expression Feedback inhibition Precursor Genes that encode enzymes 1 2 and 3 Enzyme 1 Enzyme 2 Enzyme 3 trp E trpD trpC trpB trpA Tryptophan Regulation of enzyme activity b Regulation of ID: 780404
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Slide1
Slide2Figure 18.2
Regulation
of gene
expression
Feedback
inhibition
Precursor
Genes that encode enzymes1, 2, and 3
Enzyme 1
Enzyme 2
Enzyme 3
trpE
trpD
trpC
trpB
trpA
Tryptophan
Regulation of enzymeactivity
(b) Regulation of enzymeproduction
–
–
Slide3Figure 18.3
DNA
Promoter Regulatory gene
trpR
3′
trp
operon
trp
promoter
Genes of operon
trpB
trpA
mRNA
5′
trpE
trpD
trpC
trp
operator
RNA
polymerase
Stop codon
Start codon
mRNA
5′
Protein
Inactive
trp
repressor
E
D
C
B
A
Polypeptide
subunits
that make
up enzymes
for tryptophan
synthesis
(a) Tryptophan absent, repressor inactive, operon on.
DNA
trpR
3′
trpE
No
RNA
made
mRNA
5′
Protein
Active
trp
repressor
Tryptophan
(
corepressor
)
(b) Tryptophan present, repressor active, operon off.
Slide4Figure 18.3a
Polypeptide
subunits
that make
up enzymes
for tryptophan
synthesis
DNA
Promoter Regulatory gene
trpR
3′
trp
operon
trp
promoter
Genes of operon
trpB
trpA
mRNA
5′
trpE
trpD
trpC
trp
operator
RNA
polymerase
Stop codon
Start codon
mRNA
5′
Protein
Inactive
trp
repressor
E
D
C
B
A
(a) Tryptophan absent, repressor inactive, operon on.
Slide5Figure 18.3b
DNA
trpR
3′
trpE
No
RNA
made
mRNA
5′
Protein
Active
trp
repressor
Tryptophan
(
corepressor
)
(b) Tryptophan present, repressor active, operon off.
Slide6Figure 18.4
Regulatory
gene
DNA
lac
I
3′
5′
Promoter
Operator
lacZ
No
RNA
made
mRNA
RNA
polymerase
Active
repressor
lac
operon
lac
I
lacZ
RNA
polymerase
3′
mRNA 5′
lacY
Stop codon
lacA
Protein
(a) Lactose absent, repressor active, operon off.
DNA
mRNA
5′
Protein
Allolactose
(inducer)
β
-
Galactosidase
Permease
Transacetylase
Inactive
lac
repressor
Enzymes for using lactose
(b) Lactose present, repressor inactive, operon on.
Start
codon
Slide7Figure 18.4a
DNA
Regulatory
gene
lac
I
3′
5′
Promoter
Operator
lacZ
No
RNA
made
RNA
polymerase
Active
repressor
mRNA
Protein
(a) Lactose absent, repressor active, operon off.
Slide8Figure 18.4b
lac
operon
DNA
lac
I
3′
5′
RNA polymerase
mRNA 5′
lacZ
lacY
lacA
Start
codon
mRNA
Protein
Inactive
lac
repressor
β
-
Galactosidase
Permease
Transacetylase
Allolactose
(inducer)
Enzymes for using lactose
(b) Lactose present, repressor inactive, operon on.
Stop
codon
Slide9Figure 18.5
Promoter
DNA
lac
I
CRP-binding site
cAMP
Active
CRP
Inactive
CRP
Allolactose
Operator
lacZ
RNA
polymerase
binds and
transcribes
Inactive
lac
repressor
(a) Lactose present, glucose scarce (
cAMP
level high):
abundant
lac
mRNA synthesized.
DNA
lac
I
CRP-binding site
RNA polymerase
less likely to bind
Inactive
CRP
Inactive
lac
repressor
Promoter
Operator
lacZ
(b) Lactose present, glucose present (
cAMP
level low):
little
lac
mRNA synthesized.
Slide10Figure 18.5a
Promoter
DNA
lac
I
CRP-binding site
cAMP
Active
CRP
Operator
lacZ
RNA
polymerase
binds and
transcribes
Inactive
lac
repressor
Inactive
CRP
Allolactose
(a) Lactose present, glucose scarce (
cAMP
level high):
abundant
lac
mRNA synthesized.
Slide11Figure 18.5b
DNA
lac
I
CRP-binding site
Promoter
Operator
lacZ
RNA polymerase
less likely to bind
Inactive
CRP
Inactive
lac
repressor
(b) Lactose present, glucose present (
cAMP
level low):
little
lac
mRNA synthesized.
Slide12Figure 18.6
Signal
Chromatin
Chromatin
modification:
DNA unpacking
DNA
Gene available for transcription
RNA
Cap
NUCLEUS
CYTOPLASM
Degradation
of mRNA
RNA processing
Tail
mRNA in
nucleus
Transport
to cytoplasm
Transcription
Exon
Primary
transcript
Intron
mRNA in
cytoplasm
Translation
Polypeptide
Protein processing
Active protein
Transport to cellular
destination
Cellular function
(such as enzymatic
activity or structural
support)
Degradation
of protein
Slide13Figure 18.6a
Signal
Chromatin
Chromatin
modification:
DNA unpacking
DNA
Gene available for transcription
Transcription
Exon
RNA
Primary
transcript
Intron
RNA processing
Tail
mRNA in
nucleus
Cap
Transport
to cytoplasm
NUCLEUS
CYTOPLASM
Slide14Figure 18.6b
CYTOPLASM
Degradation
of mRNA
mRNA in
cytoplasm
Translation
Polypeptide
Protein processing
Degradation
of protein
Active protein
Transport to cellular
destination
Cellular function
(such as enzymatic
activity or structural
support)
Slide15Figure 18.7
Unacetylated histone tails
Histone
tails
Amino acids
available
for chemical
modification
Nucleosome
(end view)
(a) Histone tails protrude outward
from a nucleosome.
DNA double
helix
Acetylated
histone
tails
Nucleosome
DNA
Acetylation
DNA
Compact: DNA not
accessible for transcription
Looser: DNA accessible
for transcription
(b) Acetylation of histone tails promotes loose chromatin
structure that permits transcription.
Slide16Figure 18.8
Enhancer (group of
distal control elements)
DNA
Upstream
Proximal
control elements
Transcription
start
site
Exon
Intron
Exon
Poly-A signal
sequence
Transcription
termination
region
Intron
Exon
Downstream
Poly-A
signal
Exon
Cleaved 3′ end
of primary
transcript
Promoter
Primary RNA
transcript
(pre-mRNA)
5′
Exon
Intron
Transcription
Exon
Intron
RNA
processing
Intron RNA
Coding segment
mRNA
G
P
P
P
5′ UTR
Start
codon
Stop
codon
3′ UTR
AAA
··
·
AAA
3′
5′ Cap
Poly-A
tail
Slide17Figure 18.8a
Enhancer (group of
distal control elements)
DNA
Upstream
Proximal
control elements
Transcription
start site
Exon
Intron
Exon
Poly-A signal
sequence
Transcription
termination
region
Intron
Exon
Downstream
Promoter
Slide18Figure 18.8b_1
Proximal
control elements
Transcription
start
site
DNA
Promoter
Exon
Intron
Exon
Poly-A signal
sequence
Intron
Exon
Slide19Figure 18.8b_2
Proximal
control elements
Transcription
start
site
DNA
Promoter
Primary RNA
transcript
(pre-mRNA)
5′
Exon
Intron
Exon
Intron
Exon
Poly-A signal
sequence
Intron
Exon
Transcription
Poly-A
signal
Exon
Intron
Exon
Cleaved 3′
end of
primary
transcript
Slide20Figure 18.8b_3
Proximal
control elements
Transcription
start
site
DNA
Promoter
Primary RNA
transcript
(pre-mRNA)
5′
Exon
Intron
Exon
Intron
Exon
Poly-A signal
sequence
Intron
Exon
Transcription
Poly-A
signal
Exon
Intron
Exon
RNA processing
Cleaved 3′
end of
primary
transcript
Intron RNA
Coding segment
mRNA
G
P
P
P
AAA
··
·
AAA
3′
5′
Cap
Start
codon
3′
UTR
Poly-A
tail
5
′ UTR
Stop
codon
Slide21Figure 18.10_2
DNA
Activators
Distal control
element
Promoter
Gene
Enhancer
TATA
box
General transcription
factors
DNA-bending
protein
Group of
mediator proteins
Slide22Figure 18.10_3
DNA
Activators
Distal control
element
Promoter
Gene
Enhancer
TATA
box
General transcription
factors
DNA-bending
protein
Group of
mediator proteins
RNA
polymerase
II
RNA
polymerase
II
Transcription
initiation complex
RNA synthesis
Slide23Figure 18.11
DNA in both
cells
(activators
not shown)
Control
elements
Enhancer for
albumin gene
Promoter
Albumin gene
Enhancer for
crystallin gene
Promoter
Crystallin gene
Liver cell
Liver cell
nucleus
DNA in liver cell
Available
activators
DNA in lens cell
Lens cell
Lens cell
nucleus
Available
activators
Albumin gene not expressed
Albumin gene
expressed
Crystallin gene not expressed
Crystallin gene
expressed
Slide24Figure 18.11a
DNA in both
cells
(activators
not shown)
Control
elements
Enhancer for
albumin gene
Albumin
gene
Enhancer for
crystallin gene
Promoter
Crystallin
gene
Promoter
Slide25Figure 18.11b
DNA in liver cell
Liver cell
Liver cell
nucleus
Available
activators
Albumin gene
expressed
Crystallin
gene not expressed
Slide26Figure 18.11c
DNA in lens cell
Lens cell
Lens cell
nucleus
Available
activators
Albumin gene not expressed
Crystallin
gene
expressed
Slide27Figure 18.12
Chromosomes in the
interphase nucleus
(fluorescence micrograph)
Chromosome
territory
5
µ
m
Chromatin
loop
Transcription
factory
Slide28Figure 18.13
Exons
DNA
1
2
3
4
5
Troponin T gene
Primary
RNA
transcript
1
2
3
4
5
RNA splicing
mRNA
1
2
3
5
OR
1
2
4
5
Slide29Figure 18.14
miRNA
miRNA-
protein
complex
The
miRNA
binds to a target
mRNA
mRNA
OR
mRNA degraded
Translation blocked
If bases are complementary, mRNA is degraded (left); if
the match is less complete, translation is blocked (right).
1
2
Slide30Figure 18.15
RNA transcripts
(red) produced.
Yeast enzyme
synthesizes strands
complementary to RNA
transcripts.
Double-stranded RNA
processed into
siRNAs
that associate with proteins.
The
siRNA
-protein complexes bind
RNA transcripts and become
tethered to centromere region.
The
siRNA
-protein
complexes recruit
histone-modifying
enzymes.
Formation of
heterochromatin at
the centromere.
Centromeric
DNA
RNA
polymerase
RNA
transcript
Sister
chromatids
(two DNA
molecules)
siRNA
-protein
complex
Centromeric DNA
Heterochromatin atthe centromere region
Chromatin-modifyingenzymes
1
2
3
4
5
6
Slide31Figure 18.15a
Centromeric DNA
RNA transcripts
(red) produced.
Yeast enzyme
synthesizes strands
complementary to RNA
transcripts.
RNA
polymerase
RNA
transcript
Sister
chromatids
(two DNA
molecules)
Double-stranded RNA
processed into
siRNAs
that associate with proteins.
The
siRNA
-protein complexes bind
RNA transcripts and become
tethered to centromere region.
siRNA-protein
complex
1
2
3
4
Slide32Figure 18.15b
The
siRNA
-protein
complexes recruit
histone-modifying
enzymes.
Centromeric
DNA
Formation of
heterochromatin at
the centromere.
Heterochromatin at
the centromere region
Chromatin-
modifying
enzymes
5
6
Slide33Myoblasts are cells determined to form muscle cells and produce large amounts of muscle-specific proteins
MyoD
is a
“master regulatory gene” that encodes a transcription factor that commits the cell to becoming skeletal muscle
Some target genes for MyoD (protein) encode additional muscle-specific transcription factors© 2017 Pearson Education, Inc.
Slide34Figure 18.18_2
Myoblast
(determined)
MyoD
protein
(transcription factor)
mRNA
OFFOFF
OFF
DNA
Embryonic
precursor cell
Nucleus
Master regulatory gene myoD
Other muscle-specific genes
Slide35Figure 18.23
Proto-oncogene
Proto-oncogene
Proto-oncogene
Translocation or
transposition: gene
moved to new locus,
under new controls
Gene amplification:
multiple copies of the gene
Point mutation
within a control element
Point mutation
within the gene
New
promoter
Oncogene
Oncogene
Oncogene
Normal growth-
stimulating
protein in excess
Normal growth-stimulating
protein in excess
Normal growth-
stimulating protein
in excess
Hyperactive or
degradation-
resistant protein
Slide36Figure 18.23a
Proto-oncogene
Translocation or
transposition:
gene moved to new
locus, under new
controls
New
promoter
Oncogene
Normal growth-
stimulating protein
in excess
Slide37Figure 18.23b
Proto-oncogene
Gene amplification:
multiple copies of the gene
Normal growth-stimulating
protein in excess
Slide38Figure 18.23c
Proto-oncogene
Point mutation
within a control element
Point mutation
within the gene
Oncogene
Oncogene
Normal growth-
stimulating protein
in excess
Hyperactive or
degradation-
resistant protein
Slide39Figure 18.24
P
P
P
P
P
P
GTP
GTP
Growth
factor
G
protein
Transcription
factor (activator)
Protein
kinases
Receptor
Ras
NUCLEUS
Protein that
stimulates
the cell cycle
Normal cell
division
(a) Normal cell cycle–stimulating pathway.
MUTATION
Ras
Overexpression
of protein
NUCLEUS
Transcription
factor (activator)
Ras protein active with or
without growth factor.
Increased cell
division
(b) Mutant cell cycle–stimulating pathway.
3
4
5
6
2
1
Slide40Figure 18.24a
P
P
P
P
P
P
Growth
factor
G
protein
Protein that
stimulates
the cell cycle
Ras
NUCLEUS
Transcription
factor (activator)
Receptor
Normal cell
division
(a) Normal cell cycle–stimulating pathway.
GTP
Protein
kinases
1
3
4
2
5
6
Slide41Figure 18.24b
MUTATION
Ras
GTP
Overexpression
of protein
NUCLEUS
Transcription
factor (activator)
Increased cell
division
Ras protein active with or
without growth factor.
(b) Mutant cell cycle–stimulating pathway.
Slide42Figure 18.25
Protein
kinases
Protein that
inhibits the
cell cycle
DNA damage
in genome
Active form
of p53
Transcription
Damaged DNA
is not replicated.
NUCLEUS
UV
light
No cell
division
(a) Normal cell cycle–inhibiting pathway
UV
light
DNA damage
in genome
MUTATION
Defective or
missing
transcription
factor
Inhibitory
protein
absent
Cell cycle is
not inhibited.
Increased
cell division
(b) Mutant cell cycle–inhibiting pathway
2
1
3
4
5
Slide43Figure 18.25a
Protein
kinases
Protein that
inhibits the
cell cycle
DNA damage
in genome
Active form
of p53
Transcription
Damaged DNA
is not replicated.
NUCLEUS
UV
light
No cell
division
(a) Normal cell cycle–inhibiting pathway
2
1
3
4
5
Slide44Figure 18.25b
UV
light
DNA damage
in genome
MUTATION
Defective or
missing
transcription
factor
Inhibitory
protein
absent
Cell cycle is
not inhibited.
Increased
cell division
(b) Mutant cell cycle–inhibiting pathway