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Cell Biology (MCB 2210) > Block 4 Lectures > Flashcards

Block 4 Lectures Flashcards

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1
Q

What are the two main phases of the cell cycle?

A

Mitosis and Interphase

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2
Q

What are the 3 phases of interphase?

Include a brief description

A
  1. G1- pd between completion of previous mitosis and the initiation of DNA synthesis for the next
  2. S- period of DNA synthesis for chromosome duplication
  3. G2- period between completion of DNA replication and M phase initiation
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3
Q

What is the Go phase?

A

holds cells that exit G1 and are post mitotic and non-proliferating

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4
Q

What are the 3 checkpoints of the cell cycle?

Include a brief description

A
  1. G1/S- check if cell large enough and has enough nutrients
  2. G2/M- check if DNA replicated correctly and environment favorable
  3. Spindle Assembly/Anaphase- are chromosomes correctly attached to the spindle?
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5
Q

What does a P13K pathway do?

A

drives cell growth

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6
Q

Explain the P13K pathway

A

A growth factor activates the receptor tyrosine kinases to recruit and activate P13K at plasma membrane. P13K then binds to phosphotyrisine residues in cytoplasmic domains and generates P1(3,4,5)P3 to activate Akt which activates the protein kinase mTOR

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7
Q

What does mTOR phosphorylate in the P13K pathway? (2)

A
  1. S6-kinase which phosphorylates S6 which increases translation of mRNA
  2. 4E-BP which releases elF4E from inhibition position which initiates translation
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8
Q

What are the 2 main protein degradation pathways in euks?

A
  1. Lysosome pathways

2. Proteasome pathways

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9
Q

2 main post-translational modifications to signals during cell cycle

A
  1. phosphorylation (tyrosines, serines and threonines)

2. ubiquitination (lysines)

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10
Q

What is the proteasome?

A

very large macromolecule of about 50 protein subunits that degrades many cellular proteins; hydrolyzes ATP to provide energy needed to degrade

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11
Q

3 functions of protein degradation

A
  1. removes misfolded, damaged, or potentially toxic proteins
  2. controlled degradation of normal proteins provides appropriate levels to be maintained
  3. permits rapid responses to changing conditions
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12
Q

What is ubiquitin?

A

highly conserved polypeptide of 76 a.a that marks proteins for degradation by proteasome

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13
Q

How does a ubiquitin mark a protein for degradation?

A

Poly-ubiquitination- multiple ubiquitin molecules attach to a protein and are recognized by the proteasome

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14
Q

What does a E3 Ub-ligase do?

A

achieves the specificity of the poly-ubiquitin

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15
Q

4 ways that cyclin dependent kinase (CDK) activity is tightly regulated

A
  1. activation by cyclin-binding and t-loop phosphorylation by CDK Activating Kinase (CAK)
  2. Inhibitory phosphorylation of inhibitory of the active site by Wee1 Kinases (deactivates CDKs)
  3. Dephosphorylation of inhibitory sites by Cdc25 Phosphatases (activates CDKs)
  4. Physical Inhibition by CDK Inhibitors (CKIs)
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16
Q

What does CDK Activating Kinase do?

A

phosphorylates a specific T loop which causes a shape change to the substrate which allows activation of the CDK

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17
Q

What does Wee1 Kinase do?

Cdc25 Phosphatase?

A

Wee1 Kinase- phosphorylates and deactivates CDK activity

Cdc25 Phosphatase- dephosphorylates and activates CDK activity

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18
Q

What do CDK Inhibitors do? (CKIs)

A

bind to CDK and cause a large rearrangement of CDK active sites making it inactive

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19
Q

What are heterodimeric protein complexes?

A

consists of a regulatory subunit (cyclin) and a catalytic subunit (CDK) and controls the passage through cell cycle

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20
Q

4 cyclin-CDK complexes and at which cycles they occur at

A
  1. Early G1: Cyclin D- CDK4,6
  2. Late G1/S: Cyclin E- CDK2
  3. S: Cyclin A- CDK2
  4. M: Cyclin A,B- CDK1
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21
Q

cyclin and CDK conc throughout the cell cycle

A

CDK conc is constant, cyclin conc varies

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22
Q

3 things that regulate the cell cycle

A
  1. cyclin/CDK complexes
  2. protein phosphates
  3. ubiquitin ligases
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23
Q

G1 Cyclin-CDKs

A

activate transcription of a gene required at for DNA replication and assemble pre-replication complexes at origins

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24
Q

SCF ubiquitin ligase

A

initiates passage through restriction point by polyubiquiting inhibitors of S-phase cyclin-CDKs so the inhibitors are degraded

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25
Q

S-phase cyclin-CDKs

A

activate DNA replication origins

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26
Q

Mitotic cyclin- CDKs

A

trigger entry into mitosis

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27
Q

Anaphase promoting complex (APC)

A

induces anaphase once kinetochores properly attached and triggers degradation of the cohesions that connect sister chromatids by enzyme seperase

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28
Q

4 examples of mitotic cyclin-CDKS at work

A
  1. phosphorylate condensins which condenses chromosomes
  2. phosphorylate nuclear lamines to breakdown nuclear envelope
  3. phosphorylate MT-assc. proteins to change MT dynamics
  4. phosphorylate ER or Golgi assc. proteins to reorganize the ER and Golgi
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29
Q

Definition of a cell cycle checkpoint

A

negative feedback mechanism that blocks cell cycle progression if wrong
inhibits cyclin-CDK transitions and allows time for correction or repair

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30
Q

2 main kinds of cell cycle checkpoints

A
  1. DNA damage checkpoints

2. spindle checkpoints

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31
Q

3 components of cell cycle checkpoints

A
  1. sensor proteins- detect abnormalities
  2. transducer proteins- relay or amp damaged signal
  3. effector proteins- halt cell cycle in response to damage signal
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32
Q

Cdc14 Phosphatase

A

activated when chromosomes are correctly segregated in anaphase
this phosphorylates and activates a protein that directs the APC to mitotic cyclins so they are broken down
changes cell to reshape into interphase form

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33
Q

3 ways we have studied the cell cycle

A
  1. genetic studies in yeast
  2. xenopus egg extracts
  3. cellular studies in animals
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34
Q

what did genetic studies in yeast tell us about the cell cycle?

A

found cell division cycle (cdc) mutants and helped ID kinases and phosphorylates that control entry in mitosis

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35
Q

what did xenopus egg extract studies tell us about the cell cycle?

A

helped ID cyclin B as a component of maturation-promoting factor (MPF)
MPF activity low in interphase and high as entering mitosis
eggs arrested in G2 could be induced into M phase by MPF activity

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36
Q

Cyclin B

normal vs. mutated

A

must be expressed then degraded for proper mitosis
in normal- mitosis
mutated- lacks a “destruction box” which normally promotes cyclin ubiquitination and degradation so it never breaks down and MTs don’t depolymerize

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37
Q

Cyclin D

A

required for passage through G1/S restriction point

is inhibited by microinjecting antibodies during Go or early G1, no DNA replication

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38
Q

Rec8

A

specialized cohesion unit and centromere

allows proper segregation during anaphase I and II

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39
Q

Synapsis

A

pairing along lengths of chromosomes, happens in meiosis NOT mitosis

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40
Q

when do centromeres divide in mitosis? meiosis?

A

mitosis- anaphase

meiosis- anaphase II

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41
Q

When does recombination happen in mitosis? meiosis?

A

mitosis- never

meiosis- at least once

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42
Q

5 major tissue types

A
  1. epithelial
  2. connective
  3. muscle
  4. nervous
  5. blood
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43
Q

2 ways cells have a connection

A
  1. cell-cell adhesions (directly adhere) with cell adhesion molecules (CAMs)
  2. cell-matrix adhesion (indirectly adhere) with binding of receptors to ECM
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44
Q

What is the extracellular matrix

A

complex meshwork or proteins and polysaccharides secreted by cells into extracellular spaces
holds tissues together and coordinates cellular functions by activating intracellular pathways

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45
Q

tight junctions

A

seals gaps between epithelial cells

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46
Q

adherens junctions

A

connects actin filaments bundle in one cell with that of next one

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47
Q

desmosomes

A

connects intermediate filaments in one cell to those of next

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48
Q

gap junctions

A

allows passage of small water-soluble molecules from cell to cell

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49
Q

hemi-desmosomes

A

anchors intermediate filaments of cell to ECM

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50
Q

focal adhesions

A

anchors actin filaments in cell to ECM

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51
Q

cis vs trans

A

cis- same side

trans- opposite sides

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52
Q

cell adhesion molecules (CAMs)

A

can generate very tight adhesions when many weak interactions are combines

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53
Q

2 major families of CAMs and examples

A
  1. hemophilic- same CAM both sides
    ex: cadherins or Ig superfamily
  2. heterophilic- different CAM classes
    ex: intigrins or selectins
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54
Q

Cadherin works at 2 sites of cell adhesion

A
  1. adherens junction- cadherins links directly to intracellular actin filaments via caterins
  2. desmosomes- cadherins linked indirectly to intermediate filaments
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55
Q

2 actin filament anchoring junctions

A
  1. adherens junction (cell-cell)

2. focal adhesions (cell-matrix)

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56
Q

2 intermediate filament anchoring junctions

A
  1. desmosomes (cell-cell)

2. hemi-desmosomes (cell-matrix)

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57
Q

1 occluding junction

A

tight junction`

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58
Q

1 channel forming junction

A

gap junction

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59
Q

E-cadherin

A

main location in many epithelia with adherins junctions

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60
Q

tight junctions:
function
location

A

perform a barrier function and restrict diffusion of proteins b/t apical and basolateral regions and of macromolecules in spaces b/t cells
located between adjacent epithelial cells beneath apical surface

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61
Q

gap junction function

A

allow small molecules to pass directly between adjacent cells
gap where ions and molecules

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62
Q

3 kinds of ECM proteins (description and examples)

A
  1. Proteoglycons (glycoproteins that cushion cells)
    ex: perlecan
  2. Collagens (insoluble proteins that provide structural integrity and mechanical strength
    ex: sheet forming and fibriliar collagens
  3. Multiadhesions matrix proteins (cross link receptors and other ECM components)
    ex. laminin, fibronectin, nidogen/entactin
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63
Q

2 things that the ECM comprise

A
  1. basal lamina

2. connective tissue

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64
Q

what is the basal lamina?

A

thin (260-120 nm) sheet of meshwork ECM components that underlies or surrounds many epithelial and non-epithelial tissues
links to cells by adhesion receptors

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65
Q

4 ubiquitous proteins found in the basal lamina and functions

A
  1. Type IV collagen- trimetric protein that forms a fibrous 2D network
  2. laminins- forms fibrous 2D network and binds to adhesion receptors
  3. perlecan- crosslink networks
  4. nidogen- crosslink networks
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66
Q

What is connective tissue in relation to ECM?

A

insoluble network of ECM that’s rich in collagen

volume is mostly ECM, not cells

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67
Q

examples of connective tissue

most abundant cell and protein in connective tissue?

A

bone, tendon, and cartilage
fibroblasts
collagen

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68
Q

Structure of collagen

A

triple helix of 3 polypeptide alpha chains with high abundance of glycine, proline, and hydroxyproline

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69
Q

Protoglycans

A

subset of secreted or surface attacked glycoproteins that contain glycosaminoglycans (GAGs) and are involved in cell-matrix interactions
cushion cells

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70
Q

glycosaminoglycans

A

specialized polysaccharides chains which many (-) charges

long linear polymers of repeating disaccharides

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71
Q

Hyaluronic acid

A

important GAG

surrounds migrating and proliferating cells and produces lubricating quality in joints

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72
Q

fibronectin:
structure
function

A

long, flexible molecule with multiple domains for various bindings with collagens, proteoglycans, adhesion receptors, etc
important for organizing components of ECM, influence shape and movement of cells, organizes actin cytoskeleton, essential for migration and differentiation, bind to integrins on plasma membrane on plasma membrane

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73
Q

focal adhesions

A

contain integrin which mediates linkage between fibronectin in ECM and in intracellular actin cytoskeleton

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74
Q

loss of E-cadherin activity in cancer cells..

A

converts epithelial cells to malignant carcinoma cells

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75
Q

function of Integrins

A

adhesion receptor
provide a direct link between ECM and actin filaments through ABPs like talin and vinculin
controlled by signaling pathways

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76
Q

2 conformations of integrins

why are there two?

A
  1. inactive (low affinity)
  2. active (high affinity)
    reflects changes in cytoplasmic and ER domains of proteins
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77
Q

2 kinds of signaling mediated by integrins

A
  1. inside-out: cytoskeleton can influence binding to ECM

2. outside-in: interactions with ECM can alter organization of cytoskeleton

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78
Q

how do integrins initiate signaling pathways

A

intigrins engaged by proteins in ECM signal to focal adhesion kinase and c-Src which activates P13K and Rho-family GTPases
signaling interacts with downstream

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79
Q

4 steps of cell motility

A
  1. forward PROTRUSION of lamellipodium driven by force of actin polymerization
  2. ADHESION of lamellipodia as it interacts with substrates in front of the cell
  3. cell body TRANSLOCATION occurs via a dynamic network contraction model where myosin-mediated contraction of the actin at the junction between cell body and lamellipodia pulls cell body forward
  4. De-adhesion and tail retraction as rear cell moves forward
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80
Q

3 enzymes that help drive motility

A

Rho, Rac, and Cdc42

81
Q

role of Rho, Rac, and Cdc42 in cell motility

A

Cdc42 does adhesion at the front
Rac (front)- leads to Arp2.3 complex
Rho (back) leads to myosin II activation

82
Q

normal function of:
Cdc42 and Rac
Rho

A

stimulates actin assembly and protrusion

regulates focal adhesion formation and myosin-II mediated contraction

83
Q

Arp 2/3 and Arpin

A

Arpin is Arp 2/3 inhibitor which is activated by same thing that activates the Arp 2/3 (Rac)
paradoxical circuit

84
Q

6 steps of synaptic vesicle trafficking

A
  1. import of neurotransmitter
  2. movement of vesicle to active zone
  3. vesicle docking at plasma membrane
  4. exocytosis of neurotransmitter triggered by influx of Ca+2
  5. reuptake of neurotransmitter
  6. recovery of synaptic vesicles via endocytosis
85
Q

3 classes of muscle

A
  1. skeletal 2. smooth 3. cardiac
86
Q

skeletal muscle broken down…

A

myofibers (muscle fibers) made up of multiple myobrils (contractile bundles) which are made up of sarcomeres (small contractile units)

87
Q

2 filaments that make up the sarcomere

A
  1. thin filaments (actin)

2. thick filaments (myosin II macromolecules)

88
Q

Leiomodins

A

actin nucleators that are thought to create actin in muscle cells

89
Q

CapZ and tropomodulin

A

CapZ- caps actin filament at (+) end, attaches filament to z-disk
Tropomodulin- caps (-) end of actin filaments
both stabilize a.f. by preventing polymerization and depolymerization

90
Q

nebulin

A

protein that wraps along entire length of thin filament and acts like a ruler to control length of filaments

91
Q

titin

A

huge fibrous protein that connects myosin ends to Zdisks, extends through filaments, and out on other side, keeps myosin centered

92
Q

sliding model of contraction

A

sarcomeres shorten during contraction because myosin filaments slide past a.f.
bipolar myosin pulls a.f. and Zdisks toward it and causes sarcomere to shorten causing contraction

93
Q

ATP and Ca+2 in skeletal muscle contraction

A

signal from motor neuron to muscle triggers an action potential in muscle cell that spread down t-tubule which extends into cytosol of myofibril; signal travels to sarcoplasmic reticulum which releases its stored Ca+2

94
Q

When will myosin not bind to actin filament in muscle contraction

A

if Ca+2 not present

95
Q

tropomyosin and troponin roles in muscle contraction

A

tropomyosin- forms a chain along thin filament and blocks myosin movement if no Ca+2 present
troponin- moves tropomyosin out of the way if Ca+2 is present

96
Q

Immunological Synapses

A

focal point for exocytosis, endocytosis, and signaling at physical junction between lymphocytes
activation of tcell receptors and integrins leads to signaling that drives adhesion and cytoskeletal rearrangements of IS formation

97
Q

5 steps of leukocytes crossing from blood to tissues

A
  1. resting state
  2. endothelial activation and leukocyte attachment and rolling (weak interaction b/t selectin receptors and carb ligands)
  3. leukocyte activation (PAF activates integrin)
  4. Firm adhesion via integrin/CAM bond
  5. extravasation (leukocyte shape changes and migrates b/t epithelial cells in underlying tissues)
98
Q

Cilia
Motile cilia
Flagella

A 
tiny hairlike appendages with MT arrangement at core
function is to move fluid over cell surfaces
much longer, less numerous, on sperm and flagellates
99
Q

axoneme

A

core of cilia and flagella
made up of 9+2 arrangement of MTs
9 outer doublets, 1 center doublet
arises from basal body

100
Q

structure of axoneme

A

outer MTs connected to inner MTs via radical spokes

inner MTs stabilized by inner sheath and connected by bridging protein

101
Q

nexin

A

protein that connects out doublets of MTs and provides an elastic linkage between them to allow movement relative to one another

102
Q

ciliary dynein

A

between a doublet of MT, on MT A and reach out and grabs MT B and mediates movement

103
Q

function and structure of a basal body

A

function- nucleates cilia and flagella

structure- 9 triplet MTs

104
Q

structure of a centrosome

A

pair of centrioles surrounded by pericentriolar matrix (PCM)

105
Q

primary cilium

A

present on almost every cell of the human body
originates from “mother centriole”
non-motile, acts as antenna to sense physical and biochemical signals in EC environment and transfer in

106
Q

movement of motile cilia

A

asymmetric, power stroke followed by recovery stroke

107
Q

movement of motile flagella

A

sinusoidal and symmetric

108
Q

what provides the force for cilia of flagella beating

A

ATP dependent movement of ciliary dyein along MTs

109
Q

Sliding MT hypothesis

A

ciliary and flagellar bending can be powered by sliding of outer doublet MTs relative to each other combines with nexin cross-links
sliding is powered by ATP-dependent ciliary dynein movement toward (-) ends of MTs

110
Q

Intraflagellular Transport (IFT)

A

controls cilia biogenesis and signal transduction

111
Q

totipotent

A

ability of single cell to divide and produce all the differentiated cells of organisms (only zygote)

112
Q

pluripotent (and ex.)

A

ability to form all lineages of body (embryonic stem cells)

113
Q

multipotent (and ex.)

A

ability of adult stem cells to form multiple cells of 1 lineage (hematopoetic stem cells- HSCs)

114
Q

unipotent (and ex.)

A

cells form 1 type (spermatogonial stem cells)

115
Q

3 defining properties of a stem cell

A
  1. it is not itself terminally differentiated
  2. it can divide without limit
  3. when it divides, each daughter cell has two possible fates- can remain a stem cell or go through differentiation
116
Q

what are the main roles of stem cells

A

to give rise to different cell types

provide indefinite supply of fresh differentiated cells where lost, discarded, or in need of larger number

117
Q

where are hematopoetic stem cells (HSCs) found?

A

in bone marrow, peripheral blood, and umbilical cord blood

118
Q

2 kinds of transplantations assc. with stem cells. Explain.

A
  1. bone marrow transplant (BMT)
  2. peripheral blood stem cell transplant (PBSCT)
    both restore stem cells that have been destroyed by chemo or radiation
    commonly used in leukemia or lymphoma treatments
119
Q

autologous vs, allogenic transplants

A

autologous- patients receive their own stem cells

allogenic- receive stem cells from parent or sibling

120
Q

what is the epidermis

A

forms outer covering of skins and creates a waterproof barrier that is self-repairing and continuously renewed

121
Q

where are stem cells located

A

wherever there is a recurring need to replace differentiated cells that cant themselves divide

122
Q

what is nuclear reprogramming

A

a switch in nuclear gene expression from one kind of somatic cell to that of an embryonic or other

123
Q

3 reasons that nuclear reprogramming is of interest

A
  1. if we ID reprogramming, we can better understand natural specialization and differentiation
  2. enables us to analyze nature of diseases and screen for therapeutic drugs
  3. cell-replacement therapy- defective cells replaced by normal cells of the same kind but derived from different cell type
124
Q

transdifferentiation and plasticity

A

notion that somatic stem cells have broadened potency and can generate cells of other lineages (controversial in mammals)

125
Q

2 major approaches for nuclear reprogramming

A
  1. induced pluripotency

2. nuclear transfer to eggs

126
Q

induced pluripotency

A

viral expression of 4 genes (Oct4, Sox2, Klf4, c-Myc) that can reprogram somatic cells to a state that is similar to embryonic stem cells (ES cells)
called induced pluripotent stem cells (iPS cells)

127
Q

Induced pluripotent stem cells

A

somatic cells that are reprogramed to a state similar to ES cells after activation of Oct4, Sox2, Klf4, and c-Myc

128
Q

events that could happen during reprogramming

A

changes in signal transduction pathways, chromatin reorganization and modification, actin rearrangements, methylation of DNA, miRNA expression, altered transcription patterns

129
Q

nuclear transfer to eggs

A

somatic cell nucleus is transplanted to enucleated egg and in culture can give rise to ES cells
clones with surrogate mother
new cell types/organisms generated

130
Q

examples of bacteria

A

coccus, coccobacillus, vibrio, bacillus, spirillum, spirochete

131
Q

DNA virus ex

A

poxvirus, herpes, adenovirus, papilloma virus, parvovirus

132
Q

RNA virus ex

A

influenza virus, mumps virus, rotavirus, rabies, HIV (AIDS virus), corona virus (common cold), poliovirus, LCM virus

133
Q

are viruses alive?

A

not exactly alive, they require a living thing for replications

134
Q

2 ways viruses can enter

and what does it depend on

A
  1. directly fusing with plasma membrane
  2. via endocytic-based mechanisms (within endosomes or an non-enveloped capsules)
    both depend of virus and cell type
135
Q

cells vs microbial cells in human body

A

10^13 human cells, 10^14 microbial cells

136
Q

normal flora

A

commensal microbes that are usual beneficial to the body

137
Q

definition of pathogen

A

organisms that can cause overt disease in health people

cause infectious disease

138
Q

difference between pathogen and commensal microbe

A

pathogen can breech barriers and survive in places in the host that the commensal microbe can’t

139
Q

virulence factors

A

proteins that contribute to the ability of an organism to cause diseases when grouped together

140
Q

genes of virulence factors

A

usually clustered together either in pathogenicity islands on bacterial chromosomes or on extra-chromosomal plasmids or carried on bacterial viruses

141
Q

5 tasks a pathogen must perform to be considered successful

A
  1. colonize their host (est. in specific location)
  2. multiply (grow/divide in particular environment)
  3. evade host responses- avoid or inactivate
  4. cause damage- alter or disrupt normal host
  5. spread- efficiently exit old host and go to new
142
Q

4 common virulence factors

A
  1. Toxins
  2. adhesions and/or invasins
  3. secretion systems
  4. effectors
143
Q

what are toxins

A

(virulence) proteins that are released from bacteria that alter or disrupt normal processes that occur either outside or inside the cell

144
Q

adhesions and/or invasins

A

virulence proteins expressed on bacterial surface that promote attachment to cells or entry into cells

145
Q

secretion systems

A

specialized molecular machines that translocate (inject) proteins from bacteria into host cells (Type 3 and Type 4) (T3SS and T4SS)

146
Q

effectors

A

translocated proteins that alter or disrupt normal processes within host cell

147
Q

AB Toxins

A

secreted by pathogens
has a A subunit- enzymatically active
B subunit- cell binding subunit

148
Q

antharax lethal toxin

A

AB Toxin

protease that modulates MAP kinase signaling cascades

149
Q

Shiga Toxins (Stx)

A

AB Toxin
inactivates ribosome to prevent protein synthesis
bypasses late endocytic phase and goes from TGN to ER

150
Q

Invasin protein

A

(mimics)
structural similarities to fibronectin,
surface protein that bacteria use to bid and enter host cell
ex: Yersinia

151
Q

Internalins

A

multiple surface expressed proteins that bacteria bind to invade
ex: listeria monocytogenes

152
Q

Intimin

A

surface expressed adhesion, doesn’t recognize host cell

used by EPEC and EHEC (strands of E.coli)

153
Q

Type 3 Secretion System (T3SS)

A

can deliver effector proteins into cytosol of a host cell

many bacteria use this to promote actin assembly and invasion

154
Q

zipper and trigger mechanisms

A

actin-dependent

bacteria use them to induce invasion into nonphagocytotic cells

155
Q

3 strategies of bacterial cells once inside a host

A
  1. vacuole escape
  2. prevention of lysosomal maturation
    3, growth with lysosomes
156
Q

M.Tb compartment in host cell

A

remains in compartment with early endosomal markers and continues to communicate with plasma membrane via transport vesicles

157
Q

Salmonella compartment in host cell

A

replicates in compartment with late endosomal markers and uses T3SS effector

158
Q

Legionella compartment in host cell

A

replicate in compartment that is wrapped in several layers of ER membrane (uses T4SS effectors)

159
Q

Chlamydia compartment in host cell

A

replicates in an exocytic compartment that fuses with vesicles forming from TGN (uses T3SS effector)

160
Q

3 effectors that disrupt right junctions

A
  1. pathogenic E. coli- uses T3SS effector proteins (EspF, EspG, and Map) to alter tight junction integrity
  2. Salmonella- uses 4 T3SS (SipA, SopB, SopE, SopE2) to modify right junctions
  3. Helicobacter pylori- translocates T4SS effector CagA to alter junctions
161
Q

5 Steps of Litsteria invasion

A
  1. attached to E-cadherin on cell surface of epithelial cells
  2. induce own uptake by zipper mechanism
  3. in phagosome, bacteria secretes protein Listerolysin (LLO)
  4. in cytosol, bacteria replicates and continues to secrete LLO
  5. LLO in cytosol rapidly degraded by proteasomes so host plasma membrane remains intact
162
Q

what is listerolysin

A

a protein secreted by listeria bacteria as it enters the host cells
it forms oligomers in host cell membrane creating large pores and disrupting the membrance

163
Q

ActA

A

protein on the surface of cells that stimulates actin assembly
activates Arp 2/3
structure is similar to WASP family proteins

164
Q

pathogens and actin-based motility

A

many pathrogens use actin-based motility by using the force of actin polymerization to drive movement through cytoplasm

165
Q

actin-based motility pathogens have virulence factors that work in 3 ways (examples)

A
  1. nucleate actin (Rickettsia)
  2. activate Arp2/3 Complex (Listeria and Baculorins)
  3. activate N-Wasp (shigella, vaccinia, EPEC, EHEC)
166
Q

3 Pathogen Controls of Actin Assembly

A
  1. A36R and TIR activate tyrosine kinase signaling cascades that lead to actin assembly
  2. ISSA and EspFu bind and activate N-WASP
  3. Act A binds and activates Arp2/3 and Ca2 acts as formin mimic
167
Q

EHEC 0157 characteristic

A

major foodborne pathogen assc. with undercooked ground beef of leafy veggies
-highly infectious, causes many illnesses in US, UK, Japan
hemolytic uremic syndrome (HUS) -kidney failure and death

168
Q

carcinomas
sarcomas
leukemias and lymphocytes

A

cancers that arise from epithelial cells
arise from connective or muscle tissue
arise from blood cells

169
Q

carcinogenesis

A

generation of cancer

170
Q

2 heritable properties of cancer cells

A
  1. reproduce in defiance of normal restraints on cell grown and division
  2. invade and colonize territories normally conserved for other cells
171
Q

tumor definition and the 2 options is can lead to

A

neoplasm- new growth

  1. benign- noninvasive
  2. malignant- ability to invade other cells by metastasis
172
Q

most cancers derive from…

A

single abnormal cell with a mutation causing it to out-grow, out-divide, and out-live any of its neighbors

173
Q

3 main genes when concerning cancer cells

A
  1. proto-oncogenes
  2. tumor suppressor genes
  3. caretaker genes
174
Q

normal function of proto-oncogenes

A

promote cell survival and proliferation

175
Q

normal function of tumor suppressor genes

A

inhibit cell survival or proliferation

176
Q

normal function of caretaker genes

A

repair or prevent DNA damage

177
Q

5 kinds of tumor suppressor genes

A
  1. proteins that regulate or inhibit cell cycle progression (ex. Rb)
  2. receptors at signal transducers for hormones or development signals (ex. TGF-B)
  3. checkpoint control proteins that arrest cell cycle if DNA damaged or chromosomes abnormal (ex. p53)
  4. proteins that promote apoptosis
  5. enzymes that function in DNA repair
178
Q

Loss of function vs Gain of function

A

LOF- tumor suppressor and caretaker genes

GOF- proto-oncogenes

179
Q

Function of Rb

A

regulates G1/S phase

180
Q

Un-phosphorylated Rb

A

binds to E2F transcription factor to prevent activation of many genes for DNA synthesis

181
Q

What phosphorylates Rb

A

cyclinD-CDK4

182
Q

phosphorylated Rb

A

releases E2F and activates transcription of genes needed for S phase

183
Q

cancers in Rb from..

A

overproduction of cyclinD, loss of p16, loss of Rb

184
Q

oncogenic transformation

A

cells that are rounder, less adherent to other cells, forms 3d clusters, and continue to grow which others have stopped

185
Q

proto-oncogene definition

A

any gene that, if mutated, is capable of transforming cells in culture or induce cancers in animals

186
Q

old school approach to studying proto-oncogenes

A

oncogene rasD was identified as it encodes activated form of Ras
rasD transforms some cultures of 3T3 cells

187
Q

new school approach to studying proto-oncogenes

A

hybridizating methods using DNA microarrays can detect duplications or deletions of genes in tumor cells
fluorescently labeled DNA compared to normal

188
Q

multi-hit model of cancer

A

many events are required for carcinogenesis

overexpressed proto-oncogene and rasD

189
Q

3 examples of proto-oncogenes and what oncogene they descended from

A
  1. v-ras (from GTPase Ras)
  2. v-myc (c-myc mutant)
  3. v-src (c-src mutant)
190
Q

how does p53 work

A

in response to hyperproliterative signals, DNA damage, hypoxia, and or telomere shoertening causes p53 levels to rise which causes cells to undergo cell cycle arrest, apoptosis, or replicative cell senescence

191
Q

rise in p53 leads to..

A

cell cycle arrest, apoptosis, replicative cell cycle senescence

192
Q

what is replicative cell senescence

A

cell looses ability to divide

193
Q

loss of p53 function leads to

A

abolishing of cell cycle checkpoints

194
Q

ATM-mediated phosphorylation of p53 leads to…

A

proper function of p53

195
Q

active mam2 and p53 leads to…

A

mam2 bind to p53 and causes polyuquitation and degradation of p53

196
Q

angiogenesis

A

growth of new blood cells

197
Q

how to tumors persist and spread

A

cancer cells secrete molecules that stimulate angiogenesis, and malignant cancers invade nearby tissues and continuously proliferate and spread

198
Q

cancer stem cells

A

can maintain many tumors, and can self renew to produce additional malignant stem cells and generate rapidly dividing amplifying cells

Cell Biology (MCB 2210) (2 decks)

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