The cell cycle: principles of control
The Cell Cycle: Principles of Control provides an engaging insight into the process of cell division, bringing to the student a much-needed synthesis of a subject entering a period of unprecedented growth as an understanding of the molecular mechanisms underlying cell division are revealed.
Gespeichert in:
| 1. Verfasser: | |
|---|---|
| Format: | Buch |
| Sprache: | English |
| Veröffentlicht: |
Oxford [u.a.]
Oxford Univ. Press
2007
|
| Schriftenreihe: | Primers in biology
|
| Schlagworte: | |
| Online-Zugang: | Abbildungen Inhaltsverzeichnis |
| Zusammenfassung: | The Cell Cycle: Principles of Control provides an engaging insight into the process of cell division, bringing to the student a much-needed synthesis of a subject entering a period of unprecedented growth as an understanding of the molecular mechanisms underlying cell division are revealed. |
| Beschreibung: | XXVII, 297 S. Ill., graph. Darst. |
| ISBN: | 0199206104 9780199206100 0953918122 9780953918126 0878935088 9780878935086 |
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| 100 | 1 | |a Morgan, David |d 1958- |e Verfasser |0 (DE-588)173873553 |4 aut | |
| 245 | 1 | 0 | |a The cell cycle |b principles of control |c David O. Morgan |
| 264 | 1 | |a Oxford [u.a.] |b Oxford Univ. Press |c 2007 | |
| 300 | |a XXVII, 297 S. |b Ill., graph. Darst. | ||
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| 338 | |b nc |2 rdacarrier | ||
| 490 | 0 | |a Primers in biology | |
| 520 | |a The Cell Cycle: Principles of Control provides an engaging insight into the process of cell division, bringing to the student a much-needed synthesis of a subject entering a period of unprecedented growth as an understanding of the molecular mechanisms underlying cell division are revealed. | ||
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| 856 | 4 | |u http://www.new-science-press.com/browse/cellcycle/resources |z Abbildungen | |
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Datensatz im Suchindex
| _version_ | 1804135473956782081 |
|---|---|
| adam_text | Contents in
The Author v
A Note from the Publisher on Primers in Biology
Preface
Acknowledgements
CHAPTER
1-0
Cell reproduction is a fundamental feature of all living things
Cells reproduce in discrete steps
The ordering of cell-cycle events is governed by an independent control
system
1-1
Chromosome duplication and segregation occur in distinct cell-cycle phases
that are usually separated by gap phases
Cytoplasmic components are duplicated throughout the cell cycle
Cell growth is usually coordinated with cell division
1-2
Cell-cycle structure varies in different cells and organisms
Multiple rounds of chromosome duplication or segregation can occur in the
same cell cycle
The symmetry of cell division varies in different cell types
1-3
Cell-cycle events are governed by an independent control system
The cell-cycle control system is based on oscillations in the activities of
cyclin-dependent protein kinases
Cell-cycle events are initiated at three regulatory checkpoints
Cell-cycle progression in most cells can be blocked at checkpoints
CHAPTER
2-0
Mechanisms of cell-cycle control are similar in all eukaryotes
Budding and fission yeasts provide powerful systems for the genetic
analysis of eukaryotic cell-cycle control
Early animal embryos are useful for the biochemical characterization of
simple cell cycles
Control of cell division in multicellular organisms can be dissected
genetically in Drosophila
Cultured cell lines provide a means of analyzing cell-cycle control in
mammals
2-1
Budding yeast and fission yeast divide by different mechanisms
Yeast cells alternate between haploid and diploid states and undergo
sporulation
2-2
Cell biological processes are readily dissected with yeast genetic methods
Conditional mutants are used to analyze essential cell-cycle processes
Homologous genes have different names in fission yeast and budding yeast
2-3
The early embryonic divisions of Xenopus provide a simplified system for
cell-cycle analysis
Unfertilized eggs develop from dipioid oocytes by meiosis
The early embryonic cell cycle can be reconstituted in a test tube
2-4
Drosophila allows genetic analysis of cell-cycle control in metazoans
Cells of the early Drosophila embryo divide by a simplified cell cycle
Gap phases are introduced in late embryogenesis
xviii
Adult fly structures develop from
2-5
Mammalian cell-cycle control can be analyzed in cells growing in culture
Mutations lead to immortalization and transformation of mammalian cells
Specific gene disruption is the ¡deal approach for assessing protein function
in mammalian cells
2-6
Cell-cycle position can be assessed by many approaches
Cell populations can be synchronized at specific cell-cycle stages
Complete understanding of cell-cycle control mechanisms requires the
analysis of protein structure and enzymatic behavior
CHAPTER
3-0
The cell-cycle control system is a complex assembly of oscillating protein
kinase activities
Multiple regulatory mechanisms govern Cdk activity during the cell cycle
The cell-cycle control system generates robust, switch-like and adaptable
changes in Cdk activity
3-1
The cyclin-dependent kinases are a small family of enzymes that require
cyclin subunits for activity
The active site of cyclin-dependent kinases is blocked in the absence of
cyclin
3-2
Cyclins are the key determinants of Cdk activity and can be classified in four
groups
Cyclins contain a conserved helical core
3-3
Full Cdk activity requires phosphorylation by the Cdk-activating kinase
Cdk function is regulated by inhibitory phosphorylation by Wee1 and
dephosphorylation by Cdc25
3-4
The conformation of the Cdk active site is dramatically rearranged by cyclin
binding and phosphorylation by
3-5
Cyclins are specialized for particular functions
Cyclins can interact directly with the substrates of the associated Cdk
Cyclins can direct the associated Cdk to specific subcellular locations
Cks1 may serve as an adaptor protein that targets Cdks to phosphoproteins
3-6
Cdk inhibitors help suppress Cdk activity in G1
Cip/Kip
G1-Cdks are activated by
3-7
Components of the cell-cycle control system are assembled into biochemical
switches
Switch-like behavior can be generated by various mechanisms
Bistability is required for an effective binary switch
3-8
Cdk1 activation at mitosis is based on positive feedback
Cdk switches are robust as a result of multiple partly redundant mechanisms
3-9
Many cell-cycle regulators are destroyed by ubiquitin-dependent proteolysis
SCF catalyzes ubiquitination of phosphorylated substrates using
interchangeable substrate-targeting subunits
3-10
The APC initiates anaphase and mitotic exit
Cdc20 activates the APC in anaphase
APC activity is maintained in G1 by Cdh1
APC targets contain specific recognition sequences
xix
3-11
Negative feedback can generate a repeating oscillator
Regulated braking mechanisms allow the Cdk oscillator to be paused in G1
3-12
A sequential program of gene expression contributes to cell-cycle control
Expression of a large fraction of the genes in the yeast genome is regulated
during the cell cycle
Key gene regulatory proteins in yeast are activated at the major cell-cycle
transitions
The E2F family controls cell-cycle-dependent changes in gene expression in
metazoans
3-13
The order of cell-cycle events is determined by regulatory interactions
between multiple oscillators
The cell-cycle control system is responsive to many external inputs
CHAPTER
4-0
DNA
The cell-cycle control system activates replication origins only once in each
S
Chromosome duplication requires duplication of chromatin structure
4-1
The two strands of
DNA
Discontinuous
Telomerase synthesizes
4-2
Replication origins in budding yeast contain well defined
Replication origins in animal chromosomes are defined by several factors in
addition to
4-3
The replication origin interacts with a multisubunit protein complex
The ORC and accessory proteins load the Mem
Mem loading involves ATP-dependent protein remodeling
4-4
Assembly of
mechanisms
Prereplicative
result of Cdk activity
Pre-RC assembly is controlled in animals by both Cdks and the APC
4-5
Cdks and Cdc7 trigger the initiation of
In budding yeast, the cyclins Clb5 and Clb6 are key activators of replication
origins
Yeast cells lacking
4-6
Different cyclins control initiation of
animal development
Cyclin A is a major regulator of replication initiation in cultured mammalian
cells
DNA
Cyclin E-Cdk2 is a major regulator of
4-7
Cdc7 triggers the activation of replication origins
Cdc7 is activated during
Dbf4 levels are regulated by multiple mechanisms
4-8
Replication begins with
Late-firing origins are regulated independently
XX
Replication must be completed before chromosome segregation occurs
4-9
Chromatin is complex and dynamic
The basic unit of chromatin structure is the nucleosome
Higher-order chromatin structure is also controlled by non-histone proteins,
histone H1 and histone modifications
4-10
Histone synthesis rises sharply during
Transcription of histone genes increases in
Histone mRNA processing and stability increase in
The level of free histones in the cell acts as a signal to link histone synthesis
to
4-11
Nucleosomes are distributed to both new
replication fork
Nucleosome assembly factors load histones on nascent
4-12
Heterochromatin is inherited by epigenetic mechanisms
Telomeres are packaged in a heritable heterochromatin structure
The centromere nucleates a heritable and poorly understood form of
heterochromatin
4-13
Duplication of heterochromatin structure involves proteins that recognize
and promote localized histone modification
The Sir proteins form a heritable polymer at telomeres in budding yeast
HP1 may nucleate heritable chromatin structure at the centromere and other
regions
Sister-chromatid cohesion in
CHAPTER
5-0
The central events of mitosis are sister-chromatid separation and
segregation
The events of early mitosis set the stage for sister-chromatid segregation
The completion of mitosis begins with sister-chromatid segregation
5-1
Phosphorylation and proteolysis control progression through mitosis
Mitotic events must go to completion
Mitotic entry and exit are major regulatory transitions with differing
importance in different species
5-2
Cyclin-Cdk complexes trigger mitotic entry in all eukaryotes
Fission yeast cells trigger mitosis with a single mitotic cyclin
Two pairs of mitotic cyclins control budding yeast mitosis
5-3
Mitosis in metazoans is governed by cyclins A and
Vertebrate mitosis is driven by multiple forms of cyclins A and
The active cyclin Bi-Cdki complex moves from cytoplasm to nucleus in late
prophase
Vertebrate cyclins A and
5-4
Cyclin B-Cdk1 complexes are activated rapidly in early
dephosphorylation
Multiple Wee1-related kinases and
activity in animal cells
5-5
Mitotic Cdk1 activation involves multiple positive feedback loops
Cdc25B and cyclin A-Cdk help trigger cyclin B-Cdki activation
5-6
Cyclin Bi-Cdki is regulated by changes in its subcellular localization
XXI
Cyclin Bi-Cdki
Cdc25C localization is regulated by phosphorylation
Cyclin Bi-Cdki activation and nuclear accumulation are partly interdependent
5-7
Polo-like kinases (Plks) heip control spindle assembly and mitotic exit
Spindle function and sister-chromatid segregation are controlled in part by
aurora kinases
5-8
Sister chromatids are held together by two mechanisms
Cohesin is a key mediator of sister-chromatid cohesion
Cohesion is established during
DNA
5-9
Chromosomes are dramatically reorganized in mitosis
Condensin complexes drive chromosome condensation and resolution
5-10
Mitotic Cdks act on condensin to govern the timing of chromosome
condensation
Sister-chromatid resolution is governed by
CHAPTER
6-0
Chromosome segregation depends on the mitotic spindle
The mitotic spindle must be bipolar
Multiple mechanisms drive spindle assembly
6-1
Microtubules are polymers of tubulin subunits
Microtubules exhibit dynamic instability
6-2
Cellular microtubules originate on preformed protein complexes that are
usually concentrated in a microtubule-organizing center
Microtubule dynamics are governed by a variety of stabilizing and
destabilizing proteins
Motor proteins move along microtubules
6-3
The centrosome cycle resembles the chromosome cycle
Centrosome behavior is determined by the centrioles
The yeast spindle pole body is embedded in the nuclear envelope
6-4
Duplication of the centrosome and spindle pole body is initiated in late G1
byGI/S-Cdks
Centrosome duplication normally occurs once per cell cycle
6-5
The kinetochore is the major site of microtubule-chromosome attachment
The kinetochore provides a stable attachment to a dynamic microtubule plus
end
6-6
Spindle assembly begins in
Mitotic microtubules are highly dynamic
Centrosome separation initiates spindle assembly
Centrosome maturation increases microtubule nucleation in mitosis
6-7
The nuclear envelope is composed of two membranes on an underlying
protein support
Nuclear envelope breakdown begins at nuclear pores
The endoplasmic reticulum and Golgi apparatus are reorganized in mitosis
6-8
Spindles self-organize around chromosomes
Microtubules can be stabilized by a gradient of Ran-GTP around
chromosomes
XXII
6-9 Attachment
Centrosomes search for and capture kinetochores in prometaphase
Some kinetochore microtubules originate at the kinetochore
Chromosome attachment results in tension between sister kinetochores
6-10
Kinetochore-microtubule attachment is stabilized by tension
Aurora
Merotelic attachments are processed by multiple mechanisms
6-11
Multiple forces act on chromosomes in the spindle
The kinetochore
Microtubule flux generates poleward force
A polar ejection force is generated by chromosome arms
6-12
Chromosome oscillations in prometaphase are generated by changes in the
state of kinetochores
Microtubule flux may promote chromosome
CHAPTER
7-0
The final events of mitosis occur in anaphase and telophase
The metaphase-to-anaphase transition is initiated by ubiquitination and
destruction of regulatory proteins
Dephosphorylation of Cdk targets drives the events of late
APCcdc20 initiates Cdk inactivation
7-1
дрсСсісго
Phosphorylation promotes APC0*20 activation in early mitosis
7-2
Unattached kinetochores generate a signal that prevents anaphase
The spindle checkpoint monitors defects in microtubule attachment and
kinetochore tension
7-3
Unattached kinetochores catalyze the formation of inhibitory signaling
complexes
The spindle checkpoint signal is rapidly turned off once kinetochores are
attached
7-4
Separase
In vertebrate cells Cdki inhibits
7-5
Cdk inactivation in mitosis in budding yeast is not due to APCCdc2° alone
The protein phosphatase Cdc14 is required to complete mitosis in budding
yeast
7-6
The anaphase spindle segregates the chromosomes
Dephosphorylation of Cdk targets governs anaphase spindle behavior
7-7
Dephosphorylation of Cdk substrates drives the final steps of mitosis
Spindle disassembly is the central event of telophase
Nuclear envelope assembly begins around individual chromosomes
CHAPTER
8-0
Cytokinesis distributes daughter nuclei into separate cells
Cytokinesis depends on a contractile ring and membrane deposition
The cleavage plane is positioned between the daughter nuclei
The timing of cytokinesis is coordinated with the completion of mitosis
xxiii
8-1
Bundles of actin assemble at the site of division
Force is generated in the contractile ring by non-muscle myosin II
Actin filament formation depends on formins
8-2
Contractile ring function depends on accessory factors whose importance
varies in different species
Contraction of the actin-myosin ring is regulated by activation of myosin II
The GTPase Rho controls actin and myosin behavior at the cleavage site
8-3
Membrane deposition is required during cytokinesis
Membrane addition occurs in parallel with actin-myosin contraction
8-4
Preparations for cytokinesis in budding yeast begin in late G1
Fission yeast uses the nucleus to mark the division site in early mitosis
8-5
Signals from the mitotic spindle determine the site of cleavage in animal
cells
Multiple regulatory components at the central spindle help control
cytokinesis
Cytokinesis is coordinated with mitosis by the spindle and Cdki inactivation
8-6
Cytokinesis can be blocked or incomplete in some stages of development
Cellularization is a specialized form of cytokinesis
8-7
Asymmetric spindle positioning leads to daughter cells of unequal sizes
Unequal forces on the poles underlie asymmetric spindle positioning
The orientation of cell division is controlled by the mitotic spindle
CHAPTER
9-0
Sexual reproduction is based on the fusion of haploid cells
The meiotic program involves two rounds of chromosome segregation
Homologous recombination is an important feature of meiosis
Defects in meiosis lead to aneuploidy
9-1
The meiotic program is controlled at multiple checkpoints
The transcription factor Ime1 initiates the budding yeast meiotic program
Entry into the meiotic program is driven by the protein kinase Ime2
9-2
Homologous recombination is a central feature of meiotic
9-3 Homolog
Stages of meiotic
Homolog
9-4
A small number of recombination sites are selected for crossover formation
in zygotene
Crossover sites nucleate the synaptonemal complex in some species
Chiasmata appear in diplotene
9-5
Meiosis I is initiated by M-Cdk activity
Entry into the first meiotic division of animal cells is controlled in diplotene
Ndt80 and Cdk1 promote entry into the meiotic divisions of budding yeast
Recombination defects block entry into meiosis I
9-6
Homolog
Homolog
Homolog
xxiv
9-7
Loss of sister-chromatid arm cohesion initiates anaphase I
The spindle checkpoint system helps control anaphase I
Centromeric
9-8
Meiosis I is followed by meiosis II
Partial Cdk1 inactivation occurs after meiosis I
The meiotic program is coordinated with gametogenesis
CHAPTER
10-0
Cell proliferation is controlled at a checkpoint in late G1
Progression through Start depends on an irreversible wave of Cdk activity
Progression through Start requires changes in gene expression
Cell division is often coordinated with cell growth
10-1
The gene regulatory proteins SBF and MBF drive expression of Start-specific
genes in yeast
SBF and MBF are activated by
Small changes in the amount of Cln3 help trigger cell-cycle entry
SBF and MBF are inactivated in
10-2
GVS-Cdks promote activation of S-Cdks
Multisite phosphorylation of Sid generates switch-like S-Cdk activation
G1/S- and S-Cdks collaborate to inactivate APC00*11 after Start
10-3
Yeast mating factors induce cell-cycle arrest in G1
Fari
Fari
10-4
E2F transcription factors help control G1/S gene expression in animals
Stimulation of G1/S gene expression results from a combination of
increased gene activation and decreased gene repression
E2F function is regulated by pRB proteins
10-5
G1/S gene expression at Start involves the replacement of repressor E2Fs
with activator E2Fs
Phosphorylation of pRB proteins releases E2F
Multiple mechanisms of E2F activation provide robust regulation of Start
10-6
Extracellular mitogens control the rate of cell division in animals
Activated mitogen receptors recruit signaling complexes to the cell
membrane
Ras
Activation of the PI3 kinase helps promote mitogenesis
10-7
Mitogenic signaling pathways lead to activation of cyclin D-Cdk complexes
Mitogens control cyclin D-Cdk localization and destruction
Mitogens and anti-mitogens control the concentrations of Cdk inhibitor
proteins
10-8
G1/S-Cdk activation at Start depends on removal of the inhibitor p27
Cyclin A-Cdk2 activation is promoted in part by APC inhibition
10-9
Developmental signals limit cell division to specific embryonic regions
Embryonic divisions are limited by depletion of key cell-cycle regulators
10-10
Cell division and cell growth are separate processes
XXV
Cell growth is regulated by extracellular nutrients and growth factors
Cell growth and division are coordinated by multiple mechanisms
The size of a cell depends on its genomic content
10-11
Cell growth rate is determined primarily by the rate of protein synthesis
Extracellular nutrients and growth factors stimulate cell growth by activating
the protein kinase TOR
TOR affects cell growth mainly by stimulating protein synthesis
Growth factors stimulate protein synthesis through the activation of
PI3 kinase
10-12
Yeast cell growth and division are tightly coupled
Yeast cells monitor translation rates as an indirect indicator of cell size
Growth thresholds are rapidly adjustable
10-13
Growth and division are coordinated by multiple mechanisms in animal cells
Division depends on growth in many animal cell types
Animal cell growth and division are sometimes controlled independently
10-14
Animal cell numbers are determined by a balance of cell birth and death
Survival factors suppress the mitochondrial pathway of apoptosis
DNA
CHAPTER
11-0
The
ATR and ATM are conserved protein kinases at the heart of the
response
Replication defects trigger
11-1
DNA
Base and nucleotide excision repair systems repair nucleotide damage
Double-strand breaks are repaired by two main mechanisms
11-2
ATR is required for the response to multiple forms of damage
ATM is specialized for the response to unprocessed double-strand breaks
11-3
Protein complexes assemble at
and the damage response
A PCNA-like complex is required for the ATR-mediated damage response
Adaptor proteins link
11-4
p53 is responsible for long-term inhibition of cell proliferation in animal cells
The major regulators of p53 include Mdm2,
Damage response kinases phosphorylate p53 and Mdm2
11-5
DNA
DNA
yeast
DNA
p53 has different effects in different cell types
11-6
A
ATR is the key initiator of the response to stalled replication forks
The
11-7
DNA
XXVI
DNA
DNA
11-8
Hyperproliferative signals trigger the activation of p53
Imbalances in mitogenic stimuli promote
cells
Telomere degeneration promotes cell-cycle arrest in human cells
CHAPTER
12-0
Cancer cells break the communal rules of tissues
Cancer progression is an evolutionary process driven by gene mutation
Genetic instability accelerates cancer progression
12-1
Mutations in oncogenes and tumor suppressors stimulate tumor
progression
Oncogenes can be activated by many different mechanisms
Multiple mutations are required to cripple tumor suppressor genes
Cancer can be initiated by mechanisms other than gene mutation
12-2
Cancers are a complex group of diseases
The molecular basis of tumorigenesis can vary in different tissues
12-3
Tumor cells are independent of mitogens and resistant to anti-mitogens
G1/S gene regulation is defective in most cancers
Multiple mitogenic defects are required for tumor formation
12-4
Cell growth is stimulated in tumors
Tumor cells are less dependent than normal cells on survival factors
Differentiation is often inhibited in tumor cells
Tumor cells are resistant to the hyperproliferation stress response
12-5
Most cancer cells have unstable genomes
Defects in the
Genetic instability sometimes results from an increased rate of point
mutation
Chromosomal instability is the major form of genetic instability
12-6
Defective
Degenerating telomeres can lead to chromosomal instability
12-7
Cancer cells often become aneuploid through a tetraploid intermediate
Cancer cells often contain excessive numbers of centrosomes
Mutations in mitotic spindle components contribute to chromosomal
instability
12-8
There are many genetic routes to a malignant cancer
Colon cancer progression usually begins with mutations in the gene APC
Two forms of genetic instability drive coiorectal cancer progression
12-9
Reducing cancer mortality begins with prevention and early diagnosis
Therapies must kill cancer cells but leave healthy cells intact
A detailed understanding of the molecular basis of cancer may lead to
rational and more specific cancer therapies
Glossary
References 275
Index
XXVII
|
| adam_txt |
Contents in
The Author v
A Note from the Publisher on Primers in Biology
Preface
Acknowledgements
CHAPTER
1-0
Cell reproduction is a fundamental feature of all living things
Cells reproduce in discrete steps
The ordering of cell-cycle events is governed by an independent control
system
1-1
Chromosome duplication and segregation occur in distinct cell-cycle phases
that are usually separated by gap phases
Cytoplasmic components are duplicated throughout the cell cycle
Cell growth is usually coordinated with cell division
1-2
Cell-cycle structure varies in different cells and organisms
Multiple rounds of chromosome duplication or segregation can occur in the
same cell cycle
The symmetry of cell division varies in different cell types
1-3
Cell-cycle events are governed by an independent control system
The cell-cycle control system is based on oscillations in the activities of
cyclin-dependent protein kinases
Cell-cycle events are initiated at three regulatory checkpoints
Cell-cycle progression in most cells can be blocked at checkpoints
CHAPTER
2-0
Mechanisms of cell-cycle control are similar in all eukaryotes
Budding and fission yeasts provide powerful systems for the genetic
analysis of eukaryotic cell-cycle control
Early animal embryos are useful for the biochemical characterization of
simple cell cycles
Control of cell division in multicellular organisms can be dissected
genetically in Drosophila
Cultured cell lines provide a means of analyzing cell-cycle control in
mammals
2-1
Budding yeast and fission yeast divide by different mechanisms
Yeast cells alternate between haploid and diploid states and undergo
sporulation
2-2
Cell biological processes are readily dissected with yeast genetic methods
Conditional mutants are used to analyze essential cell-cycle processes
Homologous genes have different names in fission yeast and budding yeast
2-3
The early embryonic divisions of Xenopus provide a simplified system for
cell-cycle analysis
Unfertilized eggs develop from dipioid oocytes by meiosis
The early embryonic cell cycle can be reconstituted in a test tube
2-4
Drosophila allows genetic analysis of cell-cycle control in metazoans
Cells of the early Drosophila embryo divide by a simplified cell cycle
Gap phases are introduced in late embryogenesis
xviii
Adult fly structures develop from
2-5
Mammalian cell-cycle control can be analyzed in cells growing in culture
Mutations lead to immortalization and transformation of mammalian cells
Specific gene disruption is the ¡deal approach for assessing protein function
in mammalian cells
2-6
Cell-cycle position can be assessed by many approaches
Cell populations can be synchronized at specific cell-cycle stages
Complete understanding of cell-cycle control mechanisms requires the
analysis of protein structure and enzymatic behavior
CHAPTER
3-0
The cell-cycle control system is a complex assembly of oscillating protein
kinase activities
Multiple regulatory mechanisms govern Cdk activity during the cell cycle
The cell-cycle control system generates robust, switch-like and adaptable
changes in Cdk activity
3-1
The cyclin-dependent kinases are a small family of enzymes that require
cyclin subunits for activity
The active site of cyclin-dependent kinases is blocked in the absence of
cyclin
3-2
Cyclins are the key determinants of Cdk activity and can be classified in four
groups
Cyclins contain a conserved helical core
3-3
Full Cdk activity requires phosphorylation by the Cdk-activating kinase
Cdk function is regulated by inhibitory phosphorylation by Wee1 and
dephosphorylation by Cdc25
3-4
The conformation of the Cdk active site is dramatically rearranged by cyclin
binding and phosphorylation by
3-5
Cyclins are specialized for particular functions
Cyclins can interact directly with the substrates of the associated Cdk
Cyclins can direct the associated Cdk to specific subcellular locations
Cks1 may serve as an adaptor protein that targets Cdks to phosphoproteins
3-6
Cdk inhibitors help suppress Cdk activity in G1
Cip/Kip
G1-Cdks are activated by
3-7
Components of the cell-cycle control system are assembled into biochemical
switches
Switch-like behavior can be generated by various mechanisms
Bistability is required for an effective binary switch
3-8
Cdk1 activation at mitosis is based on positive feedback
Cdk switches are robust as a result of multiple partly redundant mechanisms
3-9
Many cell-cycle regulators are destroyed by ubiquitin-dependent proteolysis
SCF catalyzes ubiquitination of phosphorylated substrates using
interchangeable substrate-targeting subunits
3-10
The APC initiates anaphase and mitotic exit
Cdc20 activates the APC in anaphase
APC activity is maintained in G1 by Cdh1
APC targets contain specific recognition sequences
xix
3-11
Negative feedback can generate a repeating oscillator
Regulated braking mechanisms allow the Cdk oscillator to be paused in G1
3-12
A sequential program of gene expression contributes to cell-cycle control
Expression of a large fraction of the genes in the yeast genome is regulated
during the cell cycle
Key gene regulatory proteins in yeast are activated at the major cell-cycle
transitions
The E2F family controls cell-cycle-dependent changes in gene expression in
metazoans
3-13
The order of cell-cycle events is determined by regulatory interactions
between multiple oscillators
The cell-cycle control system is responsive to many external inputs
CHAPTER
4-0
DNA
The cell-cycle control system activates replication origins only once in each
S
Chromosome duplication requires duplication of chromatin structure
4-1
The two strands of
DNA
Discontinuous
Telomerase synthesizes
4-2
Replication origins in budding yeast contain well defined
Replication origins in animal chromosomes are defined by several factors in
addition to
4-3
The replication origin interacts with a multisubunit protein complex
The ORC and accessory proteins load the Mem
Mem loading involves ATP-dependent protein remodeling
4-4
Assembly of
mechanisms
Prereplicative
result of Cdk activity
Pre-RC assembly is controlled in animals by both Cdks and the APC
4-5
Cdks and Cdc7 trigger the initiation of
In budding yeast, the cyclins Clb5 and Clb6 are key activators of replication
origins
Yeast cells lacking
4-6
Different cyclins control initiation of
animal development
Cyclin A is a major regulator of replication initiation in cultured mammalian
cells
DNA
Cyclin E-Cdk2 is a major regulator of
4-7
Cdc7 triggers the activation of replication origins
Cdc7 is activated during
Dbf4 levels are regulated by multiple mechanisms
4-8
Replication begins with
Late-firing origins are regulated independently
XX
Replication must be completed before chromosome segregation occurs
4-9
Chromatin is complex and dynamic
The basic unit of chromatin structure is the nucleosome
Higher-order chromatin structure is also controlled by non-histone proteins,
histone H1 and histone modifications
4-10
Histone synthesis rises sharply during
Transcription of histone genes increases in
Histone mRNA processing and stability increase in
The level of free histones in the cell acts as a signal to link histone synthesis
to
4-11
Nucleosomes are distributed to both new
replication fork
Nucleosome assembly factors load histones on nascent
4-12
Heterochromatin is inherited by epigenetic mechanisms
Telomeres are packaged in a heritable heterochromatin structure
The centromere nucleates a heritable and poorly understood form of
heterochromatin
4-13
Duplication of heterochromatin structure involves proteins that recognize
and promote localized histone modification
The Sir proteins form a heritable polymer at telomeres in budding yeast
HP1 may nucleate heritable chromatin structure at the centromere and other
regions
Sister-chromatid cohesion in
CHAPTER
5-0
The central events of mitosis are sister-chromatid separation and
segregation
The events of early mitosis set the stage for sister-chromatid segregation
The completion of mitosis begins with sister-chromatid segregation
5-1
Phosphorylation and proteolysis control progression through mitosis
Mitotic events must go to completion
Mitotic entry and exit are major regulatory transitions with differing
importance in different species
5-2
Cyclin-Cdk complexes trigger mitotic entry in all eukaryotes
Fission yeast cells trigger mitosis with a single mitotic cyclin
Two pairs of mitotic cyclins control budding yeast mitosis
5-3
Mitosis in metazoans is governed by cyclins A and
Vertebrate mitosis is driven by multiple forms of cyclins A and
The active cyclin Bi-Cdki complex moves from cytoplasm to nucleus in late
prophase
Vertebrate cyclins A and
5-4
Cyclin B-Cdk1 complexes are activated rapidly in early
dephosphorylation
Multiple Wee1-related kinases and
activity in animal cells
5-5
Mitotic Cdk1 activation involves multiple positive feedback loops
Cdc25B and cyclin A-Cdk help trigger cyclin B-Cdki activation
5-6
Cyclin Bi-Cdki is regulated by changes in its subcellular localization
XXI
Cyclin Bi-Cdki
Cdc25C localization is regulated by phosphorylation
Cyclin Bi-Cdki activation and nuclear accumulation are partly interdependent
5-7
Polo-like kinases (Plks) heip control spindle assembly and mitotic exit
Spindle function and sister-chromatid segregation are controlled in part by
aurora kinases
5-8
Sister chromatids are held together by two mechanisms
Cohesin is a key mediator of sister-chromatid cohesion
Cohesion is established during
DNA
5-9
Chromosomes are dramatically reorganized in mitosis
Condensin complexes drive chromosome condensation and resolution
5-10
Mitotic Cdks act on condensin to govern the timing of chromosome
condensation
Sister-chromatid resolution is governed by
CHAPTER
6-0
Chromosome segregation depends on the mitotic spindle
The mitotic spindle must be bipolar
Multiple mechanisms drive spindle assembly
6-1
Microtubules are polymers of tubulin subunits
Microtubules exhibit dynamic instability
6-2
Cellular microtubules originate on preformed protein complexes that are
usually concentrated in a microtubule-organizing center
Microtubule dynamics are governed by a variety of stabilizing and
destabilizing proteins
Motor proteins move along microtubules
6-3
The centrosome cycle resembles the chromosome cycle
Centrosome behavior is determined by the centrioles
The yeast spindle pole body is embedded in the nuclear envelope
6-4
Duplication of the centrosome and spindle pole body is initiated in late G1
byGI/S-Cdks
Centrosome duplication normally occurs once per cell cycle
6-5
The kinetochore is the major site of microtubule-chromosome attachment
The kinetochore provides a stable attachment to a dynamic microtubule plus
end
6-6
Spindle assembly begins in
Mitotic microtubules are highly dynamic
Centrosome separation initiates spindle assembly
Centrosome maturation increases microtubule nucleation in mitosis
6-7
The nuclear envelope is composed of two membranes on an underlying
protein support
Nuclear envelope breakdown begins at nuclear pores
The endoplasmic reticulum and Golgi apparatus are reorganized in mitosis
6-8
Spindles self-organize around chromosomes
Microtubules can be stabilized by a gradient of Ran-GTP around
chromosomes
XXII
6-9 Attachment
Centrosomes search for and capture kinetochores in prometaphase
Some kinetochore microtubules originate at the kinetochore
Chromosome attachment results in tension between sister kinetochores
6-10
Kinetochore-microtubule attachment is stabilized by tension
Aurora
Merotelic attachments are processed by multiple mechanisms
6-11
Multiple forces act on chromosomes in the spindle
The kinetochore
Microtubule flux generates poleward force
A polar ejection force is generated by chromosome arms
6-12
Chromosome oscillations in prometaphase are generated by changes in the
state of kinetochores
Microtubule flux may promote chromosome
CHAPTER
7-0
The final events of mitosis occur in anaphase and telophase
The metaphase-to-anaphase transition is initiated by ubiquitination and
destruction of regulatory proteins
Dephosphorylation of Cdk targets drives the events of late
APCcdc20 initiates Cdk inactivation
7-1
дрсСсісго
Phosphorylation promotes APC0*20 activation in early mitosis
7-2
Unattached kinetochores generate a signal that prevents anaphase
The spindle checkpoint monitors defects in microtubule attachment and
kinetochore tension
7-3
Unattached kinetochores catalyze the formation of inhibitory signaling
complexes
The spindle checkpoint signal is rapidly turned off once kinetochores are
attached
7-4
Separase
In vertebrate cells Cdki inhibits
7-5
Cdk inactivation in mitosis in budding yeast is not due to APCCdc2° alone
The protein phosphatase Cdc14 is required to complete mitosis in budding
yeast
7-6
The anaphase spindle segregates the chromosomes
Dephosphorylation of Cdk targets governs anaphase spindle behavior
7-7
Dephosphorylation of Cdk substrates drives the final steps of mitosis
Spindle disassembly is the central event of telophase
Nuclear envelope assembly begins around individual chromosomes
CHAPTER
8-0
Cytokinesis distributes daughter nuclei into separate cells
Cytokinesis depends on a contractile ring and membrane deposition
The cleavage plane is positioned between the daughter nuclei
The timing of cytokinesis is coordinated with the completion of mitosis
xxiii
8-1
Bundles of actin assemble at the site of division
Force is generated in the contractile ring by non-muscle myosin II
Actin filament formation depends on formins
8-2
Contractile ring function depends on accessory factors whose importance
varies in different species
Contraction of the actin-myosin ring is regulated by activation of myosin II
The GTPase Rho controls actin and myosin behavior at the cleavage site
8-3
Membrane deposition is required during cytokinesis
Membrane addition occurs in parallel with actin-myosin contraction
8-4
Preparations for cytokinesis in budding yeast begin in late G1
Fission yeast uses the nucleus to mark the division site in early mitosis
8-5
Signals from the mitotic spindle determine the site of cleavage in animal
cells
Multiple regulatory components at the central spindle help control
cytokinesis
Cytokinesis is coordinated with mitosis by the spindle and Cdki inactivation
8-6
Cytokinesis can be blocked or incomplete in some stages of development
Cellularization is a specialized form of cytokinesis
8-7
Asymmetric spindle positioning leads to daughter cells of unequal sizes
Unequal forces on the poles underlie asymmetric spindle positioning
The orientation of cell division is controlled by the mitotic spindle
CHAPTER
9-0
Sexual reproduction is based on the fusion of haploid cells
The meiotic program involves two rounds of chromosome segregation
Homologous recombination is an important feature of meiosis
Defects in meiosis lead to aneuploidy
9-1
The meiotic program is controlled at multiple checkpoints
The transcription factor Ime1 initiates the budding yeast meiotic program
Entry into the meiotic program is driven by the protein kinase Ime2
9-2
Homologous recombination is a central feature of meiotic
9-3 Homolog
Stages of meiotic
Homolog
9-4
A small number of recombination sites are selected for crossover formation
in zygotene
Crossover sites nucleate the synaptonemal complex in some species
Chiasmata appear in diplotene
9-5
Meiosis I is initiated by M-Cdk activity
Entry into the first meiotic division of animal cells is controlled in diplotene
Ndt80 and Cdk1 promote entry into the meiotic divisions of budding yeast
Recombination defects block entry into meiosis I
9-6
Homolog
Homolog
Homolog
xxiv
9-7
Loss of sister-chromatid arm cohesion initiates anaphase I
The spindle checkpoint system helps control anaphase I
Centromeric
9-8
Meiosis I is followed by meiosis II
Partial Cdk1 inactivation occurs after meiosis I
The meiotic program is coordinated with gametogenesis
CHAPTER
10-0
Cell proliferation is controlled at a checkpoint in late G1
Progression through Start depends on an irreversible wave of Cdk activity
Progression through Start requires changes in gene expression
Cell division is often coordinated with cell growth
10-1
The gene regulatory proteins SBF and MBF drive expression of Start-specific
genes in yeast
SBF and MBF are activated by
Small changes in the amount of Cln3 help trigger cell-cycle entry
SBF and MBF are inactivated in
10-2
GVS-Cdks promote activation of S-Cdks
Multisite phosphorylation of Sid generates switch-like S-Cdk activation
G1/S- and S-Cdks collaborate to inactivate APC00*11 after Start
10-3
Yeast mating factors induce cell-cycle arrest in G1
Fari
Fari
10-4
E2F transcription factors help control G1/S gene expression in animals
Stimulation of G1/S gene expression results from a combination of
increased gene activation and decreased gene repression
E2F function is regulated by pRB proteins
10-5
G1/S gene expression at Start involves the replacement of repressor E2Fs
with activator E2Fs
Phosphorylation of pRB proteins releases E2F
Multiple mechanisms of E2F activation provide robust regulation of Start
10-6
Extracellular mitogens control the rate of cell division in animals
Activated mitogen receptors recruit signaling complexes to the cell
membrane
Ras
Activation of the PI3 kinase helps promote mitogenesis
10-7
Mitogenic signaling pathways lead to activation of cyclin D-Cdk complexes
Mitogens control cyclin D-Cdk localization and destruction
Mitogens and anti-mitogens control the concentrations of Cdk inhibitor
proteins
10-8
G1/S-Cdk activation at Start depends on removal of the inhibitor p27
Cyclin A-Cdk2 activation is promoted in part by APC inhibition
10-9
Developmental signals limit cell division to specific embryonic regions
Embryonic divisions are limited by depletion of key cell-cycle regulators
10-10
Cell division and cell growth are separate processes
XXV
Cell growth is regulated by extracellular nutrients and growth factors
Cell growth and division are coordinated by multiple mechanisms
The size of a cell depends on its genomic content
10-11
Cell growth rate is determined primarily by the rate of protein synthesis
Extracellular nutrients and growth factors stimulate cell growth by activating
the protein kinase TOR
TOR affects cell growth mainly by stimulating protein synthesis
Growth factors stimulate protein synthesis through the activation of
PI3 kinase
10-12
Yeast cell growth and division are tightly coupled
Yeast cells monitor translation rates as an indirect indicator of cell size
Growth thresholds are rapidly adjustable
10-13
Growth and division are coordinated by multiple mechanisms in animal cells
Division depends on growth in many animal cell types
Animal cell growth and division are sometimes controlled independently
10-14
Animal cell numbers are determined by a balance of cell birth and death
Survival factors suppress the mitochondrial pathway of apoptosis
DNA
CHAPTER
11-0
The
ATR and ATM are conserved protein kinases at the heart of the
response
Replication defects trigger
11-1
DNA
Base and nucleotide excision repair systems repair nucleotide damage
Double-strand breaks are repaired by two main mechanisms
11-2
ATR is required for the response to multiple forms of damage
ATM is specialized for the response to unprocessed double-strand breaks
11-3
Protein complexes assemble at
and the damage response
A PCNA-like complex is required for the ATR-mediated damage response
Adaptor proteins link
11-4
p53 is responsible for long-term inhibition of cell proliferation in animal cells
The major regulators of p53 include Mdm2,
Damage response kinases phosphorylate p53 and Mdm2
11-5
DNA
DNA
yeast
DNA
p53 has different effects in different cell types
11-6
A
ATR is the key initiator of the response to stalled replication forks
The
11-7
DNA
XXVI
DNA
DNA
11-8
Hyperproliferative signals trigger the activation of p53
Imbalances in mitogenic stimuli promote
cells
Telomere degeneration promotes cell-cycle arrest in human cells
CHAPTER
12-0
Cancer cells break the communal rules of tissues
Cancer progression is an evolutionary process driven by gene mutation
Genetic instability accelerates cancer progression
12-1
Mutations in oncogenes and tumor suppressors stimulate tumor
progression
Oncogenes can be activated by many different mechanisms
Multiple mutations are required to cripple tumor suppressor genes
Cancer can be initiated by mechanisms other than gene mutation
12-2
Cancers are a complex group of diseases
The molecular basis of tumorigenesis can vary in different tissues
12-3
Tumor cells are independent of mitogens and resistant to anti-mitogens
G1/S gene regulation is defective in most cancers
Multiple mitogenic defects are required for tumor formation
12-4
Cell growth is stimulated in tumors
Tumor cells are less dependent than normal cells on survival factors
Differentiation is often inhibited in tumor cells
Tumor cells are resistant to the hyperproliferation stress response
12-5
Most cancer cells have unstable genomes
Defects in the
Genetic instability sometimes results from an increased rate of point
mutation
Chromosomal instability is the major form of genetic instability
12-6
Defective
Degenerating telomeres can lead to chromosomal instability
12-7
Cancer cells often become aneuploid through a tetraploid intermediate
Cancer cells often contain excessive numbers of centrosomes
Mutations in mitotic spindle components contribute to chromosomal
instability
12-8
There are many genetic routes to a malignant cancer
Colon cancer progression usually begins with mutations in the gene APC
Two forms of genetic instability drive coiorectal cancer progression
12-9
Reducing cancer mortality begins with prevention and early diagnosis
Therapies must kill cancer cells but leave healthy cells intact
A detailed understanding of the molecular basis of cancer may lead to
rational and more specific cancer therapies
Glossary
References 275
Index
XXVII |
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| author | Morgan, David 1958- |
| author_GND | (DE-588)173873553 |
| author_facet | Morgan, David 1958- |
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| discipline | Biologie |
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| id | DE-604.BV021662182 |
| illustrated | Illustrated |
| index_date | 2024-07-02T15:06:21Z |
| indexdate | 2024-07-09T20:41:04Z |
| institution | BVB |
| isbn | 0199206104 9780199206100 0953918122 9780953918126 0878935088 9780878935086 |
| language | English |
| oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-014876671 |
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| owner_facet | DE-M49 DE-BY-TUM DE-355 DE-BY-UBR DE-29T DE-19 DE-BY-UBM DE-703 DE-188 |
| physical | XXVII, 297 S. Ill., graph. Darst. |
| publishDate | 2007 |
| publishDateSearch | 2007 |
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| publisher | Oxford Univ. Press |
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| series2 | Primers in biology |
| spelling | Morgan, David 1958- Verfasser (DE-588)173873553 aut The cell cycle principles of control David O. Morgan Oxford [u.a.] Oxford Univ. Press 2007 XXVII, 297 S. Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Primers in biology The Cell Cycle: Principles of Control provides an engaging insight into the process of cell division, bringing to the student a much-needed synthesis of a subject entering a period of unprecedented growth as an understanding of the molecular mechanisms underlying cell division are revealed. Zellzyklus (DE-588)4129960-7 gnd rswk-swf (DE-588)4123623-3 Lehrbuch gnd-content Zellzyklus (DE-588)4129960-7 s b DE-604 http://www.new-science-press.com/browse/cellcycle/resources Abbildungen Digitalisierung UB Regensburg application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=014876671&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Morgan, David 1958- The cell cycle principles of control Zellzyklus (DE-588)4129960-7 gnd |
| subject_GND | (DE-588)4129960-7 (DE-588)4123623-3 |
| title | The cell cycle principles of control |
| title_auth | The cell cycle principles of control |
| title_exact_search | The cell cycle principles of control |
| title_exact_search_txtP | The cell cycle principles of control |
| title_full | The cell cycle principles of control David O. Morgan |
| title_fullStr | The cell cycle principles of control David O. Morgan |
| title_full_unstemmed | The cell cycle principles of control David O. Morgan |
| title_short | The cell cycle |
| title_sort | the cell cycle principles of control |
| title_sub | principles of control |
| topic | Zellzyklus (DE-588)4129960-7 gnd |
| topic_facet | Zellzyklus Lehrbuch |
| url | http://www.new-science-press.com/browse/cellcycle/resources http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=014876671&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
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