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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
White
1
Removed
stamens from
purple flower
Stamens
Carpel
Parents
(P)
2
Purple
Transferred
pollen from stamens of white
flower to carpel of purple flower
Fig. 9-2c-2
White
1
Removed
stamens from
purple flower
Stamens
Carpel
Parents
(P)
2
Purple
3
Transferred
pollen from stamens of white
flower to carpel of purple flower
Pollinated carpel
matured into pod
Fig. 9-2c-3
White
1
Removed
stamens from
purple flower
Stamens
Carpel
Parents
(P)
2
Purple
3
Transferred
pollen from stamens of white
flower to carpel of purple flower
Pollinated carpel
matured into pod
4
Offspring
(F1)
Planted seeds
from pod
Fig. 9-2d
Flower color
Purple
White
Axial
Terminal
Seed color
Yellow
Green
Seed shape
Round
Wrinkled
Pod shape
Inflated
Constricted
Pod color
Green
Yellow
Tall
Dwarf
Flower position
Stem length
Fig. 9-3a-1
P generation
(true-breeding
parents)
Purple flowers
White flowers
Fig. 9-3a-2
P generation
(true-breeding
parents)
Purple flowers
F1 generation
White flowers
All plants have
purple flowers
Fig. 9-3a-3
P generation
(true-breeding
parents)
Purple flowers
White flowers
F1 generation
All plants have
purple flowers
Fertilization
among F1 plants
(F1 ´ F1)
F2 generation
3
–
4
of plants
have purple flowers
1
– of
4
plants
have white flowers
Fig. 9-3b
Genetic makeup (alleles)
pp
PP
P plants
Gametes
All p
All P
F1 plants
(hybrids)
All Pp
Gametes
1
–
2
1
–
2
P
Sperm
P
F2 plants
Phenotypic ratio
3 purple : 1 white
p
P
PP
Pp
p
Pp
pp
Eggs
Genotypic ratio
1 PP : 2 Pp : 1 pp
p
Fig. 9-4
Gene loci
Genotype:
Dominant
allele
P
a
B
P
a
b
Recessive
allele
Bb
PP
aa
Homozygous
Heterozygous
Homozygous
for the
for the
dominant allele recessive allele
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 F1 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 14.11 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 14.10 Multiple alleles for the ABO blood groups
Figure 14.10x ABO blood types
Figure 14.12 A simplified model for polygenic inheritance of skin color
Figure 14.13 The effect of environment of phenotype
Figure 14.14 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?
http://www.teachersdomain.org/resource/tdc02.s
ci.life.gen.mutationstory/
Figure 14.15 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 15.10 X inactivation and the tortoiseshell cat
Figure 15.11 Meiotic nondisjunction
Figure 15.13 Alterations of chromosome structure
Figure 15.14 Down syndrome
Figure 15.x2 Klinefelter syndrome
Figure 15.x3 XYY karyotype
Figure 15.15 Genomic imprinting (Layer 3)
Fig. 9-5a
Hypothesis: Independent assortment
Hypothesis: Dependent assortment
P
generation
rryy
RRYY
ry
Gametes RY
F1
generation
rryy
RRYY
ry
Gametes RY
RrYy
RrYy
Sperm
Sperm
1
–
2
F2
generation
1
–
2
RY
1
–
2
1
–
4
ry
1
–
4
RY
Eggs
1
–
2
RY
1
–
4
ry
Hypothesized
(not actually seen)
1
–
4
rY
1
–
4
Ry
1
–
4
ry
RY
RRYY
RrYY
RRYy
RrYy
RrYY
rrYY
RrYy
rrYy
rY
Eggs
1
–
4
1
–
4
9
––
16
Ry
RRYy
RrYy
RRyy
Rryy
RrYy
rrYy
Rryy
rryy
ry
Actual results
(support hypothesis)
3
––
16
3
––
16
1
––
16
Yellow
round
Green
round
Yellow
wrinkled
Green
wrinkled
Fig. 9-5b
Blind
Phenotypes
Genotypes
Black coat, normal vision
B_N_
BbNn
Mating of heterozygotes
(black, normal vision)
Phenotypic ratio
of offspring
Black coat, blind (PRA)
B_nn
9 black coat,
normal vision
3 black coat,
blind (PRA)
Blind
Chocolate coat, normal vision Chocolate coat, blind (PRA)
bbN_
bbnn
BbNn
3 chocolate coat,
normal vision
1 chocolate coat,
blind (PRA)
Fig. 9-6
Testcross:
B_
Genotypes
bb
Two possibilities for the black dog:
BB
B
Gametes
b
Offspring
Bb
or
Bb
All black
b
B
b
Bb
bb
1 black : 1 chocolate
Fig. 9-7
F1 genotypes
Bb male
Formation of sperm
Bb female
Formation of eggs
1
–
2
1
–
2
1
–
2
B
B
B
b
B
B
1
–
4
1
–
4
1
–
2
b
b
B
1
–
4
F2 genotypes
b
b
b
1
–
4
Fig. 9-8a
Dominant Traits
Recessive Traits
Freckles
No freckles
Widow’s peak
Straight hairline
Free earlobe
Attached earlobe
Fig. 9-8aa
Freckles
No freckles
Fig. 9-8ab
Widow’s peak
Straight hairline
Fig. 9-8ac
Free earlobe
Attached earlobe
Fig. 9-8b
First generation
(grandparents)
Ff
Second generation
(parents, aunts,
and uncles)
FF
or
Ff
Third generation
(two sisters)
Female Male
Affected
Unaffected
Ff
ff
ff
ff
Ff
Ff
Ff
ff
ff
FF
or
Ff
Fig. 9-9a
Parents
Normal
Dd
Normal
Dd
´
Sperm
D
Offspring
D
d
DD
Normal
Dd
Normal
(carrier)
Dd
Normal
(carrier)
dd
Deaf
Eggs
d
Fig. 9-9b
Fig. 9-9c
Fig. 9-9ca
Fig. 9-10bb
Fig. 9-11a
P generation
Red
RR
White
rr
r
R
Gametes
F1 generation
Pink
Rr
Gametes
1
–
2
R
1
–
2
r
Sperm
1
–
2
F2 generation
R
1
–
2
r
1
–
2
R
RR
rR
1
–
2
r
Rr
rr
Eggs
Fig. 9-11b
Genotypes:
HH
Homozygous
for ability to make
LDL receptors
Hh
Heterozygous
hh
Homozygous
for inability to make
LDL receptors
Phenotypes:
LDL
LDL
receptor
Cell
Normal
Mild disease
Severe disease
Fig. 9-12
Blood
Group
(Phenotype) Genotypes
Red Blood Cells
Antibodies
Present in
Blood
Anti-A
Anti-B
O
ii
A
I AI A
or
I Ai
Carbohydrate A
Anti-B
B
IBIB
or
IBi
Carbohydrate B
Anti-A
AB
IAIB
—
Reaction When Blood from Groups Below Is Mixed
with Antibodies from Groups at Left
O
A
B
AB
Fig. 9-12a
Blood
Group
(Phenotype) Genotypes
Red Blood Cells
O
ii
A
IAIA
or
IAi
Carbohydrate A
B
IBIB
or
IBi
Carbohydrate B
AB
IAIB
Fig. 9-12b
Blood
Antibodies Reaction When Blood from Groups Below Is Mixed
Group
Present in with Antibodies from Groups at Left
(Phenotype) Blood
B
A
AB
O
O
Anti-A
Anti-B
A
Anti-B
B
Anti-A
AB
—
Fig. 9-13
Individual homozygous
for sickle-cell allele
Sickle-cell (abnormal) hemoglobin
Abnormal hemoglobin crystallizes,
causing red blood cells to become sickle-shaped
Sickle cells
Clumping of cells
and clogging of
small blood vessels
Breakdown of
red blood cells
Physical
weakness
Impaired
mental
function
Anemia
Heart
failure
Paralysis
Pain and
fever
Pneumonia
and other
infections
Accumulation of
sickled cells in spleen
Brain
damage
Damage to
other organs
Rheumatism
Spleen
damage
Kidney
failure
Fig. 9-14
P generation
aabbcc
AABBCC
(very light) (very dark)
F1 generation
AaBbCc
AaBbCc
Sperm
1
–
8
1
–
8
1
–
8
1
–
8
1
–
8
1
–
8
1
–
8
1
–
8
F2 generation
1
–
8
1
–
8
1
–
8
1
–
8
Fraction of population
Eggs
20
––
64
1
–
8
1
–
8
1
–
8
1
–
8
15
––
64
6
––
64
1
––
64
1
––
64
6
––
64
15
––
64
20
––
64
15
––
64
6
––
64
1
––
64
Skin color
Fig. 9-14a
P generation
aabbcc
(very light)
AABBCC
(very dark)
F1 generation
AaBbCc
AaBbCc
Sperm
1
–
8
F2 generation
1
–
8
1
–
8
1
–
8
1
–
8
1
–
8
1
–
8
1
–
8
1
–
8
1
–
8
1
–
8
1
–
8
Eggs
1
–
8
1
–
8
1
–
8
1
–
8
1
––
64
6
––
64
15
––
64
20
––
64
15
––
64
6
––
64
1
––
64
Fig. 9-14b
Fraction of population
20
––
64
15
––
64
6
––
64
1
––
64
Skin color
Fig. 9-16-1
F1 generation
All round yellow seeds
(RrYy)
R
r
y
Y
R
Y
r
y
Metaphase I
of meiosis
(alternative
arrangements)
r
R
Y
y
Fig. 9-16-2
F1 generation
All round yellow seeds
(RrYy)
R
r
y
Y
r
R
y
Y
R
Y
Metaphase I
of meiosis
(alternative
arrangements)
r
R
Y
y
r
Anaphase I
of meiosis
y
R
r
Y
y
Metaphase II
of meiosis
r
R
Y
y
r
R
Y
y
Fig. 9-16-3
F1 generation
All round yellow seeds
(RrYy)
R
r
y
Y
r
R
y
Y
R
Y
y
Y
y
R
R
Y
y
Anaphase I
of meiosis
r
Y
R
r
R
Y
Metaphase I
of meiosis
(alternative
arrangements)
r
Metaphase II
of meiosis
r
Y
y
r
R
Y
y
y
Y
Y
r
r
r
1
– ry
4
1
– rY
4
Fertilization among the F1 plants
F2 generation
R
Gametes
y
1
– RY
4
r
9
:3
:3
:1
y
y
R
R
1
–
4
Ry
Fig. 9-17
Experiment
Purple flower
PpLl
PpLl
Observed
offspring
Phenotypes
Purple long
Purple round
Red long
Red round
Long pollen
Prediction
(9:3:3:1)
215
71
71
24
284
21
21
55
Explanation: linked genes
PL
Parental
diploid cell
PpLl
pl
Meiosis
Most
gametes
pl
PL
Fertilization
Sperm
PL
Most
offspring
pl
PL
PL
PL
pl
pl
pl
PL
pl
PL
Eggs
pl
3 purple long : 1 red round
Not accounted for: purple round and red long
Fig. 9-17a
Experiment
Purple flower
PpLl
Phenotypes
Purple long
Purple round
Red long
Red round
PpLl
Observed
offspring
284
21
21
55
Long pollen
Prediction
(9:3:3:1)
215
71
71
24
Fig. 9-17b
Explanation: linked genes
PL
Parental
diploid cell
PpLl
pl
Meiosis
Most
gametes
pl
PL
Fertilization
Sperm
Most
offspring
PL
pl
PL
PL
PL
pl
pl
pl
PL
pl
PL
Eggs
pl
3 purple long : 1 red round
Not accounted for: purple round and red long
Fig. 9-18a
AB
a b
Tetrad
A B
A b
a B
a b
Crossing over
Gametes
Fig. 9-18b
Fig. 9-18c
Experiment
Gray body,
long wings
(wild type)
Black body,
vestigial wings
GgLl
ggll
Female
Male
Gray long
Offspring
Black vestigial Gray vestigial Black long
944
965
206
Parental
phenotypes
185
Recombinant
phenotypes
Recombination frequency = 391 recombinants = 0.17 or 17%
2,300 total offspring
Explanation
g l
GL
GgLl
(female)
GL
g l
g l
g l
Gl
gL
ggll
(male)
g l
Sperm
Eggs
GL
g l
Gl
gL
g l
g l
g l
g l
Offspring
Fig. 9-18ca
Experiment
Gray body,
long wings
(wild type)
Black body,
vestigial wings
GgLl
ggll
Female
Male
Offspring
Gray long Black vestigial Gray vestigial Black long
965
944
Parental
phenotypes
206
185
Recombinant
phenotypes
Recombination frequency = 391 recombinants = 0.17 or 17%
2,300 total offspring
Fig. 9-18cb
Explanation
gl
GL
GgLl
(female)
GL
g l
gl
g l
Gl
gL
ggll
(male)
gl
Sperm
Eggs
GL
gl
Gl
gL
gl
gl
gl
gl
Offspring
Fig. 9-19a
Chromosome
g
l
c
17%
9%
9.5%
Recombination
frequencies
Fig. 9-19b
Mutant phenotypes
Short
aristae
Black
body
(g)
Long aristae Gray
(appendages body
on head)
(G)
Cinnabar Vestigial
eyes
wings
(c)
(l)
Red
eyes
(C)
Normal
wings
(L)
Wild-type phenotypes
Brown
eyes
Red
eyes
Fig. 9-20a
X
Y
Fig. 9-20b
(male)
44
Parents’
+
diploid
XY
cells
22
+
X
(female)
44
+
XX
22
+
Y
Sperm
22
+
X
44
+
XX
44
+
XY
Offspring
(diploid)
Egg
Fig. 9-20c
22
+
XX
22
+
X
Fig. 9-20d
76
+
ZW
76
+
ZZ
Fig. 9-20e
32
16
Fig. 9-21a
Fig. 9-21b
Female
Male
Xr Y
XR XR
Sperm
Eggs XR
Xr
Y
XR Xr
XR Y
R = red-eye allele
r = white-eye allele
Fig. 9-21c
Female
Male
XR Xr
XR Y
Sperm
XR
Y
XR
XR XR
XR Y
Xr
Xr XR
Xr Y
Eggs
Fig. 9-21d
Female
Male
XR Xr
Xr Y
Sperm
Xr
Y
XR
XR XR
XR Y
Xr
Xr Xr
Xr Y
Eggs
Fig. 9-22
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 20.10 Restriction fragment analysis by Southern blotting
Figure 20.12 Sequencing of DNA by the Sanger method (Layer 4)
Figure 20.13 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 20.15 RFLP markers close to a gene
Figure 20.16 One type of gene therapy procedure
Figure 20.17 DNA fingerprints from a murder case
Figure 20.19 Using the Ti plasmid as a vector for genetic engineering in plants
Fig. 9-UN1
Fertilization
Homologous
Alleles, residing
chromosomes at the same locus
Meiosis
Paired alleles,
alternate forms
of a gene
Gamete
from other
parent
Haploid gametes
(allele pairs separate)
Diploid zygote
(containing
paired alleles)
Fig. 9-UN2
Incomplete
dominance
White
rr
Red
RR
Pink
Rr
Pleiotropy
Single
gene
Multiple
genes
Multiple characters
Polygenic
inheritance
Single characters
(such as skin color)
Fig. 9-UN3
Genes
located
on
alternative
versions called
(a)
chromosomes
at specific
locations called
(b)
if both same,
if different,
genotype called genotype called
(c)
heterozygous
expressed
allele called
(d)
unexpressed
allele called
(e)
inheritance when phenotype
In between called
(f)
Figure 18.19 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