1. Figure 13.2 Two families

2. Figure 13.x1 SEM of sea urchin sperm fertilizing egg

3. Figure 13.x4 Human male chromosomes shown by bright field G-banding

4. Fig. 9-2a

5. Figure 14.x1 Sweet pea flowers

6. Figure 14.1 A genetic cross

7. Fig. 9-2b Petal Stamen Carpel

8. Fig. 9-2c-1 Transferred pollen from stamens of white flower to carpel of purple flower Stamens Carpel Parents (P) Purple 2 White Removed stamens from purple flower 1

9. Fig. 9-2c-2 Transferred pollen from stamens of white flower to carpel of purple flower Stamens Carpel Parents (P) Purple 2 White Removed stamens from purple flower 1 Pollinated carpel matured into pod 3

10. Fig. 9-2c-3 Transferred pollen from stamens of white flower to carpel of purple flower Stamens Carpel Parents (P) Purple 2 White Removed stamens from purple flower 1 Pollinated carpel matured into pod 3 Offspring (F 1 ) Planted seeds from pod 4

11. Fig. 9-2d Flower color White Axial Purple Flower positionTerminal Yellow Seed color Green Round Seed shapeWrinkled Inflated Pod shape Constricted Green Pod colorYellow Tall Stem lengthDwarf

12. Fig. 9-3a-1 P generation (true-breeding parents) Purple flowers White flowers

13. Fig. 9-3a-2 P generation (true-breeding parents) Purple flowers White flowers F 1 generation All plants have purple flowers

14. Fig. 9-3a-3 P generation (true-breeding parents) Purple flowers White flowers F 1 generation All plants have purple flowers F 2 generation Fertilization among F 1 plants (F 1  F 1 ) of plants have purple flowers 3–43–4 of plants have white flowers 1–41–4

15. Fig. 9-3b P plants 1–21–2 1–21–2 Genotypic ratio 1 PP : 2 Pp : 1 pp Phenotypic ratio 3 purple : 1 white F 1 plants (hybrids) Gametes Genetic makeup (alleles) All All Pp Sperm Eggs PP p ppPp P p P p P P p PP pp All Gametes F 2 plants

17. Fig. 9-4 Gene loci Homozygous for the dominant allele Dominant allele Homozygous for the recessive allele Heterozygous Recessive allele Genotype: P B a P PP a aa b Bb

18. Figure 14.2 Mendel tracked heritable characters for three generations

19. Figure 14.3 Alleles, alternative versions of a gene

20. Table 14.1 The Results of Mendel’s F 1 Crosses for Seven Characters in Pea Plants

21. Figure 14.x2 Round and wrinkled peas

22. Figure 14.4 Mendel’s law of segregation (Layer 2)

23. Figure 14.5 Genotype versus phenotype

24. Figure 14.6 A testcross

25. Figure 14.7 Testing two hypotheses for segregation in a dihybrid cross

28. Figure 14.11 An example of epistasis

29. Figure 14.8 Segregation of alleles and fertilization as chance events

30. Figure 14.9 Incomplete dominance in snapdragon color

31. Figure 14.9x Incomplete dominance in carnations

32. Figure 14.10 Multiple alleles for the ABO blood groups

33. Figure 14.10x ABO blood types

34. Figure 14.12 A simplified model for polygenic inheritance of skin color

35. Figure 14.13 The effect of environment of phenotype

36. Figure 14.14 Pedigree analysis

37. Discussion Questions 1.How can a mutation be harmful in one environment and helpful in another? 2.Why should a mutation persist if it kills people? 3.Why are there more people with sickle cell disease in one part of the world than in other parts? http://www.teachersdomain.org/resource/tdc02.s ci.life.gen.mutationstory/

38. Figure 14.15 Pleiotropic effects of the sickle-cell allele in a homozygote

39. Figure 15.1 The chomosomal basis of Mendel’s laws

40. Figure 15.9 The transmission of sex-linked recessive traits

41. Figure 15.10 X inactivation and the tortoiseshell cat

42. Figure 15.11 Meiotic nondisjunction

43. Figure 15.13 Alterations of chromosome structure

44. Figure 15.14 Down syndrome

45. Figure 15.x2 Klinefelter syndrome

46. Figure 15.x3 XYY karyotype

47. Figure 15.15 Genomic imprinting (Layer 3)

49. Fig. 9-5a P generation 1–21–2 Hypothesis: Dependent assortment Hypothesis: Independent assortment 1–21–2 1–21–2 1–21–2 1–41–4 1–41–4 1–41–4 1–41–4 1–41–4 1–41–4 1–41–4 1–41–4 9 –– 16 3 –– 16 3 –– 16 1 –– 16 RRYY Gametes Eggs F 1 generation Sperm F 2 generation Eggs Gametes rryy RrYy ry RY ry RY ry RY Hypothesized (not actually seen) Actual results (support hypothesis) RRYY rryy RrYy ry RY RRYY rryy RrYy ry RY RrYy rrYYRrYY RRYyRrYY RRYy rrYy Rryy RRyy rY Ry ry Yellow round Green round Green wrinkled Yellow wrinkled RY rY Ry

50. Fig. 9-5b Phenotypes Genotypes Mating of heterozygotes (black, normal vision) Phenotypic ratio of offspring Black coat, normal vision B_N_ 9 black coat, normal vision Black coat, blind (PRA) B_nn 3 black coat, blind (PRA) Chocolate coat, normal vision bbN_ 3 chocolate coat, normal vision Chocolate coat, blind (PRA) bbnn 1 chocolate coat, blind (PRA) Blind BbNn

51. Fig. 9-6 B_ or Two possibilities for the black dog: Testcross: Genotypes Gametes Offspring1 black : 1 chocolate All black Bb bb BB Bbbb B b Bb b b B

52. Fig. 9-7 F 1 genotypes 1–21–2 1–21–2 1–21–2 1–21–2 1–41–4 1–41–4 1–41–4 1–41–4 Formation of eggs Bb female F 2 genotypes Formation of sperm Bb male B B B B B B b b b bb b

53. Fig. 9-8a Freckles Widow’s peak Free earlobe No freckles Straight hairline Attached earlobe Dominant Traits Recessive Traits

54. Fig. 9-8aa FrecklesNo freckles

55. Fig. 9-8ab Widow’s peak Straight hairline

56. Fig. 9-8ac Free earlobeAttached earlobe

57. Fig. 9-8b Ff FemaleMale Affected Unaffected First generation (grandparents) Second generation (parents, aunts, and uncles) Third generation (two sisters) Ff ff FF or

58. Fig. 9-9a Parents Normal Dd Offspring Sperm Eggs dd Deaf d Dd Normal (carrier) DD Normal D D d Dd Normal (carrier) Normal Dd 

59. Fig. 9-9b

60. Fig. 9-9c

61. Fig. 9-9ca

62. Fig. 9-10bb

63. Fig. 9-11a P generation 1–21–2 1–21–2 1–21–2 1–21–2 1–21–2 1–21–2 F 1 generation F 2 generation Red RR Gametes Eggs Sperm RR rR Rrrr R r R r R r Pink Rr R r White rr

64. Fig. 9-11b HH Homozygous for ability to make LDL receptors hh Homozygous for inability to make LDL receptors Hh Heterozygous LDL receptor LDL Cell Normal Mild disease Severe disease Genotypes: Phenotypes:

65. Fig. 9-12 Blood Group (Phenotype) Genotypes O A ii I A or I A i Red Blood Cells Carbohydrate A Antibodies Present in Blood Anti-A Anti-B Reaction When Blood from Groups Below Is Mixed with Antibodies from Groups at Left Anti-B O AB AB B I B or I B i Carbohydrate B AB IAIBIAIB — Anti-A

66. Fig. 9-12a Blood Group (Phenotype) Genotypes O A ii I A or I A i Red Blood Cells Carbohydrate A B I B or I B i Carbohydrate B AB IAIBIAIB

68. Fig. 9-12b Antibodies Present in Blood Anti-A Anti-B Reaction When Blood from Groups Below Is Mixed with Antibodies from Groups at Left Anti-B O A B AB — Anti-A Blood Group (Phenotype) O A B AB

69. Fig. 9-13 Clumping of cells and clogging of small blood vessels Pneumonia and other infections Accumulation of sickled cells in spleen Pain and fever Rheumatism Heart failure Damage to other organs Brain damage Spleen damage Kidney failure Anemia Paralysis Impaired mental function Physical weakness Breakdown of red blood cells Individual homozygous for sickle-cell allele Sickle cells Sickle-cell (abnormal) hemoglobin Abnormal hemoglobin crystallizes, causing red blood cells to become sickle-shaped

70. Fig. 9-14 P generation 1–81–8 F 1 generation F 2 generation Fraction of population Skin color Eggs Sperm 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 aabbcc (very light) AABBCC (very dark) AaBbCc 1 –– 64 15 –– 64 6 –– 64 1 –– 64 15 –– 64 6 –– 64 20 –– 64 1 –– 64 15 –– 64 6 –– 64 20 –– 64

71. Fig. 9-14a P generation 1–81–8 F 1 generation F 2 generation Eggs Sperm 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 1–81–8 aabbcc (very light) AABBCC (very dark) AaBbCc 1 –– 64 15 –– 64 6 –– 64 1 –– 64 15 –– 64 6 –– 64 20 –– 64

72. Fig. 9-14b Fraction of population Skin color 1 –– 64 15 –– 64 6 –– 64 20 –– 64

73. Fig. 9-16-1 F 1 generation R Metaphase I of meiosis (alternative arrangements) r Y y R r Y y R r Y y All round yellow seeds (RrYy)

74. Fig. 9-16-2 F 1 generation R Metaphase I of meiosis (alternative arrangements) r Y y R r Y y R r Y y All round yellow seeds (RrYy) Anaphase I of meiosis Metaphase II of meiosis R y r Y r y R Y R r Y y R r Y y

75. Fig. 9-16-3 F 1 generation R Metaphase I of meiosis (alternative arrangements) r Y y R r Y y R r Y y All round yellow seeds (RrYy) Anaphase I of meiosis Metaphase II of meiosis R y r Y r y R Y R r Y y R r Y y 1–41–4 R y Ry R y r Y 1–41–4 rY r Y 1–41–4 ry r y 1–41–4 RY R Y R Y Gametes Fertilization among the F 1 plants :3 9 :1 F 2 generation r y

76. Fig. 9-17 Purple long Purple round Red long Red round Explanation: linked genes Parental diploid cell PpLl Experiment Purple flower PpLl Long pollen PpLl Prediction (9:3:3:1) Observed offspring Phenotypes 284 21 55 215 71 24 Most gametes Meiosis PL pl PL pl Fertilization Sperm Most offspring Eggs 3 purple long : 1 red round Not accounted for: purple round and red long PL pl PL pl

77. Fig. 9-17a Purple long Purple round Red long Red round Experiment Purple flower PpLl Long pollen PpLl Prediction (9:3:3:1) Observed offspring Phenotypes 284 21 55 215 71 24

78. Fig. 9-17b Explanation: linked genes Parental diploid cell PpLl Most gametes Meiosis PL pl PL pl Fertilization Sperm Most offspring Eggs 3 purple long : 1 red round Not accounted for: purple round and red long PL pl PL pl

79. Fig. 9-18a Gametes Tetrad Crossing over Baba a b A B A B A b

80. Fig. 9-18b

81. Fig. 9-18c Experiment Parental phenotypes Recombination frequency = Black vestigial Black body, vestigial wings GgLl Offspring FemaleMale Gray long 965 944 206 185 ggll Gray vestigial Black long Gray body, long wings (wild type) Recombinant phenotypes 391 recombinants 2,300 total offspring Explanation = 0.17 or 17% G L g l GgLl (female) ggll (male) G L g l g L g l G L Sperm Eggs Offspring g L G l

82. Fig. 9-18ca Experiment Parental phenotypes Recombination frequency = Black vestigial Black body, vestigial wings GgLl Offspring Female Male Gray long 965 944206 185 ggll Gray vestigial Black long Gray body, long wings (wild type) Recombinant phenotypes 391 recombinants 2,300 total offspring = 0.17 or 17%

83. Fig. 9-18cb Explanation G L g l GgLl (female) ggll (male) G L g l g L g l G L Sperm Eggs Offspring g L G l

84. Fig. 9-19a Chromosome 9.5% Recombination frequencies 9% 17% g c l

85. Fig. 9-19b Mutant phenotypes Short aristae Black body (g) Cinnabar eyes (c) Vestigial wings (l) Brown eyes Long aristae (appendages on head) Gray body (G) Red eyes (C) Normal wings (L) Red eyes Wild-type phenotypes

86. Fig. 9-20a X Y

87. Fig. 9-20b (male) Sperm (female) 44 + XY Parents’ diploid cells 44 + XX 22 + X 22 + Y 22 + X 44 + XY 44 + XX Egg Offspring (diploid)

88. Fig. 9-20c 22 + X 22 + XX

89. Fig. 9-20d 76 + ZZ 76 + ZW

90. Fig. 9-20e 16 32

91. Fig. 9-21a

92. Fig. 9-21b Female Male X R X r Y X R Y X R X r Y XrXr XRXR Sperm Eggs R = red-eye allele r = white-eye allele

93. Fig. 9-21c Female Male X R X r X R Y X R Y XRXR XRXR Sperm Eggs X r X R X r Y XrXr

94. Fig. 9-21d Female Male X R X r X r Y X R Y X R Y XrXr XRXR Sperm Eggs X r X r Y XrXr

95. Fig. 9-22 Queen Victoria Albert Alice Louis Alexandra Czar Nicholas II of Russia Alexis

96. Fig. 9-UN4

97. Figure 20.9 Using restriction fragment patterns to distinguish DNA from different alleles

98. Figure 20.10 Restriction fragment analysis by Southern blotting

99. Figure 20.12 Sequencing of DNA by the Sanger method (Layer 4)

100. Figure 20.13 Alternative strategies for sequencing an entire genome

101. Table 20.1 Genome Sizes and Numbers of Genes

102. Figure 21.6 Nuclear transplantation

103. Figure 21.7 Cloning a mammal

104. Figure 20.15 RFLP markers close to a gene

105. Figure 20.16 One type of gene therapy procedure

106. Figure 20.17 DNA fingerprints from a murder case

107. Figure 20.19 Using the Ti plasmid as a vector for genetic engineering in plants

108. Fig. 9-UN1 Homologous chromosomes Alleles, residing at the same locus Meiosis Gamete from other parent Fertilization Diploid zygote (containing paired alleles) Paired alleles, alternate forms of a gene Haploid gametes (allele pairs separate)

109. Fig. 9-UN2 Incomplete dominance Red RR Single gene Single characters (such as skin color) Multiple characters Pleiotropy Polygenic inheritance Multiple genes White rr Pink Rr

110. Fig. 9-UN3 Genes located on (b) (a) at specific locations called alternative versions called if both same, genotype called expressed allele called inheritance when phenotype In between called unexpressed allele called if different, genotype called chromosomes heterozygous (d) (c) (f) (e)

111. Figure 18.19 Regulation of a metabolic pathway

112. Figure 18.20a The trp operon: regulated synthesis of repressible enzymes

113. Figure 18.20b The trp operon: regulated synthesis of repressible enzymes (Layer 2)

114. Figure 18.21a The lac operon: regulated synthesis of inducible enzymes

115. Figure 18.21b The lac operon: regulated synthesis of inducible enzymes

116. Figure 18.22a Positive control: cAMP receptor protein

117. Figure 18.22b Positive control: cAMP receptor protein

119. Figure 19.3 The evolution of human  -globin and  -globin gene families

120. Figure 19.7 Opportunities for the control of gene expression in eukaryotic cells

121. Figure 19.8 A eukaryotic gene and its transcript

122. Figure 19.9 A model for enhancer action