Exam 4 Flashcards
(116 cards)
1
Q
What is the cytoskeleton?
A
a three dimensional, interconnected network of filaments and tubules
2
Q
What are the three major components of the cytoskeleton?
A
microtubules, microfilaments, intermediate filaments
3
Q
What do microtubules do?
A
move chromosomes, intracellular transport of versicles and movement of organelles, and makes up cilia and flagella
4
Q
What is the diameter of microtubules?
A
largest of the three parts of the cytoskeleton, 25 nm outer diameter, and 15 nm inner diameter
5
Q
How is the microtubule built?
A
alpha tubulin and beta tubulin forms a heterodimer to make a literal tube
6
Q
How is the microfilament arranged with the alpha and beta tubulins?
A
alpha is at the bottom of the protofilament and the beta is at the top of the protofilament - the beta subunit is the positive end and the alpha subunit is at the minus end. This makes the microtubule polar
7
Q
What is a tubule heterodimer?
A
a microtubule subunit that makes up the protofilaments, which come together to make microtubules
8
Q
What does elongation do in tubule formation?
A
it adds the subunits
9
Q
What is the critical concentration?
A
concentration of dimers where assembly and disassembly of microtubules is balanced, meaning MTs are not getting longer or shorter
10
Q
What are the basal bodies in microtubules?
A
microtubule organizing center which can be found at the base of the cilia and flagella
11
Q
What is dynamic instability?
A
microtubules can oscillate between growth and shrinking phases rapidly
12
Q
How does MT assembly use GTP?
A
GTP is bound to subunits which are at the GTP-caps, when the MT needs to shrink, GDP-bound subunits are at the GTPs caps (this causes the end to be unstable making the protofilaments not stick together)
13
Q
How does microtubule stability work?
A
Microtubule Associated Proteins (MAPs) interact with other cellular structures
14
Q
What do motor MAPs do?
A
Use ATP to drive transport and generate force (help with movement)
15
Q
What do nonmotor MAPs do?
A
important for MT organization
16
Q
Describe the structure of microfilaments.
A
smallest of the three, with a diameter of 7 nm and a solid center/helix shape
17
Q
How are microfilaments used?
A
muscle movement, amoeboid movement, cytoplasmic streaming, cleavage furrows, cell chape, microvilli
18
Q
How are microfilaments linked to the plasma membrane?
A
they are concentrated in the cell cortex, right underneath the plasma membrane
19
Q
What are the monomers of microfilaments?
A
actin
20
Q
What is the G-actin in microfilaments?
A
globular form/monomer form of actin (has ATP bound)
21
Q
What is F-actin?
A
filamentous actin/polymer form of actin that has ADP bound
22
Q
Are actin molecules polar?
A
yes
23
Q
What structures do cells assemble actin into?
A
contractile bundles, gels, branched networks, parallel bundles
24
Q
What is the structure of microfilaments in contractile bundles/stress fibers?
A
MFs point in opposite directions, which allow things to contract (like muscle cells)
25
How are microfilaments arranged in cell cortexes/gels arranged?
3-D meshwork of MF's
26
How are MFs arranged in lamellipodium/branched networks?
branched networks produce wide, flat extensions
27
How are MFs arranged in filopodium/parallel bundles?
parallel structures of MFs that cause pointed extensions of membrane
28
How are microfilaments regulated?
capping proteins that stop growth/assembly, branched networks are formed by binding Arp213 proteins, and actin crosslinking proteins stabilize microfilaments into bundles (like those found in microvilli)
29
What are microvilli made of?
several MFs put together with actin binding proteins
30
How are MFs linked to the plasma membrane?
ankyrin bunds to integral membrane proteins, which bind to spectrin and forms a sheath under the PM, and actin (MFs) bind to spectrin
31
What are intermediate filaments?
8-12 nm in diameter with no polarization and very stable
32
What are the three types of intermediate filaments?
keratins (epithelial cells strength), desmins (maintain structure in muscle cells), nuclear lamins (line the interior of nuclear envelope)
33
What is special about intermediate filaments?
different tissues/cell types have different types of intermediate filaments
34
What drugs affect microtubules?
colchicine - inhibits MT assembly
taxol - stabilizes MTs
35
What drugs affect microfilaments?
cytochalasin D - inhibits MF assembly
phalloidin - stabilizes MFs
36
What are motor proteins?
proteins that use energy from ATP to change shape, and that shape change either generates force or creates movement
37
What are microtubule motor proteins?
kinesins - move towards positive ends of MTs
dynesins - move towards negative ends of MTs
38
What is the microfilament motor protein?
myosin
39
What are MTOCs?
microtubule organizing centers (centrosomes)
40
Where are the positive and negative ends of microtubules attached in cells?
negative are attached to the MTOC and positives go out towards the periphery
41
What do kinesins do and how do they work?
they do anterograde axonal transport (move vesicles towards positive ends of MTS) and they bind directly to vesicles
42
What do dyneins do and how do they work?
retrograde axonal transport (move vesicles towards the negative end of MTs) and bind vesicles through intermediates (dynactin)
43
What is the structure of kinesins?
two globular heads that bind ATP that interacts with MTs, heavy chain stalk with light chain region for attachment to cargo, and walks along beta-tubulin in 8 nm steps
44
What is the structure of dyneins?
consists of heavy globular heads, an intermediate stalk, and light bottom chains (ankyrin/spectrin are used to bind vesicle)
45
How do Motor MAPs work in the endomembrane system?
kinesins - move vesicles towards the cell periphery along MTs
dyneins - move vesicles from cell edge into cell interior along MTs
46
Describe cilia.
microtubule-based motility that are tiny and short, but appear in large numbers. They use a perpendicular force of power stroke and are like oars to move things in or past the cells
47
Describe flagella.
small, long microtubule-based motility that uses parallel force
48
What is the axoneme?
The MT structure inside the cilia and flagella, which consists a 9a+2 arrangement (9 outer MT doublets, and 2 single MTs aka the central pair)
49
What is the structure of myosin?
two heavy-chain tails
50
Describe how myosin works.
during muscle contraction, sarcomeres shorten when thick filaments (myosin) and thin filaments (actin) slide past each other. Globular heads of myosin bind to the actin to move them along
51
How does cell crawling work?
the leading edge extends due to polymerization of actin to form lamellipodium, new adhesions to the substrate anchored by actin form attachments to the underside of the lamellipodium, the trailing edge detaches and comes forward by contraction of the cell
52
What are the three parts of interphase and what do they do?
G1 - gap 1, make decision if gonna divide
S = synthesis
G2 = gap 2
53
What is depurination?
the removal of a purine base from a nucleotide (more common than deamination)
54
What is deamination?
removal of an amino group from a base (most often results in a C being converted to a U)
55
What is a thymine dimer?
two adjacent Ts are covalently attached (can be caused by UV)
56
What is BER and NER?
base excision repair - corrects a single base (depurination, deamination)
nucleotide excision repair - corrects larger lesions (T dimers)
57
How does the cell know which strand to repair in mismatched nucleotides?
lack of methylation
58
What happens during prophase?
chromosomes condense, centrosomes migrate to poles, mitotic spindles form
59
What happens in prometaphase?
centrosomes reach poles, nuclear envelope breaks down, spindle fiber attach to chromosomes
60
What happens telophase?
chromosomes arraive at poles, chromosomes decondense, spindles disappear, and nuclear envelope reforms, cytokinesis usually occurs
61
What is mitosis promoting factor (MPF)?
injection of dividing cell cytoplasm into quiescent cell causes mitosis
62
What is MPF made of?
cyclin-dependent kinase - protein kinase that controls progression through cell cycle by phosphorylating target protein (only bound to cyclin)
cyclin-activated with CDK bound to them - protein level cycle in abundance
63
How does MPF work?
CDK remains at constant levels, cyclin levels slowly rise during G2 and push cells into mitosis
64
What are the three major checkpoints in the cell cycle?
restriction point (start) - just before G1--> S transition and is controlled by growth factors and cell size
G2-M transition - controlled by DNA replication
Metaphase-Anaphase transition - controlled by chromosome attachment to spindle fibers
65
Which proteins regulate the start point?
E2F - transcription factor required for transcription of DNA replication genes - bound to and inhibited to Rb protein
66
Describe how E2F is released.
at restriction point, phosphorylation by CDK cause Rb to release E2F and no longer inhibit it and growth factors stimulate production of G1 cyclin that binds activate CDK
67
What do growth factors do in the cell cycle?
promote entry into the cell cycle from G1 (expressed in tissue growth, liver regeneration, and wound healing)
68
How does the Ras/Raf pathway work?
Ras is a monomeric G protein that activates Raf, and then Raf activates MAPK (mitogen-activate protein kinase)
69
What happens when Ras is mutated (or abnormally activated)?
constantly sending signals to grow and divide (in ~25-30% of cancers)
70
How does activated MAPK work?
moves into the nucleus, phosphorylates, and activates transcription regulators that turn on the genes that stimulate cell division
71
What protein works with the G2-M transition?
Mitosis promoting factor (MPF)
72
What does MPF do and how is it structured?
can trigger mitosis or meiosis to progress in halted cells and is composed of cyclin and Cdk
73
What happens to MPF if DNA replication is not completed?
the cyclin-CDK complexes are not activated and the cell pauses in G2
74
How is MPF degraded?
the cyclin in MPF is flagged for degradation by the Anaphase Promoting Complex (APC/C)
75
What does APC/C do?
stimulates the destruction of cohesion which holds sister chromatids together (becomes active at the metaphase-anaphase transition)
76
What is the metaphase-anaphase transition also called?
spindle checkpoint
77
How does the metaphase-anaphase checkpoint work?
the checkpoint is activated by kinetochores not being attached to spindle fibers, proteins inhibit APC/C until all kinetochores are correctly attached to spindle fibers
78
What is p53 and what does it do?
DNA damage causes accumulation of p53, which inhibits cdk-cyclin complexes, at least in part by inducing the transcription of p21
79
What is the contractile ring in cytokinesis in animal cells?
belt-like bundle of actin MFs that forms beneath the PM and tightens to pinch the cell in half
80
How does plant cytokinesis work?
has cell plate that is a flattened sac that is formed from Golgi-cleaved vesicles fusing together - the vesicles fuse together and then contain the components of the cell wall
81
What are stem cells?
undifferentiated cells that can self-renew
82
What are totipotent stem cells?
can give rise to any cell of the body or placenta
83
What are pluripotent cells?
stem cells that can give rise to any cell in the body
84
What are multipotent cells?
stem cells that can give rise to more than one cell type, but are more limited than pluripotent
85
Which stem cell types are used in experiments today?
embryonic stem cells, adult stem cells, induced pluripotent stem cells
86
What are embryonic stem cells?
pluripotent from inner cell mass of embryo
87
What are adult stem cells?
multipotent from various tissues and are important for things such as bone marrow transplants
88
What are induced pluripotent stem cells?
genetically reprogrammed that are made from differentiated cells that have certain genes reactivated to revert the cells to a stem cell state (they are pluripotent and this won the Nobel Prize in 2012)
89
Describe apoptosis vs. necrosis
apoptosis - programmed cell death where contents are disposed of without spilling into extracellular space or causing inflammation (tidier form)
necrosis - death by injury or disease
90
What are the major steps of apoptosis?
1. chromosomes condense and cytoplasm shrinks
2. nucleus is fragmented and DNA cut at regular intervals and cytoplasm extends blebs
3. Eventually the remnants of the cell (apoptotic bodies) are ingested by phagocytic cells
91
What are caspases?
proteases that cleave other cellular proteins to mediate the events of apoptosis
92
How does apoptosis occur through a cascade of caspase activation?
initiator caspases begin the apoptotic process, and then effector caspases catalyze the widespread cleavage events that kill the cell
93
Describe the two ways apoptosis can be triggered.
extrinsic pathway - begins with a signal from outside the cell that binds to death receptor
intrinsic pathway - begins inside the cell; initiated by the release of cytochrome C from the mitochondria
94
What is the important note about apoptosis?
activation of p53 after DNA damage can trigger apoptosis
95
What are the four major types of cancer?
carcinoma, sarcoma, lymphoma, leukemia
96
What is carcinoma?
90% of cancers - cells of epithelial origin
97
What is sarcoma?
mesenchymal origin (bone, fat, muscle)
98
What is lymphoma?
blood or lymph origin; form a solid mass
99
What is leukemia?
blood of lymph origin; circulate in the bloodstream
100
When is a tumor named malignant?
when the tumor cells break through the basal lamina and invade the underlying tissue
101
What traits lead to uncontrolled proliferation?
growth signaling pathways are always on, cell checkpoint are inactivated, apoptosis pathways are off, telomerase is always on so that cell division stays continuous and the telomeres do not get smaller
102
How does angiogenesis work with cancer cells?
vascular endothelial growth factor is released from tumor cells
103
How do cancers metastasize?
cells have to lose adhesion to become unstuck from where they are, have the ability to move to other areas, and be able to secrete proteases to break down the extracellular matrix
104
What are oncogenes?
a mutated version of proto-oncogene that is constantly on
105
What are tumor suppressor genes?
their absence leads to cancer (encode things that normally control cell division)
106
How do cells acquire oncogenes?
mutations in proto-oncogenes or by infection with certain viruses
107
Which genes are protooncogenes?
growth factors
receptors
G-proteins (Ras)
protein kinase (MAPK)
transcription regulators
108
What are examples of tumor suppressor genes?
Rb, p53 (which is mutated in 50% of cancer)
109
What does HPV to do tumor suppressor genes (specifically Rb and p53)?
E6 binds to and destroys p53
E7 binds to and inhibits Rb
110
What is the APC gene with colon cancer an example of?
tumor suppressor genes
111
What is the two hit hypothesis?
the loss of tumor suppressor genes is recessive
112
What is familial cancer?
when people already have one recessive "hit", so they just need another to develop cancer
113
What is dynamic instability?
Ability of microtubules
to rapidly oscillate between growth and shrinking
phases
114
What iis XERODERMA PIGMENTOSUM?
Genetic disease
with increased rate of skin cancer resulting from defective NER
115
What is procaspase?
the inactive precursor of caspase
116
