figure 13.2 two families
DESCRIPTION
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. Petal. Fig. 9-2b. Stamen. Carpel. White. Removed - PowerPoint PPT PresentationTRANSCRIPT
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Figure 13.2 Two families
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Figure 13.x1 SEM of sea urchin sperm fertilizing egg
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Figure 13.x4 Human male chromosomes shown by bright field G-banding
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Fig. 9-2a
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Figure 14.x1 Sweet pea flowers
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Figure 14.1 A genetic cross
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Fig. 9-2b
Petal
Stamen
Carpel
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Fig. 9-2c-1
Transferredpollen from stamens of whiteflower to carpel of purple flower
StamensCarpel
Parents(P)
Purple
2
White
Removedstamens frompurple flower
1
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Fig. 9-2c-2
Transferredpollen from stamens of whiteflower to carpel of purple flower
StamensCarpel
Parents(P)
Purple
2
White
Removedstamens frompurple flower
1
Pollinated carpelmatured into pod
3
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Fig. 9-2c-3
Transferredpollen from stamens of whiteflower to carpel of purple flower
StamensCarpel
Parents(P)
Purple
2
White
Removedstamens frompurple flower
1
Pollinated carpelmatured into pod
3
Offspring(F1)
Planted seedsfrom pod
4
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Fig. 9-2d
Flower color White
Axial
Purple
Flower position Terminal
YellowSeed color Green
RoundSeed shape Wrinkled
InflatedPod shape Constricted
GreenPod color Yellow
TallStem length Dwarf
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Fig. 9-3a-1P generation(true-breedingparents)
Purple flowers White flowers
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Fig. 9-3a-2P generation(true-breedingparents)
Purple flowers White flowers
F1 generation All plants havepurple flowers
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Fig. 9-3a-3P generation(true-breedingparents)
Purple flowers White flowers
F1 generation All plants havepurple flowers
F2 generation
Fertilizationamong F1 plants(F1 F1)
of plantshave purple flowers
3–4 of plants
have white flowers
1–4
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Fig. 9-3b
P plants
1–2
1–2
Genotypic ratio1 PP : 2 Pp : 1 pp
Phenotypic ratio3 purple : 1 white
F1 plants(hybrids)
Gametes
Genetic makeup (alleles)
All
All Pp
Sperm
Eggs
PP
p
ppPp
Pp
P
pP
pP
P
p
PP pp
All
Gametes
F2 plants
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Fig. 9-4
Gene loci
Homozygousfor thedominant allele
Dominantallele
Homozygousfor therecessive allele
Heterozygous
Recessive allele
Genotype:
P Ba
P
PP
a
aa
b
Bb
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Figure 14.2 Mendel tracked heritable characters for three generations
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Figure 14.3 Alleles, alternative versions of a gene
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Table 14.1 The Results of Mendel’s F1 Crosses for Seven Characters in Pea Plants
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Figure 14.x2 Round and wrinkled peas
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Figure 14.4 Mendel’s law of segregation (Layer 2)
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Figure 14.5 Genotype versus phenotype
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Figure 14.6 A testcross
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Figure 14.7 Testing two hypotheses for segregation in a dihybrid cross
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Figure 14.11 An example of epistasis
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Figure 14.8 Segregation of alleles and fertilization as chance events
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Figure 14.9 Incomplete dominance in snapdragon color
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Figure 14.9x Incomplete dominance in carnations
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Figure 14.10 Multiple alleles for the ABO blood groups
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Figure 14.10x ABO blood types
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Figure 14.12 A simplified model for polygenic inheritance of skin color
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Figure 14.13 The effect of environment of phenotype
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Figure 14.14 Pedigree analysis
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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.sci.life.gen.mutationstory/
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Figure 14.15 Pleiotropic effects of the sickle-cell allele in a homozygote
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Figure 15.1 The chomosomal basis of Mendel’s laws
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Figure 15.9 The transmission of sex-linked recessive traits
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Figure 15.10 X inactivation and the tortoiseshell cat
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Figure 15.11 Meiotic nondisjunction
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Figure 15.13 Alterations of chromosome structure
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Figure 15.14 Down syndrome
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Figure 15.x2 Klinefelter syndrome
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Figure 15.x3 XYY karyotype
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Figure 15.15 Genomic imprinting (Layer 3)
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Fig. 9-5a
P generation
1–2
Hypothesis: Dependent assortment Hypothesis: Independent assortment
1–2
1–2
1–2
1–4
1–4
1–4
1–4
1–4
1–4
1–4
1–4
9––16
3––16
3––16
1––16
RRYY
Gametes
Eggs
F1
generation
SpermSperm
F2
generation
Eggs
Gametes
rryy
RrYy
ryRY
ryRY
ry
RY
Hypothesized(not actually seen)
Actual results(support hypothesis)
RRYY rryy
RrYy
ryRY
RRYY
rryy
RrYy
ry
RY
RrYy
RrYy
RrYy
rrYYRrYY
RRYyRrYY
RRYy
rrYy
rrYy
Rryy
Rryy
RRyy
rY
Ry
ry
Yellowround
Greenround
Greenwrinkled
Yellowwrinkled
RY rY Ry
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Fig. 9-5b
PhenotypesGenotypes
Mating of heterozygotes(black, normal vision)
Phenotypic ratioof offspring
Black coat, normal visionB_N_
9 black coat,normal vision
Black coat, blind (PRA)B_nn
3 black coat,blind (PRA)
Chocolate coat, normal visionbbN_
3 chocolate coat,normal vision
Chocolate coat, blind (PRA)bbnn
1 chocolate coat,blind (PRA)
Blind Blind
BbNn BbNn
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Fig. 9-6
B_
or
Two possibilities for the black dog:
Testcross:
Genotypes
Gametes
Offspring 1 black : 1 chocolateAll black
Bb
bb
BB
Bb bb
B
b
Bb
b
bB
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Fig. 9-7F1 genotypes
1–2
1–2
1–2
1–2
1–4
1–4
1–4
1–4
Formation of eggs
Bb female
F2 genotypes
Formation of sperm
Bb male
B
BB B B
B
b
b
bbbb
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Fig. 9-8a
Freckles
Widow’s peak
Free earlobe
No freckles
Straight hairline
Attached earlobe
Dominant Traits Recessive Traits
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Fig. 9-8aa
Freckles No freckles
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Fig. 9-8ab
Widow’s peak Straight hairline
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Fig. 9-8ac
Free earlobe Attached earlobe
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Fig. 9-8b
Ff
Female MaleAffected
Unaffected
First generation(grandparents)
Second generation(parents, aunts,and uncles)
Third generation(two sisters)
Ff Ff
Ff
Ff Ff
Ff
ff
ff ff ff
ff
FF
FF
or
or
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Fig. 9-9a
Parents NormalDd
Offspring
Sperm
Eggs
ddDeafd
DdNormal(carrier)
DDNormalD
D d
DdNormal(carrier)
NormalDd
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Fig. 9-9b
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Fig. 9-9c
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Fig. 9-9ca
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Fig. 9-10bb
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Fig. 9-11aP generation
1–2
1–2
1–2
1–2
1–2
1–2
F1 generation
F2 generation
RedRR
Gametes
Gametes
Eggs
Sperm
RR rR
Rr rr
R
r
R r
R r
PinkRr
R r
Whiterr
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Fig. 9-11b
HHHomozygous
for ability to makeLDL receptors
hhHomozygous
for inability to makeLDL receptors
HhHeterozygous
LDL receptor
LDL
CellNormal Mild disease Severe disease
Genotypes:
Phenotypes:
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Fig. 9-12
BloodGroup(Phenotype) Genotypes
O
A
ii
IAIA
orIAi
Red Blood Cells
Carbohydrate A
AntibodiesPresent inBlood
Anti-AAnti-B
Reaction When Blood from Groups Below Is Mixedwith Antibodies from Groups at Left
Anti-B
O A B AB
BIBIB
orIBi
Carbohydrate B
AB IAIB —
Anti-A
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Fig. 9-12a
BloodGroup(Phenotype) Genotypes
O
A
ii
IAIA
orIAi
Red Blood Cells
Carbohydrate A
BIBIB
orIBi
Carbohydrate B
AB IAIB
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Fig. 9-12b
AntibodiesPresent inBlood
Anti-AAnti-B
Reaction When Blood from Groups Below Is Mixedwith Antibodies from Groups at Left
Anti-B
O A B AB
—
Anti-A
BloodGroup(Phenotype)
O
A
B
AB
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Fig. 9-13
Clumping of cellsand clogging of
small blood vessels
Pneumoniaand otherinfections
Accumulation ofsickled cells in spleen
Pain andfever
Rheumatism
Heartfailure
Damage toother organs
Braindamage
Spleendamage
Kidneyfailure
Anemia
ParalysisImpairedmental
function
Physicalweakness
Breakdown ofred blood cells
Individual homozygousfor sickle-cell allele
Sickle cells
Sickle-cell (abnormal) hemoglobin
Abnormal hemoglobin crystallizes,causing red blood cells to become sickle-shaped
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Fig. 9-14P generation
1–8
F1 generation
F2 generation
Fra
ctio
n o
f p
op
ula
tio
n
Skin color
Eggs
Sperm1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
aabbcc(very light)
AABBCC(very dark)
AaBbCc AaBbCc
1––64
15––64
6––64
1––64
15––64
6––64
20––64
1––64
15––64
6––64
20––64
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Fig. 9-14aP generation
1–8
F1 generation
F2 generation
Eggs
Sperm1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
1–8
aabbcc(very light)
AABBCC(very dark)
AaBbCc AaBbCc
1––64
15––64
6––64
1––64
15––64
6––64
20––64
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Fig. 9-14b
Fra
ctio
n o
f p
op
ula
tio
n
Skin color
1––64
15––64
6––64
20––64
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Fig. 9-16-1
F1 generation R
Metaphase Iof meiosis(alternative
arrangements)
r
Y
y
Rr
Y y
R r
Y y
All round yellow seeds(RrYy)
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Fig. 9-16-2
F1 generation R
Metaphase Iof meiosis(alternative
arrangements)
r
Y
y
Rr
Y y
R r
Y y
All round yellow seeds(RrYy)
Anaphase Iof meiosis
Metaphase IIof meiosis
R
y
r
Y
r
y
R
Y
R r
Y y
Rr
Y y
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Fig. 9-16-3
F1 generation R
Metaphase Iof meiosis(alternative
arrangements)
r
Y
y
Rr
Y y
R r
Y y
All round yellow seeds(RrYy)
Anaphase Iof meiosis
Metaphase IIof meiosis
R
y
r
Y
r
y
R
Y
R r
Y y
Rr
Y y
1–4
R
y
Ry
R
y
r
Y
1–4 rY
r
Y
1–4 ry
r
y
1–4 RY
R
Y
R
YGametes
Fertilization among the F1 plants
:39 :3 :1F2 generation
r
y
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Fig. 9-17
Purple longPurple roundRed longRed round
Explanation: linked genes
Parentaldiploid cellPpLl
Experiment
Purple flower
PpLl Long pollenPpLl
Prediction(9:3:3:1)
ObservedoffspringPhenotypes
284212155
215717124
Mostgametes
Meiosis
PL
pl
PL
PL pl
pl
Fertilization
Sperm
Mostoffspring Eggs
3 purple long : 1 red roundNot accounted for: purple round and red long
PL PL
PL
PL
plPL
pl
pl
plpl
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Fig. 9-17a
Purple longPurple roundRed longRed round
Experiment
Purple flower
PpLl Long pollenPpLl
Prediction(9:3:3:1)
ObservedoffspringPhenotypes
284212155
215717124
![Page 78: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/78.jpg)
Fig. 9-17bExplanation: linked genes
Parentaldiploid cellPpLl
Mostgametes
Meiosis
PL
pl
PL
PL pl
pl
Fertilization
Sperm
Mostoffspring Eggs
3 purple long : 1 red roundNot accounted for: purple round and red long
PL PL
PL
PL
plPL
pl
plpl
pl
![Page 79: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/79.jpg)
Fig. 9-18a
Gametes
Tetrad Crossing over
Ba baa b
A BA B A b
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Fig. 9-18b
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Fig. 9-18c Experiment
Parentalphenotypes
Recombination frequency =
Black vestigial
Black body,vestigial wings
GgLl
Offspring
Female Male
Gray long
965 944 206 185
ggll
Gray vestigial Black long
Gray body,long wings(wild type)
Recombinantphenotypes
391 recombinants2,300 total offspring
Explanation
= 0.17 or 17%
G L
g l g l
g lGgLl
(female)ggll
(male)
G L g l g L
g l
g l
g l g l
g l
g l
G L
SpermEggs
Offspring
g L
G l
G l
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Fig. 9-18caExperiment
Parentalphenotypes
Recombination frequency =
Black vestigial
Black body,vestigial wings
GgLl
Offspring
Female Male
Gray long
965 944 206 185
ggll
Gray vestigial Black long
Gray body,long wings(wild type)
Recombinantphenotypes
391 recombinants2,300 total offspring
= 0.17 or 17%
![Page 83: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/83.jpg)
Fig. 9-18cb
ExplanationG L
g l g l
g lGgLl
(female)ggll
(male)
G L g l g L
g l
g l
g l g l
g l
g l
G L
SpermEggs
Offspring
g L
G l
G l
![Page 84: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/84.jpg)
Fig. 9-19a
Chromosome
9.5%
Recombinationfrequencies
9%
17%
g c l
![Page 85: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/85.jpg)
Fig. 9-19b
Mutant phenotypes
Shortaristae
Blackbody(g)
Cinnabareyes(c)
Vestigialwings(l)
Browneyes
Long aristae(appendageson head)
Graybody(G)
Redeyes(C)
Normalwings(L)
Redeyes
Wild-type phenotypes
![Page 86: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/86.jpg)
Fig. 9-20a
X
Y
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Fig. 9-20b
(male)
Sperm
(female)
44+
XYParents’diploidcells
44+
XX
22+X
22+Y
22+X
44+
XY
44+
XX
Egg
Offspring(diploid)
![Page 88: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/88.jpg)
Fig. 9-20c
22+X
22+
XX
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Fig. 9-20d
76+
ZZ
76+
ZW
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Fig. 9-20e
1632
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Fig. 9-21a
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Fig. 9-21bFemale Male
XR XR Xr Y
XR YXR Xr
YXr
XR
Sperm
Eggs
R = red-eye alleler = white-eye allele
![Page 93: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/93.jpg)
Fig. 9-21cFemale Male
XR Xr XR Y
XR YXR XR
YXR
XR
Sperm
Eggs
Xr XR Xr YXr
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Fig. 9-21dFemale Male
XR Xr Xr Y
XR YXR XR
YXr
XR
Sperm
Eggs
Xr Xr Xr YXr
![Page 95: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/95.jpg)
Fig. 9-22
QueenVictoria
Albert
Alice Louis
Alexandra CzarNicholas IIof Russia
Alexis
![Page 96: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/96.jpg)
Fig. 9-UN4
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Figure 20.9 Using restriction fragment patterns to distinguish DNA from different alleles
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Figure 20.10 Restriction fragment analysis by Southern blotting
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Figure 20.12 Sequencing of DNA by the Sanger method (Layer 4)
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Figure 20.13 Alternative strategies for sequencing an entire genome
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Table 20.1 Genome Sizes and Numbers of Genes
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Figure 21.6 Nuclear transplantation
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Figure 21.7 Cloning a mammal
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Figure 20.15 RFLP markers close to a gene
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Figure 20.16 One type of gene therapy procedure
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Figure 20.17 DNA fingerprints from a murder case
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Figure 20.19 Using the Ti plasmid as a vector for genetic engineering in plants
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Fig. 9-UN1
Homologouschromosomes
Alleles, residingat the same locus
MeiosisGametefrom otherparent
Fertilization
Diploid zygote(containingpaired alleles)
Paired alleles, alternate formsof a gene Haploid gametes
(allele pairs separate)
![Page 109: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/109.jpg)
Fig. 9-UN2
Incompletedominance
RedRR
Singlegene
Single characters(such as skin color)
Multiple characters
Pleiotropy
PolygenicinheritanceMultiple
genes
Whiterr
PinkRr
![Page 110: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/110.jpg)
Fig. 9-UN3
Genes
locatedon
(b)
(a)
at specificlocations called
alternativeversions called
if both same,genotype called
expressedallele called
inheritance when phenotypeIn between called
unexpressedallele called
if different,genotype called
chromosomes
heterozygous
(d)
(c)
(f)
(e)
![Page 111: Figure 13.2 Two families](https://reader036.vdocuments.us/reader036/viewer/2022062408/568144de550346895db1ab83/html5/thumbnails/111.jpg)
Figure 18.19 Regulation of a metabolic pathway
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Figure 18.20a The trp operon: regulated synthesis of repressible enzymes
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Figure 18.20b The trp operon: regulated synthesis of repressible enzymes (Layer 2)
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Figure 18.21a The lac operon: regulated synthesis of inducible enzymes
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Figure 18.21b The lac operon: regulated synthesis of inducible enzymes
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Figure 18.22a Positive control: cAMP receptor protein
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Figure 18.22b Positive control: cAMP receptor protein
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Figure 19.3 The evolution of human -globin and -globin gene families
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Figure 19.7 Opportunities for the control of gene expression in eukaryotic cells
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Figure 19.8 A eukaryotic gene and its transcript
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Figure 19.9 A model for enhancer action