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Biol 413: Cell Bio > ch 17, 18, 22 (cell cycle, death, and stem cells) > Flashcards

ch 17, 18, 22 (cell cycle, death, and stem cells) Flashcards

1
Q

What is the cell cycle control system?

A

a timer that triggers events of the cell cycle in a specific sequence
made up from cyclins and cdks
controls 3 major transitions:
1. start (transition from G1 to S)
2. Transition from G2 to M
3. Transition from metaphase to anaphase (separation into 2 cells)

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2
Q

How was cell cycle control system discovered?

A

1960s: cell cycle was defined as succession of 4 phases (G1, S, G2, M) and an extra G0
1971: Masui discovered cytosolic unknown factor that can drive cells to enter mitosis
1980s: protein components of cell cycle control system identifified by Maller, Lohka, Hunt, etc

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3
Q

how were cyclins identified and purified

A
  • by observing protein levels in sea urchin eggs during different stages of the cell cycle
  • protein was degraded periodically in the cell cycle.
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4
Q

how does CDK activity turn on abruptly?

A

rapid increase in cyclin availability

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5
Q

how does CDK activity turn off abruptly?

A

due to the rapid degradation of its cyclin by the APC (which marks the cyclin for destruction by the proteasome)

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6
Q

What are the different cyclin-cdk complexes

A

G1/S-cyclin: Start–> S ; phase resulting in a commitment to cell-cycle entry.
S-cyclins: after Start –> mitosis; stimulate chromosome duplication
M-cyclins: G2/M transition –> mid-mitosis; entry into mitosis
G1 cyclins – regulate G1/S cyclin activity, respond to extracellular signals

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7
Q

Wee1, p27, PP2A, cdc25

A

wee1: phosphorylates and inhibits complex
cdc25: dephosphorylates and activates
p27: wraps around complex and inactivates
PP2A: dephosphorylates cdk substrates (does NOT act on complex)

cdk-cyclin complex

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8
Q

CAK

A

along with cyclin, fully activate complex

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9
Q

when is cdk activity highest?

A

M-phase

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10
Q

APC/C in regulating cell cycle

A

Cdc20 activates APC/C when anaphase starts –> APC/C ubiquinates and destructs cyclins → cdk inactivation→ PP2A dephosphorylates targets (negative feedback)

Cdh1 activates APC/C –> Cdk inactivation and cyclin degradation during G1

APC/C ubiquitylates securin –> separase is activated –> cohesin rings are cleaved –> chromatid are separated by being pulled to spindle poles

trigger metaphase to anaphase transition
activates separase for chromatid separation
Cdh1 can only be activated during mid M-phase when M-cyclins are destroyed

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11
Q

What do M-Cdks do?

A
  • inhibit Cdh1 and activates Cdc20
  • induce assembly of mitotic spindle
  • ensure each sister chromatid is attached to oppsite spindle pole
  • trigger chromosome condensaiton
  • promote breakdown of nuclear envelope
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12
Q

Cohesins vs condensins

A

cohesins: form a ring around each of the 2 sister chromatids (glues replicated sister chromatids together until they split at anaphase)
condensin: form ring that encircles DNA, promoting compaction of chromatids

both protein complexes

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13
Q

What does separase do?

A

cleaves and dissociates cohesin rings

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14
Q

why is chromosome condensation critical?

A

to avoid DNA breaks during sister chromatid separation

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15
Q

p53/ p21 checkpoint activity

A

p53 activates the transcription of p21, which arrests cell cycle at the G1 phase (cant go to S phase)

p53 promotes expression of pro-apoptotic proteins like Puma

p21 inhibits cdk

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16
Q

Describe the role of Rb

A

binds and inhibits E2F
phosphorylation of Rb by G1-cdk reduces binding to E2F –> activates E2F

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17
Q

three examples of events that would trigger checkpoint arrest

A

DNA damage, incomplete DNA replication, improper chromosome attachment to spindle fibers during mitosis, extreme cellular stress, lack of essential nutrients, and significant changes in cellular environmen

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18
Q

what could happen in cell cycle if cell did not have centrosomes?

A

cell will still divide and become 2 cells, with chromosome abnormalities

dont need centrosome for microtubules, just y-tubulin ring

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19
Q

When does nuclear envelope break down and chromosomes attach to spindle?

A

prometaphase

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20
Q

Explain the fundamental difference between meiosis and mitosis

A

meiosis: duplicated homolog chromosomes pair during prophase

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21
Q

what do kinetichores do?

A

attach sister chromatids to opposite spindle poles

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22
Q

anaphase A vs B

A

A: kinetichore microtubules shorten & chromosomes pulled towards poles
B: movement of spindles themselves; poles are pushed and pulled apart

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23
Q

shugoshin

A
  • kinetichore-associated protein that protects cohesins from degradation
  • keeps 2 sister chromatids attached
  • without it, all chromatids separate prematurely in anaphase I
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24
Q

When does nuclear envelope reform?

A

telophase

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25
When is nuclear envelope broken down?
prophase
26
midbody
a tether between 2 daughter cells remaining after contractile ring has been disassembled (aka cytoplasmic bridge)
27
What is the final step in cytokinesis?
**abscission**- membrane on both sides of midbody constricts and is severed by ESCRT-III protein
28
Define the mechanisms that regulate tissue growth
29
Compare mitogens and growth factors
**mitogens**: stimulate cell division by triggering G1/S-cdk activity **growth factors**: stimulate cell growth by promoting protein and other molecule synthesis and inhibiting their degradation
30
how do mitogens control cell division?
promote cell division by activating Ras-MAPK pathway to induce transcription of Myc
31
what divides cytoplasm into 2?
contractile ring made of actin and myosin
32
what marks the start of cytokinesis?
cleavage furrow
33
what is the force for cytokinesis that forms contractile ring?
actin and myosin
34
bivalent pairing
a 4-chromatid structure with duplicated homolog chromosomes
35
chiasma
connection between homolog chromosomes during recombination
36
how does APC/C promote anaphase 1 and 2?
separase activation and cohesin cleavage
37
what does TGFB do?
mitogen that blocks growth by inhibiting cell cycle progression in G1
38
Explain how Myc regulates growth
expression of G1-cyclin genes --> G1-cdk activated --> phosphorylates and inactivates Rb --> active E2F transcribes cyclines that activate S-cdk --> DNA synthesis ## Footnote promotes cell division
39
E2F
* promote gene expression of multiple protiens needed for S-phase * inhibited by Rb
40
Differences between apoptosis and necrosis
apoptosis * form of cell death by suicide occurring only in animal cells * cell undergoes characteristic morphological and biochemical changes * cell debris are engulfed by phagocytic cells * IRREVERSIBLE
41
Examples of apoptosis in healthy organisms
1. quality control during development- eliminating damaged/misplaced cells 2. digit formation during development 3. tail disappearance during frog metamorphosis
42
intrinsic and extrinsic pathway apoptosis induction
**extrinsic** : initated following activaiton of cell surface death receptors (belong to TNF) **intrinsic** : depends on proteins released from the mitochondria: Bcl2 and MOMP proteins (apoptosis is induced when Cytochrome c is released in the cytosol)
43
Bcl2 proteins
* control permeabilization of mitochondria outer membrane, thus regulating release of cytochrome c to the cytosol * can be pro or anti-poptotic
44
What happens when anti-poptotic proteins are inhibited?
allows Bak to oligomerize and induce MOMP
45
MOMP
* mitochondrial outer membrane permeabilization (when apoptosis starts) * can be reversed * only way to stop apoptosis is to stop MOMP from happening
46
Caspase cascade
**Caspase activation cascade:** Activated caspase-9 triggers activation of caspase-3, which ultimately leads to cell death
47
Inititator vs executioner caspase
**Initiatior**: begin apoptotic program --> activate executioner caspases (8 & 9 in mammals) **Executioner**: orchestrate apoptotic program in vertebrates Caspase-6: cleaves nuclear lamin --> breakdown of nuclear lamina Caspase-3: cleaves iCAD (inhibitor protein of DNA-degrading nucelase enzyme) Caspase-7
48
Procaspase
inactive caspase precursor in cytosol
49
FLIP
* dimerizes with caspase-8 and inhibits it from activating executioner caspases to initiate apoptosis * inhibits the extrinsic pathway of apoptosis
50
role of mitochondria in the apoptosis process
When MOMP occurs, cytochrome c is released, binds to Apaf-1 and procaspase-9 to form the apoptosome, leading to caspase-9 activation. Caspase activation cascade: Activated caspase-9 triggers a cascade of caspase activation, including caspase-3, which ultimately leads to cell death.
51
Where is cytochrome c released to?
from the mitochondrial intermembrane space into the cytosol
52
What does Fas ligand promote?
apoptosis through extrinsic pathway
53
In a tissue with high cell turnover, why dont we see large numbers of dead cells present within that tissue?
phagocytosis: find and clear out apoptosised cells
54
What happens when cleave of cytoskeleton-regulating proteins?
Causes actin polymerization to form membrane blebbing and detachment from other cells
55
# (How apoptosis is activated) Which signals activate the initiator caspases?
extrinsic and intrisic pathway (mitochondria)
56
Apoptosis extrinsic pathway
* death receptors have intracellular death domain that activates the apoptotic program * TNF: includes death receptor and ligands
57
Apoptosome
complex containing Apaf 1 and caspase-9
58
what happens when recruit caspase-9 to apoptosome?
dimerizes --> starts apoptosis
59
Would WT or injected MOMP-defective cells to undergo apoptosis?
Both- extrinsic pathway links intrinsic pathway dont care if MOMP is working if already have cytochome C in cytosol
60
IAP and anti IAP
**IAP**: XIAP: inactivates-9,3, 7 **anti-IAP** Omi and Smac: released by MOMP, promoting apoptosis; bind XIAP
61
What are IAP?
* inhibitor of apoptosis * in cytosol, protect cell from unwatnted apoptosis induction
62
survival factors
* extracellular signaling molecules that inhbit apoptosis, thus promoting cell survival; cells that do not receive signals wil undergo apoptosis * increase production of anti-apoptotic Bcl2 * inactivate BH3
63
flippase and scramblase
flippase: enzyme that ensures correct membrane localization of PS; active in healthy cell membranes scramblase: enzyme that flips phospholipids from one membrane leaflet to another indiscrimnately; inactive in healthy cells' membrane
64
what inactivates flippase?
caspase
65
what does collective function of caspases to inactive flippase and activate scamblase do?
increased presence of PS on the outer membrane leaflet--> signaling for phagocytic cells to engulf the cell
66
which way does PS face in healthy cells?
cytosol
67
PS
phospholipid that serves as "eat me" signal for phagocytosis
68
What are stem cells?
* undifferentiated self-replicating cells that have the potential to differentiate into multiple cell types supplying tissues with renewable cells for tissue repair and regneration * Have 2 fundamental properties: self renewal and ability to produce differentiated cells
69
Tissues that do not have stem cells and cannot renew
auditory epithelium retinal photoreceptive epithelium
70
Tissues that regenerate without presence of stem cells
* pancreatic beta cells * hepatocytes
71
Difference between multipotent stem cell, transit-amplifying progenitor, and terminally differentiated cell
**multipotent progenitor**: can form different types of cells **unipotent progenitor**: can form one cell type **terminally differentiated**: fully differentiated cell ## Footnote progenitor: transit-amplifying; will have limited number of divisions prior to differentiation
72
Describe the role of stem cells in tissue renewal – epithelium in the gut
73
Cell types of the gut epithelium and define the areas where they form
1. **absorptive cell**: take up nutrients from gut lumen; digestion; villi 2. **goblet cell**; secrete mucus into gut lumen, which acts as protective coat; villi 3. **paneth cell**: role in innate immune defense by secreting proteins that kill bacteria; secrete wnt needed to maintain stem cell population; crypts 4. **enteroendocrine cell**: secrete serotonin and peptide hormones; act on neurons to regulate growth, poliferation, and digestion; both ## Footnote Villus: structure in gut lumen coated by a layer of epithelial cells crypt: area within connective tissue; location of replicating stem cells that produce differntiated cell types
74
where do differentiated cells go in the gut?
migrate out of the crypt to populate the villi
75
Structure of the epidermis and the location of the stem cells
* **transient amplifying progenitors in basal cell laye**r: give rise to epidermis cell types * **squames**: dead cells marking the outermost layer of the skin; shed from the surface * **granular cell layer**: waterproof barrier of the skin formed by cells
76
How is the epidermis renewed by new differentiated cells?
continously renewed by stem cells proliferation in basal cell layer
77
hematopoietic cells
* stem cells that give rise to RBC and WBC * located in adult bone marrow
78
Describe lineage tracing technique using cre/loxp system. What do we learn about the characteristics of the cells by conducting this experiment?
Cre/loxP: edit genome and express a reporter under desired promoter activity of cre is dependent on the presence of tamoxifen allowing temporal control of genome editing
79
Why are satellite cells in muscles difficult to observe through traditional lineage tracing experiments?
Satellite cells are quiescent until activated and therefore are not detectable by most lineage tracing
80
Difference between totipotent and pluripotent stem cells. what type of cells are ES cells?
totipotent- can create a complete organism pluripotent- can only create the different cell types within the body ES are pluripotent
81
How can hematopoietic cells be used in transplantation studies?
* multipotent cells that give rise to transit-amplifying progenitors * ** cell transplantation**- to replace damaged or dysfunctional bone marrow in patients by infusing healthy stem cells from a donor, allowing the patient to regenerate a healthy blood cell population in their body * transplantation of bone marrow fro healthy mouse can repopulate the hematopoietic stem cells destroyed by X-irradiation
82
Describe the stem cell niche
* specialized microenvironment in the tissue containing necessary signaling molecules to promote proliferation and inhibit differentiation * supporting cells, ECM, excreted factors
83
Cell fate determinant
molecules required to maintain stem cell identity
84
what will uneven distribution of cell fate determinant molecules produce?
one stem cell and one differentiatied cell
85
mechanisms that control the numbers of stem cells within tissues
1. limiting size of niche 2. asymmetric cell division 3. stochastic cell fate determination (randomly decides)
86
Describe how some animals can regenerate their limbs and organs, give examples
blastema- small bud forming at the site of amputation includes activated stem cells and progenitor cells that regenerate the limb ex: axolotol Neoblast- restore the regenerative ability of planarian
87
compare ES and iPS cells
overexpression of ES genes can induce iPS
88
How is transdifferentiation different from reprogramming cells to iPS cells?
**reprogramming**: converts cells into pluripotent stem cells **transdifferentiation**: converts cells directly into another cell type
89
At which two major time points during the cell cycle does the cell-cycle control system normally arrests the cycle if DNA damage is detected?
G1 and G2
90
What is mainly responsible for maintaining low levels of M-cyclin protein during G1?
Cdh1–APC/C
91
Teratoma
tumor with a mixture of cell types that did not receive appropriate differentiation cues
92
organoid
3D organ-like tissues generated by reprogramming ES cells

Biol 413: Cell Bio (5 decks)

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