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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

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Biology 101 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
Q

When is nuclear envelope broken down?

A

prophase

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26
Q

midbody

A

a tether between 2 daughter cells remaining after contractile ring has been disassembled
(aka cytoplasmic bridge)

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27
Q

What is the final step in cytokinesis?

A

abscission- membrane on both sides of midbody constricts and is severed by ESCRT-III protein

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28
Q

Define the mechanisms that regulate tissue growth

A
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29
Q

Compare mitogens and growth factors

A

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

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30
Q

how do mitogens control cell division?

A

promote cell division by activating Ras-MAPK pathway to induce transcription of Myc

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31
Q

what divides cytoplasm into 2?

A

contractile ring made of actin and myosin

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32
Q

what marks the start of cytokinesis?

A

cleavage furrow

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33
Q

what is the force for cytokinesis that forms contractile ring?

A

actin and myosin

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34
Q

bivalent pairing

A

a 4-chromatid structure with duplicated homolog chromosomes

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35
Q

chiasma

A

connection between homolog chromosomes during recombination

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36
Q

how does APC/C promote anaphase 1 and 2?

A

separase activation and cohesin cleavage

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37
Q

what does TGFB do?

A

mitogen that blocks growth by inhibiting cell cycle progression in G1

38
Q

Explain how Myc regulates growth

A

expression of G1-cyclin genes –> G1-cdk activated –> phosphorylates and inactivates Rb –> active E2F transcribes cyclines that activate S-cdk –> DNA synthesis

promotes cell division

39
Q

E2F

A
  • promote gene expression of multiple protiens needed for S-phase
  • inhibited by Rb
40
Q

Differences between apoptosis and necrosis

A

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
Q

Examples of apoptosis in healthy organisms

A
  1. quality control during development- eliminating damaged/misplaced cells
  2. digit formation during development
  3. tail disappearance during frog metamorphosis
42
Q

intrinsic and extrinsic pathway apoptosis induction

A

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
Q

Bcl2 proteins

A
  • control permeabilization of mitochondria outer membrane, thus regulating release of cytochrome c to the cytosol
  • can be pro or anti-poptotic
44
Q

What happens when anti-poptotic proteins are inhibited?

A

allows Bak to oligomerize and induce MOMP

45
Q

MOMP

A
  • mitochondrial outer membrane permeabilization (when apoptosis starts)
  • can be reversed
  • only way to stop apoptosis is to stop MOMP from happening
46
Q

Caspase cascade

A

Caspase activation cascade:
Activated caspase-9 triggers activation of caspase-3, which ultimately leads to cell death

47
Q

Inititator vs executioner caspase

A

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
Q

Procaspase

A

inactive caspase precursor in cytosol

49
Q

FLIP

A
  • dimerizes with caspase-8 and inhibits it from activating executioner caspases to initiate apoptosis
  • inhibits the extrinsic pathway of apoptosis
50
Q

role of mitochondria in the apoptosis process

A

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
Q

Where is cytochrome c released to?

A

from the mitochondrial intermembrane space into the cytosol

52
Q

What does Fas ligand promote?

A

apoptosis through extrinsic pathway

53
Q

In a tissue with high cell turnover, why dont we see large numbers of dead cells present within that tissue?

A

phagocytosis: find and clear out apoptosised cells

54
Q

What happens when cleave of cytoskeleton-regulating proteins?

A

Causes actin polymerization to form membrane blebbing and detachment from other cells

55
Q

(How apoptosis is activated)

Which signals activate the initiator caspases?

A

extrinsic and intrisic pathway (mitochondria)

56
Q

Apoptosis extrinsic pathway

A
  • death receptors have intracellular death domain that activates the apoptotic program
  • TNF: includes death receptor and ligands
57
Q

Apoptosome

A

complex containing Apaf 1 and caspase-9

58
Q

what happens when recruit caspase-9 to apoptosome?

A

dimerizes –> starts apoptosis

59
Q

Would WT or injected MOMP-defective cells to undergo apoptosis?

A

Both- extrinsic pathway links intrinsic pathway
dont care if MOMP is working if already have cytochome C in cytosol

60
Q

IAP and anti IAP

A

IAP:
XIAP: inactivates-9,3, 7
anti-IAP
Omi and Smac: released by MOMP, promoting apoptosis; bind XIAP

61
Q

What are IAP?

A
  • inhibitor of apoptosis
  • in cytosol, protect cell from unwatnted apoptosis induction
62
Q

survival factors

A
  • 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
Q

flippase and scramblase

A

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
Q

what inactivates flippase?

A

caspase

65
Q

what does collective function of caspases to inactive flippase and activate scamblase do?

A

increased presence of PS on the outer membrane leaflet–> signaling for phagocytic cells to engulf the cell

66
Q

which way does PS face in healthy cells?

A

cytosol

67
Q

PS

A

phospholipid that serves as “eat me” signal for phagocytosis

68
Q

What are stem cells?

A
  • 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
Q

Tissues that do not have stem cells and cannot renew

A

auditory epithelium
retinal photoreceptive epithelium

70
Q

Tissues that regenerate without presence of stem cells

A
  • pancreatic beta cells
  • hepatocytes
71
Q

Difference between multipotent stem cell, transit-amplifying progenitor, and terminally differentiated cell

A

multipotent progenitor: can form different types of cells
unipotent progenitor: can form one cell type
terminally differentiated: fully differentiated cell

progenitor: transit-amplifying; will have limited number of divisions prior to differentiation

72
Q

Describe the role of stem cells in tissue renewal – epithelium in the gut

A
73
Q

Cell types of the gut epithelium and define the areas where they form

A
  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

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
Q

where do differentiated cells go in the gut?

A

migrate out of the crypt to populate the villi

75
Q

Structure of the epidermis and the location of the stem cells

A
  • transient amplifying progenitors in basal cell layer: 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
Q

How is the epidermis renewed by new
differentiated cells?

A

continously renewed by stem cells proliferation in basal cell layer

77
Q

hematopoietic cells

A
  • stem cells that give rise to RBC and WBC
  • located in adult bone marrow
78
Q

Describe lineage tracing technique using cre/loxp system. What do we learn about the characteristics of the cells by conducting this experiment?

A

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
Q

Why are satellite cells in muscles difficult to observe through traditional lineage tracing experiments?

A

Satellite cells are quiescent until activated and therefore are not detectable by most lineage tracing

80
Q

Difference between totipotent and pluripotent stem cells. what type of cells are ES cells?

A

totipotent- can create a complete organism
pluripotent- can only create the different cell types within the body

ES are pluripotent

81
Q

How can hematopoietic cells be used in transplantation studies?

A
  • 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
Q

Describe the stem cell niche

A
  • specialized microenvironment in the tissue containing necessary signaling molecules to promote proliferation and inhibit differentiation
  • supporting cells, ECM, excreted factors
83
Q

Cell fate determinant

A

molecules required to maintain stem cell identity

84
Q

what will uneven distribution of cell fate determinant molecules produce?

A

one stem cell and one differentiatied cell

85
Q

mechanisms that control the numbers of stem cells within tissues

A
  1. limiting size of niche
  2. asymmetric cell division
  3. stochastic cell fate determination (randomly decides)
86
Q

Describe how some animals can regenerate their limbs and organs, give examples

A

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
Q

compare ES and iPS cells

A

overexpression of ES genes can induce iPS

88
Q

How is transdifferentiation different from reprogramming cells to iPS cells?

A

reprogramming: converts cells into pluripotent stem cells
transdifferentiation: converts cells directly into another cell type

89
Q

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?

A

G1 and G2

90
Q

What is mainly responsible for maintaining low levels of M-cyclin protein during G1?

A

Cdh1–APC/C

91
Q

Teratoma

A

tumor with a mixture of cell types that did not receive appropriate differentiation cues

92
Q

organoid

A

3D organ-like tissues generated by reprogramming ES cells

Biol 413: Cell Bio (5 decks)

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