Figure 13.2 Two families

Figure 13.x1 SEM of sea urchin sperm fertilizing egg

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

Fig. 9-2a

Figure 14.x1 Sweet pea flowers

Figure 14.1 A genetic cross

Fig. 9-2b Petal Stamen Carpel

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

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

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

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

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

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

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

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

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

Figure 14.2 Mendel tracked heritable characters for three generations

Figure 14.3 Alleles, alternative versions of a gene

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

Figure 14.x2 Round and wrinkled peas

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

Figure 14.5 Genotype versus phenotype

Figure 14.6 A testcross

Figure 14.7 Testing two hypotheses for segregation in a dihybrid cross

Figure An example of epistasis

Figure 14.8 Segregation of alleles and fertilization as chance events

Figure 14.9 Incomplete dominance in snapdragon color

Figure 14.9x Incomplete dominance in carnations

Figure Multiple alleles for the ABO blood groups

Figure 14.10x ABO blood types

Figure A simplified model for polygenic inheritance of skin color

Figure The effect of environment of phenotype

Figure Pedigree analysis

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? ci.life.gen.mutationstory/

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

Figure 15.1 The chomosomal basis of Mendel’s laws

Figure 15.9 The transmission of sex-linked recessive traits

Figure X inactivation and the tortoiseshell cat

Figure Meiotic nondisjunction

Figure Alterations of chromosome structure

Figure Down syndrome

Figure 15.x2 Klinefelter syndrome

Figure 15.x3 XYY karyotype

Figure Genomic imprinting (Layer 3)

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

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

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

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

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

Fig. 9-8aa FrecklesNo freckles

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

Fig. 9-8ac Free earlobeAttached earlobe

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

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 

Fig. 9-9b

Fig. 9-9c

Fig. 9-9ca

Fig. 9-10bb

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

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:

Fig 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

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

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

Fig 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

Fig 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 6 –– 64 1 –– –– 64 6 –– –– 64 1 –– –– 64 6 –– –– 64

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 6 –– 64 1 –– –– 64 6 –– –– 64

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

Fig 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)

Fig 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

Fig 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

Fig 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 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

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

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

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

Fig. 9-18b

Fig. 9-18c Experiment Parental phenotypes Recombination frequency = Black vestigial Black body, vestigial wings GgLl Offspring FemaleMale Gray long 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

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

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

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

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

Fig. 9-20a X Y

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)

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

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

Fig. 9-20e 16 32

Fig. 9-21a

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

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

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

Fig Queen Victoria Albert Alice Louis Alexandra Czar Nicholas II of Russia Alexis

Fig. 9-UN4

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

Figure Restriction fragment analysis by Southern blotting

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

Figure Alternative strategies for sequencing an entire genome

Table 20.1 Genome Sizes and Numbers of Genes

Figure 21.6 Nuclear transplantation

Figure 21.7 Cloning a mammal

Figure RFLP markers close to a gene

Figure One type of gene therapy procedure

Figure DNA fingerprints from a murder case

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

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)

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

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)

Figure Regulation of a metabolic pathway

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

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

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

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

Figure 18.22a Positive control: cAMP receptor protein

Figure 18.22b Positive control: cAMP receptor protein

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

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

Figure 19.8 A eukaryotic gene and its transcript

Figure 19.9 A model for enhancer action