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Biol 413 > ch 17, 22 > Flashcards

ch 17, 22 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 partner by the Anaphase Promoting Complex (APC), which marks the cyclin for destruction by the proteasome, causing a sudden drop in its activity

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6
Q

Compare different cyclin-cdk complexes and which cell cycle phase they regulate

A

G1/S-cyclin: in G1 help trigger progression through Start, resulting in a commitment to cell-cycle entry. Levels fall in S phase
S-cyclins: bind after Start to stimulate chromosome duplication. Levels high until mitosis and contribute to the control of early mitotic events
M-cyclins: activate Cdks that stimulate entry into mitosis at the G2/M transition. Levels fall in mid-mitosis
G1 cyclins – regulate G1/S cyclin activity, respond to extracellular signals

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7
Q

Describe cyclin-cdk regulatory molecules and explain the cellular pathways they activate

A
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8
Q

CAK, wee1, p27, PP2A, cdc25

A

CAK: along with cyclin, fully activates complex
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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9
Q

APC/C in regulating cell cycle mitosis and meiosis

A
  • trigger metaphase to anaphase transition
  • APC/C ubiquinates and destructs cyclins → cdk inactivation→ PP2A dephosphorylates targets (negative feedback)

ADD MORE

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10
Q

p53/ p21 checkpoint activity

A

protein p53, acting as a tumor suppressor, activates the transcription of p21, which arrests cell cycle at the G1 phase, effectively acting as a checkpoint to prevent damaged cells from replicating, thus preventing potential mutations and tumor development

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11
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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12
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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13
Q

describe meiosis, different phases including proteins involved

A
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14
Q

Explain the fundamental difference between meiosis and mitosis

A

meiosis: duplicated homolog chromosomes pair during prophase

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15
Q

shugoshin

A

shugoshin: kinetichore-associated protein that protects cohesins from degradation
keeps 2 sister chromatids attached

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16
Q

Define the mechanisms that regulate tissue growth

A
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17
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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18
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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19
Q

Explain how Myc regulates growth

A

promotes expression of G1-cyclin genes –> increase cyclin-cdk activity –> associate with cdk –> cdk activated

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20
Q

E2F

A
  • promote gene expression of multiple protiens needed for S-phase
  • inhibited by retinoblastoma protein (Rb)
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21
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

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22
Q

Examples of processes that involve apoptosis in healthy organisms

A
  1. quality control during development- eliminating damaged or misplaced cells
  2. digit formation during limb development
  3. tail disappearance during frog metamorphosis
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23
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)

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24
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
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25
Q

What happens when anti-poptotic proteins are inhibited?

A

allows Bak to oligomerize and induce MOMP (Bad)

26
Q

MOMP

A
  • mitochondrial outer membrane permeabilization (when apoptosis starts)
  • can be reversed
  • only way to stop apoptosis is to stop MOMP from happening
27
Q

Caspase cascade

A

Caspase activation cascade:
Activated caspase-9 triggers a cascade of caspase activation, including caspase-3, which ultimately leads to the execution of cellular components and cell death.

28
Q

Types of caspases and their roles

A

Procaspase- inactive caspase precursor in cytosol
Initiatior: begin apoptotic program (caspase-8 & 9 in mammals) –> activate executioner caspases
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

29
Q

FLIP

A
  • caspase inhibitor that prevents apoptosis
  • dimerizes with caspase-8 and prevents it from activating executioner caspases to initiate apoptosis
30
Q

role of mitochondria in the apoptosis process

A

When MOMP occurs, cytochrome c is released from the mitochondrial intermembrane space into the cytosol, where it 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 the execution of cellular components and cell death.

31
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

32
Q

What happens when cleave of cytoskeleton-regulating proteins?

A

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

33
Q

(How apoptosis is activated)

Which signals activate the initiator caspases?

A

extrinsic and intrisic pathway (mitochondria)

34
Q

Apoptosis extrinsic pathway

A
  • death receptors have intracellular death domain that activates the apoptotic program
  • TNF: includes death receptor and ligands
35
Q

Apoptosome

A

complex containing Apaf 1 and caspase-9

36
Q

what happens when recruit caspase-9 to apoptosome?

A

dimerizes –> starts apoptosis

37
Q

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

A

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

38
Q

IAP and anti IAP

A

IAP:
XIAP: binds caspade-9,3, and 7 –> inactivates them
anti-AP
Omi and Smac: released by MOMP, promoting apoptosis; bind XIAP

39
Q

survival factors

A

extracellular signaling molecules that inhbit apoptosis, thus promoting cell survival; cells that do not receive signals wil undergo apoptosis

40
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

41
Q

what inactivates flippase?

A

caspase

42
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

43
Q

PS

A

phospholipid that serves as “eat me” signal for phagocytosis

44
Q

What are stem cells?

A
  • undifferentiated self-replicating cells that have the potential to differentiate into multiple cell types supplying tissus with renewable cells for tissue repair and regneration
  • Have 2 fundamental properties: self renewal and ability to produce differentiated cells
45
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

46
Q

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

A
47
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

48
Q

where do differentiated cells go in the gut?

A

migrate out of the crypt to populate the villi

49
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
50
Q

How is the epidermis renewed by new
differentiated cells?

A

continously renewed by stem cells proliferation in basal cell layer

51
Q

hematopoietic cells

A
  • stem cells that give rise to RBC and WBC
  • located in adult bone marrow
52
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

expressing a fluorescent reporter to label progenitors/stem cells and their progen

53
Q

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

A

totipotent cells have the potential to create a complete organism, whereas pluripotent can only create the different cell types within the body

ES are pluripotent

54
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
55
Q

Describe the stem cell niche

A
  • specialized microenvironment in the tissue containing necessary signaling molecules to promote proliferation and inhibit differentiation
  • can be formed by niche supporting cells or ECM
  • signaling molceules include wnt, hedgehog, or TGF family
56
Q

Describe the stem cells in the gut epithelia, their location and ability to differentiate, compare with stem cells in the skin and
muscle

A
57
Q

Explain the 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
58
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

59
Q

Define reprogramming and compare ES and iPS cells

A

overexpression of ES genes can induce iPS

60
Q

Explain how cells can be reprogrammed from differentiated cells to stem cells, and which genomic mechanisms are involved

A
61
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

Biol 413 (4 decks)

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