected, what isthe probability that their second child is affected?Ans:0.5 (or 50%)Level:MTopic:Huntington diseasePages:1011d. If child A marries an unaffected woman and has two children, what is the probability thatbothchildren areunaffected?Ans:0.5×0.5 = 0.25Level:DTopic:Huntington diseasePages:10114. The figure below shows part of a PKU pedigree:a. Using K as the symbol for the normal allele and k as the symbol for the PKU allele, give the possiblegenotypes of the unaffected children (A,B,C).Ans:A = KK or Kk B = KK or Kk C= KK or KkLevel:MTopic:Phenylketonuria (PKU)Pages:1112b. Given that child A is anunaffectedbrother of a PKU child, what is the probability that he is a PKU carrier?Ans:0.66 (or 2/3)Level:M

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Topic:Phenylketonuria (PKU)Pages:1112c. Assume A is a carrier. What genotype would his mate have to be for a child of the couple to be at risk forPKU?Ans:Kk (or kk, but this is less likely)Level:ETopic:Phenylketonuria (PKU)Pages:1112d. What are A’s chances (assuming he is a carrier) of marrying and producing children who arenotat risk forhaving PKU? (see Box 2.2, page 13 of text)Ans:A cannot marry Kk or kk; mate has to be KKFrequency of Kk = 2%Frequency of kk = 1/10000So, frequency of KK = 1(0.2+ 0.00001) = 0.97999 around 98%Level:DTopic:Phenylketonuria (PKU)Pages:12135.A mouse geneticist discovers two recessive alleles, each of which causes the mice to be deaf when two copiesare present.a. How could the geneticist determine whether the alleles occur at the same locus (i.e., are alleles of the samegene)?Ans:Cross mice with two copies of one allele with mice having two copies of the other allele. If offspring aredeaf, then the alleles are at the same locus. If none of the mice are deaf, then the alleles are at separate loci.Level:DTopic:Mendel’s Second Law of HeredityPages:1417b. If it is discovered that the alleles are at different loci, how could the geneticist discover if they were locatedtogether on the same chromosome?Ans:Do a test for linkage: Cross second-generation offspring (F2) from the mating of mice with both types ofdeafness and look for a departure from the expected ratio of 9:3:3:1. A lack of recombinants would indicatelinkage.Level:DTopic:Mendel’s Second Law of HeredityPages:1417

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CHAPTER 3Beyond Mendel’s LawsVOCABULARYMatch the phrases to the terms below. Each term may be used once, more than once, or not at all.Phrases1.)Chromosomes that differ for males and females2.)Describes genes on a sex chromosome3.)Recessive alleles of this type produce disorders more common in males4.)Describes a female that has an X-linked recessive allele for a disorder5.)Having three copies of a chromosome instead of the usual two6.)Process that produces incorrect numbers of chromosomes in cells7.)Type of mutation caused by repeated three-nucleotide units8.)Describes the situation where a disorder gets more severe as it is passed down generations9.)Fragile X is caused by this type of mutation10.)Describes a trait influenced by many genesTermsautosomescarriercorrelationfirst-degree relativegenetic anticipationgenomic imprintingliability-threshold modelmethylationmonosomymRNAnondisjunctionnucleotidepolygenicpermutationprobandqualitative traitsecond-degree relativesex chromosomestranscriptiontranslationtriplet repeattrisomyX-linkedAns:

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1.)sex chromosomes2.)X-linked3.)X-linked4.)carrier5.)trisomy6.)nondisjunction7.)tripletrepeat8.)genetic anticipation9.)triplet repeat10.)polygenicLevel:ETopic:Beyond Mendel’s LawsPages:2038PROBLEMS1.Red-green color blindness is an X-linked recessive trait in humans. In four different families, the parents havechildren together. For each of the families (A,B,C,D) shown in the table below, give a possible combination ofgenotypes for the parents that could have resulted in the combinations of children found in each family. (UseXCto indicate the color-blind allele and X to indicate the normal allele.)Possible genotype:FamilyChildren PhenotypeMOMDADA2 males normal2 females normalB2 females color-blind3 females normal2 males color-blindC4 males color-blind4 females normalD2 femalescolor-blind2 males normalAns:There may be several possible answers for the genotypes of the parents, but given that the normal alleleis more common than the color-blindness allele, the following are the most likely genotypes:Family A XX and XY; Family B XCX and XC;Y; Family C XCX and XY;Family D XCX and XCYLevel:MTopic:X-linked inheritancePages:20232.Draw a pedigree for Family B from the question above. Label the genotypes under the symbols for eachperson.Ans:Level:MTopic:X-linked inheritancePages:2023

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3.Down syndrome is caused by the presence of an extra copy of chromosome 21 and is also known as Trisomy21.a. Name the process that occurs in gamete formation to produce an abnormal number of chromosomes.b. Name a prenatal test that a woman might need inorder to detect the presence of genetic abnormalities.c. Why is Down syndrome generally non-familial?d. Why is it that mothers who are older than 40 have an increased risk of having a child with Down syndrome?Ans:a.non-disjunctionb.amniocentesis, chorionic villi samplingc.Non-disjunction is a spontaneous chromosome mutation, and people with Down syndrome generally do notreproduce, hence all occurrences are newly arisen.d.The completion of cell division in females only takes place on ovulation (not continuously as in males) afterpuberty, and the activation of immature eggs after many years gives rise to imperfect separation ofchromosomes.Level:MTopic:Chromosome mutationsPages:23254.Huntington disease and fragile X syndrome are caused by a section of DNA that is repeated many times.a. Explain how this type of mutation can give rise toi. genetic anticipationii. premutationb. What are the consequences of genetic anticipation and premutation in the families of those with Huntingtondisease and fragile X?Ans:a. i.The expanded repeat section of DNA is unstable and may increase between each generation, resulting inmore severe cases in later generations. This phenomenon is known as genetic anticipation.ii.A lower number of repeats than necessary to produce the disorder is recognized in relatives of those withthe disorder. This intermediate number of repeats between normal and full expansion is known as apremutation.b.For Huntington disease, genetic anticipation results in the appearance of HD at an earlier age and greaterseverity as it is passed on. For fragile X, the symptoms become more severe as it is passed on. Premutationcarriers for both disorders are at greater than average risk of producing a child with the disorder.Level:DTopic:Expanded triplet repeatsPages:25265.a. Look at the figures taken from the text, and explain how they show there is evidence that both schizophreniaand general cognitive ability are influenced by genes.

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Figure 3.6 Risk for schizophrenia and genetic relatednessFigure 3.7 Resemblance for general cognitive ability and genetic relatednessb. Both correlations and morbidity risk estimates are measures that show familiality. Correlations aregenerally more accurate measures of similarity between relatives. Why is it that correlations are given betweenrelatives for general cognitive ability but not for schizophrenia?c. Continuous variation for a trait can be produced by many genes, each obeying Mendelian laws, and many ofthe alleles are recognized to act in an “additive” manner. Explain what “additive” means in this context.Ans:a.Figure 3.6 shows the risk for schizophrenia increases the more genetically related someone is to a personwho has the disorder, and allrelatives have an increased risk compared to population prevalence. Figure 3.7
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