figure 13.2 two families. figure 13.x1 sem of sea urchin sperm fertilizing egg
TRANSCRIPT
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
Transferredpollen from stamens of whiteflower to carpel of purple flower
StamensCarpel
Parents(P)
Purple
2
White
Removedstamens frompurple flower
1
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
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
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
Fig. 9-3a-1P generation(true-breedingparents)
Purple flowers White flowers
Fig. 9-3a-2P generation(true-breedingparents)
Purple flowers White flowers
F1 generation All plants havepurple flowers
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
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
Fig. 9-4
Gene loci
Homozygousfor thedominant allele
Dominantallele
Homozygousfor therecessive allele
Heterozygous
Recessive allele
Genotype:
P Ba
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 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.sci.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
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
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
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
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
Fig. 9-8a
Freckles
Widow’s peak
Free earlobe
No freckles
Straight hairline
Attached earlobe
Dominant Traits Recessive Traits
Fig. 9-8aa
Freckles No freckles
Fig. 9-8ab
Widow’s peak Straight hairline
Fig. 9-8ac
Free earlobe Attached earlobe
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
Fig. 9-9a
Parents NormalDd
Offspring
Sperm
Eggs
ddDeafd
DdNormal(carrier)
DDNormalD
D d
DdNormal(carrier)
NormalDd
Fig. 9-9b
Fig. 9-9c
Fig. 9-9ca
Fig. 9-10bb
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
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:
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
Fig. 9-12a
BloodGroup(Phenotype) Genotypes
O
A
ii
IAIA
orIAi
Red Blood Cells
Carbohydrate A
BIBIB
orIBi
Carbohydrate B
AB IAIB
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
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
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
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
Fig. 9-14b
Fra
ctio
n o
f p
op
ula
tio
n
Skin color
1––64
15––64
6––64
20––64
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)
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
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
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
Fig. 9-17a
Purple longPurple roundRed longRed round
Experiment
Purple flower
PpLl Long pollenPpLl
Prediction(9:3:3:1)
ObservedoffspringPhenotypes
284212155
215717124
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
Fig. 9-18a
Gametes
Tetrad Crossing over
Ba baa b
A BA B A b
Fig. 9-18b
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
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%
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
Fig. 9-19a
Chromosome
9.5%
Recombinationfrequencies
9%
17%
g c l
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
Fig. 9-20a
X
Y
Fig. 9-20b
(male)
Sperm
(female)
44+
XYParents’diploidcells
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
1632
Fig. 9-21a
Fig. 9-21bFemale Male
XR XR Xr Y
XR YXR Xr
YXr
XR
Sperm
Eggs
R = red-eye alleler = white-eye allele
Fig. 9-21cFemale Male
XR Xr XR Y
XR YXR XR
YXR
XR
Sperm
Eggs
Xr XR Xr YXr
Fig. 9-21dFemale Male
XR Xr Xr Y
XR YXR XR
YXr
XR
Sperm
Eggs
Xr Xr Xr YXr
Fig. 9-22
QueenVictoria
Albert
Alice Louis
Alexandra CzarNicholas IIof 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
Homologouschromosomes
Alleles, residingat the same locus
MeiosisGametefrom otherparent
Fertilization
Diploid zygote(containingpaired alleles)
Paired alleles, alternate formsof a gene Haploid gametes
(allele pairs separate)
Fig. 9-UN2
Incompletedominance
RedRR
Singlegene
Single characters(such as skin color)
Multiple characters
Pleiotropy
PolygenicinheritanceMultiple
genes
Whiterr
PinkRr
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)
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