Epigenetics:
Gespeichert in:
| 1. Verfasser: | |
|---|---|
| Format: | Buch |
| Sprache: | English |
| Veröffentlicht: |
New York [u.a.]
Garland Science
2014
|
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis Klappentext |
| Beschreibung: | XII, 306 S. Ill., graph. Darst. |
| ISBN: | 9780815365112 |
Internformat
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| 245 | 1 | 0 | |a Epigenetics |c Lyle Armstrong |
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Datensatz im Suchindex
| _version_ | 1804150654560632832 |
|---|---|
| adam_text | Contents
CHAPTER
1
INTRODUCTION TO
THE STUDY OF EPIGENETICS
1.1
THE CORE ISSUE: CONTROLLING THE
EXPRESSION OF SPECIFIC GENES
1.2
DEFINING EPIGENETICS
1.3
THE NATURE OF EPIGENETIC MARKS
1.4
THE IMPORTANCE OF EPIGENETICS
FURTHER READING
CHAPTER
2
THE BASIS OF THE
TRANSCRIPTION PROCESS
2.1
THE NEED FOR SPECIFICITY
2.2
PROMOTERS AND THEIR TATA
BOXES
2.3
ASSEMBLY OF THE PRE-INITIATION
COMPLEX
2.4
INITIATION OF TRANSCRIPTION
KEY CONCEPTS
FURTHER READING
CHAPTER
3 DNA
PACKAGING
AND CHROMATIN ARCHITECTURE
3.1
NUCLEOSOME STRUCTURE AND
CHROMATIN
Chromatin consists of
DNA
plus many
proteins
The nucleosome is the basic unit of
chromatin
DNA
binds to the histone octamer
3.2
CHROMATIN ARCHITECTURE
21
Chains of nucleosomes organize into
chromatin fibers
21
1
Chromatin fibers are further organized
into euchromatin and heterochromatin
23
1
2
A variety of mechanisms are involved in
compacting chromatin beyond the
30
nm
fiber stage
24
2
Chromatin compaction restricts access
to the information content of
DNA
26
4
KEY CONCEPTS
26
FURTHER READING
27
8
10
11
12
12
15
15
16
17
CHAPTER
4
MODIFYING THE
STRUCTURE OF CHROMATIN
4.1
CHROMATIN REMODELING
29
Chromatin remodeling transiently
exposes
DNA
to binding proteins
29
Chromatin remodeling is mediated by
the SWI/SNF family of proteins in
eukaryotes
30
Chromatin remodeling by SWI/SNF works
by repositioning nucleosomes
31
Transcription factor binding sites are
often located in regions of low
nucleosome occupancy
32
4.2
CHROMATIN MODIFICATION
33
Spontaneous conformational changes and
covalent modifications can also expose
DNA
to transcription factors
33
Epigenetic modification of
DNA
or
histones regulates nucleosome occupancy
and repositioning
35
KEY CONCEPTS
37
FURTHER READING
37
VIII
CONTENTS
CHAPTERS
DNA
METHYLATION
5.1
PATTERNS OF
DNA
METHYLATION
39
CpG-rich islands are infrequently
methylated
40
CpG-poor islands are frequently
methylated
40
5.2
EFFECTS OF
DNA
METHYLATION ON
TRANSCRIPTION
42
Proteins controlling cellular function
interact with methylated
DNA 42
Transcription factors and
methylated-DNA-binding proteins can
repress transcription
44
5.3
THE MOLECULES THAT METHYLATE
DNA 45
De novo
methylation of cytosine
establishes the methylation pattern
45
Existing patterns of
DNA
methylation
are maintained
47
5.4 DNA METHYLTRANSFERASE
ACTIVITY
48
Enzyme activity can be controlled by
small molecules in vivo
48
DNA methyltransferase
activity can be
controlled transcriptionally
49
5.5
METHYLATION REGULATION AT
SPECIFIC GENE LOCI
51
Histone interaction with
DNA
methyltransferases affects where
DNA
is methylated
51
Transcription factors may control
DNA
methyltransferases
52
Noncoding
RNA
may control
DNA
methyltransferases
53
Noncoding
RNA
can influence chromatin
regulation directly
55
5.6
GENOME FUNCTION CONTROL
ACROSS SPECIES
56
KEY CONCEPTS
57
FURTHER READING
57
CHAPTER
6
POST-TRANSLATIONAL
MODIFICATION OF HISTONES
6.1
ACETYLATION AND METHYLATION
OF
LYSINE
60
Lysine
is often acetylated in histone tails
Proteins with bromodomains recognize
and bind to acetylated histones
The multiple methylation states of
lysine
can alter transcriptional response
6.2
PHOSPHORYLATION OF
SERINE
AND
THREONINE
6.3
ADDITION OF UBIQUITIN TO SPECIFIC
LYSINES
6.4
SUMOYLATION OF LYSINES
6.5
BIOTINYLATION OF HISTONES
6.6
ADP-RIBOSYLATION OF HISTONES
6.7
THE HISTONE CODE HYPOTHESIS
KEY CONCEPTS
FURTHER READING
CHAPTER
7
HISTONE
MODIFICATION MACHINERY
7.1
ENZYMES THAT ACETYLATE OR
DEACETYLATE HISTONES
Acetyl
groups are added by a class of
enzymes known as histone
acetyltransferases
Histone acetyltransferases add
acetyl
groups to specific
lysine
residues
Histone deacetylase enzymes remove
acetyl
groups from histone
lysine
residues
7.2
ENZYMES THAT METHYLATE
OR DEMETHYLATE HISTONES
The histone methyltransferases add
methyl groups to histone residues
The SET domain
SET
7/9
EZH2
Human SET domain proteins
MLL-family proteins
Non-SET-dependent methyltransferases
The histone arginyl methyltransferases
Histone methylation is reversible using
histone demetfiyiases
Lysine-specific demethylase
1
Demethylating trimethylated
lysine
4
on H3
Demethylating methylated
arginine
61
62
63
65
66
68
69
71
71
73
73
77
77
77
80
80
80
83
83
85
85
86
87
87
90
90
93
93
CONTENTS
IX
7.3
ENZYMES
THAT PHOSPHORYLATE
OR DEPHOSPHORYLATE HISTONES
Kinases catalyze the phosphorylation of
specific
amino
acids on histones
A variety of
serine
kinases phosphorylate
serine
10
on histone H3
Ribosomal S6 kinases
MSK1and MSK2
Aurora kinases
MST1 kinase phosphorylates
ser
14
on
histone H2B
Histone phosphatases remove phosphates
from histone residues
7.4
ENZYMES THAT ADD AND REMOVE
UBIQUITIN ON HISTONES
E3 ubiquitin
ligases
add ubiquitin to
lysine
A variety of enzymes remove ubiquitin
from
lysine
7.5
ENZYMES THAT ADD AND REMOVE
THE SUMO GROUP ON HISTONES
E3
SUMO ligases
add the SUMO group to
lysine
SUMO-specific proteases remove the
SUMO group from
lysine
7.6
ENZYMES THAT ADD AND REMOVE
BIOTIN ON HISTONES
Biotinidase and biotin holocarboxylase
synthetase can biotinylate histones
Enzymes that remove biotin from histone
lysine
residues
KEY CONCEPTS
FURTHER READING
CHAPTER
8
LOCUS-SPECIFIC
CONTROL OF HISTONE-MODIFYING
ENZYME ACTION
8 1
HISTONE ACETYLATION AND
DEACETYLATION AS A PROTEIN
COMPLEX ACTIVITY
NURD is a well-known deacetylation
complex
109
SIN3A acts as a scaffold on which
repressor
proteins may assemble
110
Protein complexes containing histone
acetyltransferases promote transcription
112
8.2
COMPLEXES OF THE HISTONE
96
METHYLTRANSFERASES
115
8.3
KINASE COMPLEXES FOR HISTONE
PHOSPHORYLATION
118
98
8.4
COORDINATION AMONG
98
CHROMATIN-MODIFYING
98
COMPLEXES
119
99
HDAC complexes respond to other
histone modifications
119
99
Noncoding
RNA
can regulate
histone-mocfifying complexes
119
100
Polycomb and trithorax are examples
of chromatin activator and
repressor
102
complexes controlled by noncoding
RNA
120
KEY CONCEPTS
125
102
FURTHER READING
125
102
CHAPTER
9
EPIGENETIC
103
CONTROL OF CELL-SPECIFIC
103
GENE EXPRESSION
9.1
EPIGENETIC CONTROL OF
104
CHROMOSOME ARCHITECTURE
129
The position of
dna
within separate
subnuclear compartments reflects the
104
expression or repression of genes
129
The nuclear skeleton is central to
104
subnucfear organization
131
105
9.2
SPATIAL ORGANIZATION OF GENE
TRANSCRIPTION IN THE NUCLEUS
132
106
The nucleolus is formed from multiple
107
chromatin loops
132
lu/
rRNA genes are clustered for transcription
in the nucleus
133
rRNA gene structure
134
f*
Regulation of rRNA gene transcription
134
G
Proteins that protect or target rDNA for
methylation and demethylation
136
Genes transcribed by
RNA
polymerase II
show a different organization
137
109
Transcription factories may be
semi-permanent structures
139
9.3
THE EPIGENETIC CONTRIBUTION TO
TRANSCRIPTION FACTORY
ORGANIZATION
140
The
ß-globin
locus control region is
subj ect to epigeneti
с
control
140
CONTENTS
The
НОХ
clusters are also subject to
epigenetic control of gene expression
142
RARES
occur in open-chromatin regions
144
HOX gene expression levels
146
KEY CONCEPTS
147
FURTHER READING
147
Genes of progenitor germ cells undergo
two rounds of demethylation
165
11.4
THE NEED FOR IMPRINTING
168
KEY CONCEPTS
169
FURTHER READING
169
CHAPTER
10
EPIGENETIC
CONTROL OF THE MITOTIC
CELL CYCLE
10.1
S
PHASE INVOLVES
DNA
REPLICATION
149
10.2
THE CELL DIVIDES IN
M
PHASE
153
KEY CONCEPTS
154
FURTHER READING
155
CHAPTER
11
THE EPIGENETIC
BASIS OF GENE IMPRINTING
11.1
CONTROLLING MONOALLELIC
EXPRESSION OF IMPRINTED GENES
157
imprinted genes share few characteristics
in common
157
imprinting control regions OCRs) regulate
the imprinted expression of genes
158
Differentially methylated regions contain
imprinting signals
159
Chromatin modifications at DMR sites
affect gene imprinting
159
11.2
EXAMPLES OF IMPRINTING
160
The imprinting of IGF2/H19 is well
documented I60
Binding of CTCF at the IGF2/H19 imprint
control region to an insulator mechanism
to control imprinted gene expression 16I
The mechanism by which insulation occurs
is uncertain
162
There are other examples of imprinting on
the same stretch of
DNA 163
11.3
ESTABLISHING DIFFERENTIALLY
METHYLATED REGIONS
164
Most genes undergo demethylation after
fertilization
164
Imprinted genes retain their
DNA
methylation patterns at their DMRs during
fertilization
165
CHAPTER
12
EPIGENETIC
CONTROL OF CELLULAR
DIFFERENTIATION
12.1
FROM CELLULAR TOTIPOTENCY TO
PLURIPOTENCY
171
12.2
MAINTENANCE OF PLURIPOTENCY
IN EMBRYONIC STEM CELLS
173
12.3
DIFFERENTIATION OF EMBRYONIC
STEM CELLS
174
12.4
BIVALENT CHROMATIN DOMAINS
IN NEURAL STEM CELLS
176
12.5
CHROMATIN PROFILE OF
HEMATOPOIETIC PROGENITORS
177
KEY CONCEPTS
178
FURTHER READING
179
CHAPTER
13
REVERSIBILITY
OF EPIGENETIC MODIFICATION
PATTERNS
13.1
REPROGRAMMING THE
EPIGENOME
BY SOMATIC CELL NUCLEAR
TRANSFER
182
What happens to the somatic genome
during SCNT?
Epigenetic modification is the basis of
SCNT reprogramming
185
Epigenetic reprogramming
¡s a
normal feature
of fertilization that is hijacked by SCNT
186
There are several possible mechanisms by
which the
somate
genome might be
remodeled in SCNT
183
187
The epigenetic remodeling that occurs in
SCNT differs from the remodeling that
occurs after fertilization
Some aspects of reprogramming of the
somatic epigenome are outside the
oocyte s capacity
189
190
CONTENTS Xi
Somatic gene expression must be turned
off for epigenetic reprogramming to occur
in SCNT embryos
191
13.2
REPROGRAMMING THE
EPIGENOME
BY CELL FUSION
192
Fusion of somatic cells with pluripotent
cells can
reprogram
the somatic genome
192
OCT4 is involved in genome reprogramming
in heterokaryons
194
There are several possible mechanisms by
which the OCT4/SOX2/NANOG trinity
of pluripotency factors may work to
reprogram
genomes
195
Reprogramming may not be the sole
purview of ESCs
196
13.3
REPROGRAMMING THE
EPIGENOME
BY CELL EXTRACTS
197
Cell extracts can effect epigenetic
reprogramming by providing the needed
regulatory factors
197
Cell extract reprogramming has the
potential to be clinically useful
198
13.4
REPROGRAMMING THE
EPIGENOME
BY INDUCED PLURIPOTENCY
199
Epigenetic reprogramming occurs during
iPSC derivation
201
Making iPSCs safe for clinical application
203
KEY CONCEPTS
204
FURTHER READING
205
chapter™ epigenetic
predisposition to disease and
imprinting-based disorders
14.1
PREDISPOSITION TO DISEASE
208
Life-course epidemiology seeks to explain
disease
208
Epigenetics may be the basis of stochastic
variation in disease
210
14.2
IMPRINTING-BASED DISORDERS
210
imprinting disorders can persist beyond
embryogenesis
211
Prader-Willi and
Angelman
syndromes
result from disruptions on chromosome
15 212
Beckwith-Wiedemann and Silver-Russell
syndromes are consequences of disruptions
of the/GF-H
7 9
locus
216
Assisted reproductive technologies may
increase the incidence of imprinting diseases
218
14.3
EPIGENETICS OF MAJOR DISEASE
GROUPS
219
Cardiovascular disease is the major killer
in high-income countries
219
The basic problem in cardiovascular disease
is atherosclerosis
220
Epigenetic events may promote
atherosclerosis by increasing known risk
factors
221
Epigenetics has a role in the regulation of
arterial hypertension
224
Hypertension increases with age
224
Cardiac hypertrophy and heart failure also
have an epigenetic component
227
Epigenetic drift may contribute to
cardiovascular disease
228
14.4
EPIGENETICS OF KIDNEY DISEASE
229
14.5
EPIGENETICS OF DIABETES
231
KEY CONCEPTS
233
FURTHER READING
234
CHAPTER
15
EPIGENETICS OF
MEMORY, NEURODEGENERATION,
AND MENTAL HEALTH
15.1
MEMORY
235
Memory formation relies on specific regions
of the brain
235
Structural changes and plasticity of
synapses could be the basis of long-term
memory
237
Epigenetic control of synaptic plasticity may
contribute to memory maintenance
237
15.2
EPIGENETIC INVOLVEMENT IN
NEURODEGENERATION
240
Epigenetic alterations may contribute to the
development of Alzheimer s disease
240
There is some evidence that epigenetic
mechanisms may contribute to Parkinson s
disease
243
15.3
THE IMPACT OF EPIGENETIC CONTROL
OF GENE EXPRESSION ON MENTAL
HEALTH
244
Disruption of epigenetic regulation may
explain some features of bipolar disorder
245
Xii CONTENTS
Epigenetic regulation is a factor in major
depressive disorder
15.4
SUMMARY
KEY CONCEPTS
FURTHER READING
CHAPTER
16
EPIGENETICS OF
CANCER
16.1
UNCONTROLLED CELL REPLICATION
Loss of control of tissue homeostasis is a
root cause of cancer
Tissue homeostasis requires cell death
Loss of control of cell division is also
known as cell transformation
Dysfunctional genes are the basis of
transformation
16.2
CHANGES LEADING TO NEOPLASTIC
TRANSFORMATION
Oncogenes and tumor suppressor genes
are often altered during cancer
progression
Genomic instability is a common trait of
cancer cells
Cancer cells frequently show major
disruption in their
DNA methylation
profiles
impairment of DNA-repair mechanisms
enhances cancer progression
16.3
ABNORMAL PATTERNS OF
DNA
METHYLATION IN CANCER
DNA hypermethylation
is typically
mediated by DNMT1
247
251
251
252
254
254
256
256
257
258
258
260
261
262
The mechanisms controlling
DNA
methylation are imperfect
Abnormal
DNA
hypomethylation contributes
to cancer formation and progression
Oxidative stress has additional effects
on epigenetic processes that impinge
on cancer
The influence of microRNA on
DNA
methylation in cancer
16.4
HISTONE MODIFICATION PATTERNS
AND CANCER
How does histone acetylation contribute
to tumorigenesis?
The HAT/HDAC balance requires
dysregulation of other factors
Histone methylation contributes to
tumorigenesis
16.5
EXAMPLES OF EPIGENETIC
DYSREGULATION LEADING TO
CANCER
Hematological malignancies such as
leukemia are good examples of epigenetic
dysregulation
DNA
hypermethylation and hypomethylation
contribute to the
leukemie
phenotype
How epigenetics contributes to lung
cancers
KEY CONCEPTS
FURTHER READING
263
GLOSSARY
263
INDEX
264
267
270
271
273
273
274
275
276
276
278
281
284
285
287
291
Epigenetics
by Lyle Armstrong provides a concise and unified view of
epigenetics, bringing together the structure and machinery of epigenetic
modification, how epigenetic modification influences cellular functions, and the
evidence for the relationship between epigenetics and disease. With full-color
figures throughout, Epigenetics is a valuable resource for graduate students
and researchers.
Lyle Armstrong is a Reader in Cellular Reprogramming at the Institute of
Genetic Medicine in Newcastle University where his research program
contributed to the derivation of some of the UK s first human embryonic stem
cell lines and the development of the world s first cloned human embryos.
He is now working on new methods to
reprogram
cells into medically useful
cells—epigenetics is the cornerstone of this reprogramming process.
Garland Science
Taylor
&
Francis Group
ISBN
978-08153-6511-2
|
| any_adam_object | 1 |
| author | Armstrong, Lyle |
| author_GND | (DE-588)1047028875 |
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| classification_rvk | WG 1900 |
| classification_tum | BIO 180f |
| ctrlnum | (OCoLC)869849486 (DE-599)OBVAC10721090 |
| discipline | Biologie |
| format | Book |
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| id | DE-604.BV041218624 |
| illustrated | Illustrated |
| indexdate | 2024-07-10T00:42:22Z |
| institution | BVB |
| isbn | 9780815365112 |
| language | English |
| oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-026193235 |
| oclc_num | 869849486 |
| open_access_boolean | |
| owner | DE-703 DE-20 DE-355 DE-BY-UBR DE-29T DE-91 DE-BY-TUM |
| owner_facet | DE-703 DE-20 DE-355 DE-BY-UBR DE-29T DE-91 DE-BY-TUM |
| physical | XII, 306 S. Ill., graph. Darst. |
| publishDate | 2014 |
| publishDateSearch | 2014 |
| publishDateSort | 2014 |
| publisher | Garland Science |
| record_format | marc |
| spelling | Armstrong, Lyle Verfasser (DE-588)1047028875 aut Epigenetics Lyle Armstrong New York [u.a.] Garland Science 2014 XII, 306 S. Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Epigenetik (DE-588)7566079-9 gnd rswk-swf Epigenetik (DE-588)7566079-9 s DE-604 Digitalisierung UB Bayreuth - ADAM Catalogue Enrichment application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=026193235&sequence=000003&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis Digitalisierung UB Bayreuth - ADAM Catalogue Enrichment application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=026193235&sequence=000004&line_number=0002&func_code=DB_RECORDS&service_type=MEDIA Klappentext |
| spellingShingle | Armstrong, Lyle Epigenetics Epigenetik (DE-588)7566079-9 gnd |
| subject_GND | (DE-588)7566079-9 |
| title | Epigenetics |
| title_auth | Epigenetics |
| title_exact_search | Epigenetics |
| title_full | Epigenetics Lyle Armstrong |
| title_fullStr | Epigenetics Lyle Armstrong |
| title_full_unstemmed | Epigenetics Lyle Armstrong |
| title_short | Epigenetics |
| title_sort | epigenetics |
| topic | Epigenetik (DE-588)7566079-9 gnd |
| topic_facet | Epigenetik |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=026193235&sequence=000003&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=026193235&sequence=000004&line_number=0002&func_code=DB_RECORDS&service_type=MEDIA |
| work_keys_str_mv | AT armstronglyle epigenetics |