Cell Cycle Control, Cell Growth Regulation, and Cell Death Flashcards
(119 cards)
1
Q
what is the most basic function of the cell cycle
A
to accurately replicate DNA
2
Q
what is the duration of the cell cycle
A
it varies depending on cell type
3
Q
what are the phases in the eukaryotic cell cycle
A
- M phase mitosis and cytokinesis
- S phase DNA replication
- G1 and G2 phases cell growth
4
Q
where are the main cell cycle checkpoints
A
- late G1 phase
- G2 to M phase
- Mid M phase
5
Q
what is checked at the late G1 phase checkpoint
A
ensures favourable environment before DNA replication
6
Q
what is checked at the G2 to M phase checkpoint
A
confirms DNA is undamaged and fully replicated
7
Q
what is checked at the mid M phase checkpoint
A
chromosomes are appropriately attached to the mitotic spindle before separation
8
Q
what is the core of the cell cycle control system
A
- a series of molecular switches that operate in a defined sequence
9
Q
how is cell cycle machinery regulated
A
- phosphorylation kinases (type of enzyme that adds phosphates to other molecules)
- dephosphorylation phosphatases
10
Q
how are the kinases regulated in cell cycle control
A
by another set of proteins called cyclins
11
Q
the kinases involved in cell cycle control are referred to as what
A
cyclin-dependent kinases (Cdks)
12
Q
the ______ of Cdks is cyclical and the ______ of cyclins is cyclical
A
- activity
- concentration
13
Q
what does G1-Cdk do
A
drive progress through G1 toward S phase
14
Q
what does G1/S-Cdk do
A
initiate transition into S phase
15
Q
what does S-Cdk do
A
- launch S phase
- trigger DNA replication
16
Q
what does M-Cdk do
A
- triggers entry into M phase
- mediate many changes during itosis
17
Q
what is a cyclin
A
set of proteins that regulate Cdks
18
Q
which cyclin is used for G1-Cdk
A
cyclin D
19
Q
which cyclin is used for G1/S-Cdk
A
cyclin E
20
Q
which cyclin is used for S-Cdk
A
cyclin A
21
Q
which cyclin is used for M-Cdk
A
cyclin B
22
Q
the [ ] of cyclin ____ due to continual transcription and protein synthesis
A
increases
23
Q
the [ ] of cyclin increased due to what
A
continual transcription and protein synthesis
24
Q
the [ ] of cyclin ____ due to targeted degradation via ubiquitylation
A
decreases
25
the [ ] of cyclin decreases due to what
targeted degradation via ubiquitylation
26
the activity of Cdks can be modulated by what
- **inhibitor proteins**
- these block the assembly or activity of cyclin-Cdk complexes
27
cyclin-Cdk complexes contain what key thing that needs to be removed to make them active
- **inhibitory phosphates**
- they are removed by phosphatases
28
what are some roles of protein phosphatases
- removing inhibitory phosphates from cyclin-Cdk complexes to activate them
- reverse downstream effects of Cdks by removing phosphates that Cdks add to their targets
29
are protein phosphatases regulated
- **yes**
- including by cyclin-Cdk complexes
30
what is used in the cell cycle to pause the cycle in various ways
- inhibitor proteins
- phosphate regulation
- cyclin regulation
31
what happens if the environment is not favourable for the cell cycle
Cdk inhibitors block entry into cell cycle
32
what happens if DNA replication is not complete
inhibition of activating phosphatase Cdc25 blocks entry to mitosis
33
what happens if there is DNA damage
inhibition of activating phosphatase Cdc25 blocks entry to mitosis
34
what happens if chromosomes are not properly attached to the spindle
inhibition of APC/C activation delays completion of mitosis
35
are Cdks stable or unstable in early g1 phase
stably inactive
36
what happens when conditions are suitable in g1 phase
the cell can transition into S-phase and through the rest of the cell cyclel
37
what happens when conditions are not suitable in G1 phase
- cell-cycle machinery can transiently hold the cell in G1
- or enter a more prolonged nonproliferative state G0
38
what happens to the machinery active in late M phase as the cell re-enters G1 phase
must be inactivated
39
what do mitogens do
activate signaling pathways that stimulate the synthesis of cyclins and other proteins involved in DNA synthesis/ chromosome duplication
40
what does accululation of cyclins synthesized by mitogens do
will lead to G1/S-Cdk activity to allow progress into S phase
41
some cells will only divide upon stimulation from extraceullular signals called what
mitogens
42
what happens in G1 when there is DNA damage
- leads to an increase in [ ] and activity of p53, a transcription regulator
- p53 then activates transcription of a protein called p21- Cdk inhibitor
- p21 prevents entry into S phase and allows time for DNA repair before replication
43
how ong can cells delay cell cycle progression
temporarily or permanently
44
when do many cells in the human body stop dividing
once they differentiate
45
what happens to many cells in the human body once they differentiate
- stop dividing
- dismantle the cell cycle control system
46
what happens when cells enter G0
- are in an arrested state
- retain the ability to reassemble the cell cycle control system
47
what phase does DNA replication happen in
S phase
48
what happens in S phase
DNA is replicated w extreme accuracy to prevent mutations
49
how many times is the genome duplicated and why
- only once
- to prevent damage from gene amplification
50
where does preparation for DNA replication begin
early g1
51
what happens in early g1 regarding DNA
- chromosome configuration
- origin recognition complexes recruit Cdc6 to that helicase can open the double strand
52
what happens in S phase regarding DNA replication
- DNA helicase is activated
- promotes recruitment of the proteins involved in DNA synthesis
- prevents re-replication by phosphorylating Cdc6 and the origin recognition complexes
53
what happens if DNA replication is incomplete
entry into M phase will be delayed
54
what happens during G2 phase
cell continues to grow and prepare for M phase
55
what happens regarding M-Cdk complexes during g2 phase
- they accumulate throughout G2
- are not active until the end of G2 to help transition into M phase
56
what happens in late G2 phase
- the phosphatase Cdc25 removes inhibitory phosphates to activate M-Cdks which in turn indirectly activates more Cdc25
- active M-Cdk complexes suppress inhibitory kinases
- M-Cdks also turn on APC/C
57
what happens when M-Cdks turn on APC/C in late G2 phase
eventually directs the degredation of M-cyclin, inactivation of M-Cdks, and exit from M phase
58
what happens during interphase
- cell size increases
- chromosomes are replicated
- centrosome is duplicated
59
what are the two phases of M phase
- **mitosis** nuclear division
- **cytokenesis** cytoplasmic division
60
what are the stages of mitosis
- prophase
- prometaphase
- metaphase
- anaphase
- telophase
61
what happens during prophase
- duplicated chromosomes condense in the nucleus
- mitotic spindle assembles between the 2 centrosomes
- centrosomes begin to move apart
62
what is required to ensure duplicated chromosomes are properly segregated during mitosis
- cohesins
- condensins
63
what do cohesins do
assemble along DNA as it is replicated to hold sister chromatids together
64
what do condensins do
reorganize and condense each sister chromatid into discreet structures
65
what happens during chromosome condensation
- cohesion rings are partially removed
- this alows the sisters to remain associated but safely pull apart in later mitosis
66
after chromosome condensation, what assembles
- mitotic spindle
- contractile ring
67
what is the mitotic spindle composed of and what does it do
- comprised of microtubules and associated proteins
- pulls duplicated chromosomes apart
68
what is the contractile ring composed of and what does it do
- comprised of actin and myosin filaments around the equator
- splits the cell in 2
69
when does centrosome duplication occur
- begins in S phase
- completed by the end of G2 phase
70
what is centrosome duplication initiated by
- same Cdks that initiate DNA replication
71
when are the poles of the mitotic spindle formed
- **prophase**
- two centrosomes move to opposite sides of the nucleus
72
what is radiated out of the centrosome
an array of microtubules called **an aster**
73
what happens during prometaphase
- phosphorylation of nuclear pores and lamina
- breakdown of the nuclear envelope into small membrane vesicles
- chromosomes attach to spindle microtubules and undergo active movement
74
what prevents the spindle microtubules from making contact with the chromosomes in prophase
the nuclear envelope
75
what happens once the nuclear envelope breaks down in prometaphase
microtubules attach to the chromosome at the kinetochores
76
when do kinetochores assemble at the centromere
prophase
77
where are kinetochores located on sister chromatids
- each chromatid has one
- they face in opposite directions
78
what happens once the microtubules attach to the kinetochores
- the chromosomes are oriented under tension
- which signals that they are ready to be separated
79
when does dynamic instability rises and why
- at the start of mitosis
- partially due to M-Cdk mediated phosphorylation of proteins that influence microtubule stability
80
what are 3 kinda of microtubules
- astral
- interpolar
- kinetochore
81
what do astral microtubules do
position the centrosomes at the poles via attachment to the cell cortex
82
what are interpolar (non kinetochore)
- microtubules in a constant state of flux
- form the basic framework of the mitotic spindle along w associated proteins
83
what do kinetochore microtubules do
encounter and attach to the chromosomes
84
what happens during metaphase
- chromosomes align at the equator
- kinetochore microtubules keep each chromosome under tension from attachment at opposite poles
85
what happens during anaphase
- sister chromatids separate and are pulled towards poles
- kinetochore microtubules get shorter, and the spindle pores move apart contributing to segregation
86
when are cohesions broken down and why
- start of anaphase
- allows the sisters to be pulled apart
87
what allows cohesion linkages to be degraded
- protease called **separase**
- held in an inactive state by inhibtory protein called **securin**
- securin is degraded by **APC/C** so separase can be free to sever cohesion linkages
88
what happens to kinetochore microtubules when chromatids separate
they shorten via loss of tubulin subunits
89
what happens in anaphase A
- the sister chromatids are pulled toward opposite poles as the kinetochore microtubules depolymerize
- The force driving this movement is generated mainly at the kinetochore
90
what happens during anaphase B
- force between non-kinetochore microtubules from opposite poles...
- pushes and pulls the poles apart
91
what is the driving force in anaphase B
- **kinesin** act on overlapping non-kinetochore microtubules, sliding them past one another (push)
- **dyneins** anchored to the plasma membrane, move along the astral microtubules (pull)
92
what happens during telophase
- chromosomes arrive at poles
- new nuclear envelope forms around each set
- division of the cytoplasm begins w the assembly of the contractile ring
93
what happens once the chromosomes arrive at the poles
- vesicles of nuclear membrane surround the chromosome clusters and fuse to reform the nuclear envelope
- nuclear pores and lamina are dephosphorylated
94
what happens once the nuclear envelope is reformed
- nuclear pores restore the localization of cytosolic and nuclear components
- chromosome decondence
95
when does cytokinesis occur
- begins in anaphase
- is not completed until the 2 daughter nuclei have reformed in telophase
96
where does the plane of cleavage occur
perpendicular to the axis of the mitotic spindle
97
what is the contractile ring made up on
actin and myosin filaments
98
what divides a cell in 2
- sliding of actin against myosin generates the force
- as the ring contracts, it becomes smaller and eventually disassembles once the cell is split
99
how is the ER segregated during cell division
cut in 2 during cytokinesis
100
how is the golgi segregated in cell division
fragmented and distributed via motor proteins
101
how are mitochondria/ chloroplasts segregated in cell division
inherited randomly
102
how is the number of cells in a multicellular organism regulated
- rate of cell division
- rate of cell death
103
if cells are no longer needed, what happens
they enter programmed cell death (apoptosis)
104
what happens during development regarding toes and fingers
cells between them die
105
what happens when a cell dies of acute injury
- it releases their contents across their neighbours
- triggers a potentially damaging inflammatory response
106
what is cell necrosis
a cell dying of acute injury (typically accidental)
107
what is apoptosis
programmed/ intentional cell death
108
what happens when a cell dies of apoptosis
- cell collapses and the cell surface is altered to attract phagocytic cells- macrophages
- cell is engulfed before it can release its contents and trigger an inflammatory response
109
what is the difference between apoptosis and necrosis
- **apoptosis** intentional/ programmed death
- **necrosis** accidental
110
the molecular machinery responsible for apoptosis is what
a family of proteases called **caspases**
111
what are caspases used for
the molecular machinery responsible for apoptosis
112
which caspases work together to take a cell apart
- **initiator caspases** activate downstream
- **executioner caspases** dismember numerous key proteins in the cell
113
describe an example of caspases at work
degrade lamins to cause irreversible breakdown of the nuclear lamina which allows nucleases to enter the nucleus and degrade DNA
114
what are the main family of proteins that regulate the activation of caspases
members of the **Bcl2 family**
115
what do Bax and Bak do
- promote cell death
- by inducing the release of cytochrome c from the mitochondria to the cytosol
116
what are two members of the Bcl2 family that promote cell death
Bax and Bak
117
what members of the Bcl2 family prevent apoptosis and how
- others including Bcl2
- preventing the action of Bax and Bak
118
how can cell death be mediated by extracellular signals
- from neighbouring cells or the environment
- directly via cell surface receptors which trigger a caspase cascade
- or due to lack of extracellular signaling
119
