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lecture 6 Flashcards

apoptosis

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1
Q

what does apoptosis do

A

physiological method to eliminate unwanted/unnecessary cells

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2
Q

example of apoptosis

A

during development, paws/hands have extra tissue which is webbing between digits; to get rid of it is apoptosis is triggered

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3
Q

define apoptosis

A

controlled, polite cell death

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4
Q

define necrosis

A

bad; uncontrolled cell death

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5
Q

what happens in necrosis

A

cells burst, release intracellular contents into extracellular space (which is bad because harmful enzymes spill out into space which is dangerous and can trigger more necrotic death)

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6
Q

what else can necrosis trigger

A

can trigger immune response by promoting inflammation; white blood cells infiltrate which is damaging to normal tissues

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7
Q

what happens in apoptosis

A

cells don’t burst and release; they are broken into small components so they dissasemble

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8
Q

describe apoptosis (how regulated it is)

A

highly regulated; everything in cell remains contained in barrier; b/c job of machinery is to make sure stuff remains where its supposed to be

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9
Q

how does stuff get taken away in apoptosis

A

when broken into chunks, things like macrophages come in and phagocytose, clean up dead cell, make sure tissue operates as healthily as possible

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10
Q

irreversible injury

A

cell can no longer function, structural integrity is disrupted

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11
Q

what happens in irreversible injruy

A

cell needs to die; prefers to do so through apoptosis

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12
Q

what happens in normal cell injury

A

cells usually bounce back; thru homeostasis they upregulate or downregulate certain genes

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13
Q

when does necrosis happen

A

if you have a massive injury, happens very quickly, not enough time for cells to undergo apoptosis

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14
Q

what are signs of reversible cell injury

A

reduced oxphos (E production) and depletion of ATP –> sign that mitochondria is injured
physical injury –> cell swelling
morphological changes to cell as injuries accumulate –> ER, mitochondria, cytoskeleton change function and appearance

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15
Q

what’s the end result if these things are allowed to progress

A

cell death

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16
Q

how can u tell necrosis happens

A

cell burst

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17
Q

how can u tell apoptosis happened

A

cellular fragmentation, not bursting

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18
Q

what does apoptosis depend on / what molecular mechanisms allow it to occur

A

depends on intracellular proteolytic cascade mediated by caspases

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19
Q

important mediator of apoptotic process

A

caspase

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20
Q

what happens when apoptosis is triggered

A

apoptotic signal –> caspase becomes active, initiate apoptotic signaling cascade resulting in morphological changes like cell fragmentation & packing into smaller pieces for engulfment by macrophages

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21
Q

what are caspases

A

proteases

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22
Q

what happens when caspases are activated

A

bind and cleave other proteins within cytoplasm

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23
Q

what is caspase / how does it transmit signal

A

caspase is a signaling protein, transmits signals by cleaving downstream proteins

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24
Q

how are caspases activated

A

cleave themselvse

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25
Q

describe inactivated caspases

A

monomers floating around in cytoplasm; intact, full length

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26
Q

what happens when cell decides to undergo apoptosis

A

apoptotic signal arrives, signal is gonna assemble an adaptor complex –> a dimer

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27
Q

what is the adaptor complex

A

2 identical dimers that can each bind and recruit a caspase to the complex

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28
Q

what is the job of adaptor

A

to bring caspases close enough together so they can cleave each otehr

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29
Q

what is this cleavage analagous to

A

trans autophosphorylation

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30
Q

what happens after the dimerization event hapens

A

proteins enzymatic activity gets close enough to act on their neighbors (in RTKs thats a phosphate group added) (in caspases, one cleaves the other)

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31
Q

what does cleavage do

A

initiates activation

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32
Q

what is this cleavage process called, and where is it in

A

cross cleavage; common to all mechanisms of caspase activation

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33
Q

what happens once cleaved

A

active caspase dimers are released, labeled as mature active caspases

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34
Q

what do mature active caspases do

A

cleave other proteins downstream in apoptotic pathway

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35
Q

initiator caspases

A

caspases that are initially activated; these are caspases that get things going

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36
Q

what do initiator caspases do

A

start process in response to upstream signal; go and activate executioner caspases next

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37
Q

executioner caspases

A

go and cleave all downstream targets needed for apoptosis to occur

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38
Q

what’s on top of next step of pathway

A

active initiator caspase that’s been cleaveed

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39
Q

what do active initiator caspases do next

A

goes and cleaves executioner caspases to activate them

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40
Q

how are executioners different from initiator caspases

A

executioners are already dimerized, but inactive

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41
Q

why don’t executioners do cross cleavage

A

if they did, they wouldn’t be able to exist as inactive dimers b/c they would just cleave each other

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42
Q

who cleaves executioner caspases

A

initiator caspases

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43
Q

what happens when initiator caspases cleave executioner caspases

A

similar rearrangement; executioners go and cleave multiple types of cell proteins

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44
Q

what does this process of cleavage by executioners result in

A

process of apoptosis

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45
Q

how many pathways needed for apoptosis to occur

A

MANY; we are just looking at one specific oen

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46
Q

how many targets do executioners have

A

multiple

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47
Q

how much does one set of initiator caspase activate

A

multiple dimers of executioner caspase; not a one to one

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48
Q

what does each downstream step represent

A

amplification where one upstream protein can activate multiple copies of downstream proteins amplifying signal

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49
Q

describe example pathway of what an executioner caspase is gonna do

A

dna cleaved into regular sized fragments

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50
Q

what is one hallmark of apoptosis

A

dna structure of cells undergoing apoptosis is cleaved in regular sized fragments

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51
Q

what does this dna cleaving allow you to determine

A

help determine when cell undergoes apoptosis vs necrossi

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52
Q

what is the end result of this specific pathway

A

it cuts DNA b/w histones [histones are regularly spaced in genomic DNA, cuts regularly spaced, so you get spaced out DNA ladders]

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53
Q

what happens if this dna cleavage pathway happens in healthy cells

A

NEVER want this to happen; cells will die if you cleave DNA ; hella rightly regulated

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54
Q

what are key players in executioner caspases controlling cleavage of DNA

A

CAD proteins, caspase activated DNase

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55
Q

what is activated by executioner caspase

A

CAD

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56
Q

what is CAD activity

A

DNase activity; cuts DNA

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57
Q

what happens when there’s no apoptosis

A

CAD is inhibited by the inhibitor iCAD –> held in place

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58
Q

what does active executioner caspase do to CAD

A

it cleaves iCAD or inhibitor of CAD; CAD is ready

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59
Q

what happens when iCAD / CAD inhibitor is degraded

A

CAD is released and becomes active

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60
Q

what can CAD do when its active

A

cleaves DNA between histones, resulting in regular DNA pattern

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61
Q

what is net result of inhibiting the inhibitor

A

activation of protein

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62
Q

what is the normal resting state

A

it’s held in inactive inhibited state; to activate you inhibit the inhibitor

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63
Q

what does CAD degrade

A

degrades DNA between histones to begin orderly destruction of nuclear contents

64
Q

what does CAD convert

A

converts genomic DNA into ladder of regularly sized pieces (experimental hallmark of cells undergoing apoptosis)

65
Q

why is immune system good at triggering apoptosis

A

immune cells kill cancer cells; T cells kill tumor cells; tumor cells have ways to evade apoptotic signals, so immune system needs to get good at triggering apoptosis

66
Q

two pathways of apoptosis triggered by immune cells

A

extrinsic and intrinsic pathway

67
Q

extrinsic pathway

A

cell receives apoptosis signal from outside / external environment

68
Q

example scenario of extrinsic pathway

A

imagine a virus infected cell that’s gonna be taken out by T cell

69
Q

what are key players in extrinsic pathway

A

caspase 8, adaptor protein: FADD, Fas death receptors

70
Q

what is caspase 8

A

initiator caspase of extrinsic apoptotic pathway

71
Q

what are adaptor proteins

A

bring inactive initiator caspases together so they can close cleave each other to become activated

72
Q

what is specific adaptor protein in extrinsic apoptosis

A

FADD protein

73
Q

what is the other key thing in extrinsic apoptosis

A

needs to be a receptor involved since signal is coming from outside; receptor need to be able to recognize signal to transmit info across hydrophobic barrier of plasma membrane

74
Q

specific receptor in extrinsic pathway

A

Fas death receptor

75
Q

describe receptors in cell when it’s normal and not undergoing extrinsic apoptosis

A

death receptors at surface; inactive, not bound

76
Q

describe adaptor proteins in cell when it’s normal and not undergoing extrinsic apoptosis

A

adaptor proteins in cytoplasm; folded up & inactive, not bringing anything together

77
Q

describe caspases in cell when it’s normal and not undergoing extrinsic apoptosis

A

caspase 8 is monomer, floating around cytoplasm, inactive

78
Q

what comes from top

A

signal; killer lymphocyte or killer T cell

79
Q

job of killer T cell

A

go in and trigger death of cells (cancer cells, infected or damaged cells, etc.)

80
Q

how does killer T cell trigger death

A

expresses fast ligand on its surface –> contact dependent signaling

81
Q

describe fast ligand

A

ligand is a trimer; binds to 3 Fas death receptors

82
Q

what does fast ligand bind to

A

Fas death receptors

83
Q

what happens once fast ligand activates fas death receptors

A

can now bind and unfold FADD adaptor proteins

84
Q

what happens when FADD adaptor proteins are unfolded

A

they are active can bind to initiator caspases

85
Q

what do adaptor proteins do

A

bring caspases close enough together so they can cleave each other to activate

86
Q

what happens when caspase 8s are cleaved

A

release as dimers (caspase-8 dimer), go and activate executioner caspases

87
Q

what are executioner caspases in extrinsic pathways

A

caspases 3 and 7

88
Q

what happens after to killer T cell

A

job is done; gonna go and find other affected cells

89
Q

general features that show up in apoptosis pathways

A

adaptor proteins, cross-cleavage, initiator caspases activate downstream executioners

90
Q

what do adaptor proteins do

A

bring initiator caspases close enough together for cross cleavage

91
Q

what is specific to extrinsic pathway

A

caspase 8, trimers of receptors, signal comes from T cell, specific FADD adaptor proteins

92
Q

where does extrinsic pathway occur

A

contained within cell

93
Q

what is intrinsic pathway

A

even more polite way to die; cell decides for itself to die for betterment of group

94
Q

what is central regulatory node of intrinsic apoptotic pathway

A

mitochondria

95
Q

what happens to mitochondria in intrinsic pathway

A

mitochondria can’t function as efficiently, ATP production drops, cell homeostasis goes out the window

96
Q

what happens if ATP production drops

A

cell is metabolically not active enough and dies

97
Q

what is key factor cell is gonna listen to in inactive pathway

A

when ATP can’t be produced in enough abundance

98
Q

what does intrinsic pathway of apoptosis depend on

A

mitochondria

99
Q

how do cells know mitochondria isn’t working properly

A

if mitochondria is leaky

100
Q

what happens if mitochondria membrane is leaky

A

proton gradient of oxphos is gonna be destroyed –> ATP production is gonna crater; apoptosis

101
Q

what should mitochondrial membrane be for regular cell

A

intact

102
Q

how does cell know when mitochondria membrane is leaky

A

cytochrome c

103
Q

what’s up w/ cytochrome c in healthy mitochondria

A

cytochrome C always held within mitochondria; never exposed to cytoplasm [good thing; membrane is intact and fully producing ATP]

104
Q

how is mitochondria damaged

A

UV radiation, triggers oxygen radicals that damage membranes and make them leaky

105
Q

where is cytochromes not supposed to be

A

in cytoplasm (green)

106
Q

what is trigger for intrinsic apoptotic pathway

A

cytochromes in cytoplasm (supposed to be in membrane)

107
Q

describe damaged mitochondria in signaling pathway

A

cytochrome c released into cytoplasm

108
Q

what detects cytochrome c in cytoplasm

A

adaptor protein Apaf1

109
Q

job of adaptor protein

A

assemble initiator caspases so they are close enough to cleave each other

110
Q

what does Apaf1 do

A

binds cytochrome c

111
Q

what does Apaf1-cytochrome c binding do

A

triggers conformational change in adaptor that allows it to assemble into oligomerized form

112
Q

what does cytochrome c do (important)

A

cytochrome c binds one copy of adaptor, triggers conformational change that allows it to form higher order oligomer

113
Q

what happens once oligomer is formed

A

recruits initiator caspases

114
Q

what is caspase for intrinsic pathway

A

caspase 9

115
Q

what happens after cross-cleaving (intrinsic)

A

activated caspase 9 dimers are released, cleave & activate executioner caspases & trigger apoptosis

116
Q

what happens in some situations w/ intrinsic pathway (in diagram apoptotic stimulus pointing at mitochondria)

A

some signaling pathways purposefully cause release of cytochrome c (even tho mitochondria is healthy)

117
Q

what pathway can trigger intrinsic pathway

A

PI 3-kinase pathway AKA survival signaling pathway

118
Q

what regulatory proteins have the job of controlling if cytochrome c is released or not from mitochondria

A

Bcl2 family (Bcl2, Bak, Bad)

119
Q

how do Bcl2 family of proteins regulate intrinsic apoptosis

A

by controlling mitochondrial permeability

120
Q

3 varieties of Bcl2 fam

A

anti-apoptotic fam proteins, 2 pro-apoptotic fam proteins

121
Q

name the anti-apoptotic fam protein

A

Bcl2

122
Q

name the pro-apoptotic proteins

A

Bak and Bad

123
Q

what do these apoptotic proteins do

A

control permeability of mitochondria in response to upstream signals

124
Q

what happens when Bak is activated

A

cell is gonna wanna undergo apoptosis (b/c it’s pro apoptotic)

125
Q

where is Bak found

A

outermembrane of mitochondria

126
Q

describe inactive Bak

A

exists as monomers in outer membrane of mitochondria

127
Q

describe inactive Bak again

A

membrane is intact, no cytochrome c is leaking out, bak is inactive

128
Q

what does bak directly control

A

permeability of outermembrane

129
Q

what happens when apoptotic stimulus acts on Bak

A

activation of Bak, it clusters into an oligomer that forms a channel thru which cytochrome c floods cytoplasm

130
Q

what does Bak channel cytochrome cytoplasm trigger

A

Apaf1 adaptor protein complex, caspase 9 activation, all steps necessary for intrinsic apoptosis

131
Q

what about Bcl2

A

anti-apoptitic; when active it sits in outer membrane of mitochondria

132
Q

what does Bcl2 do

A

Bcl2 binds Bak and blocks cytochrome channels from forming

133
Q

what is Bcl2 similar to

A

safety mechanism; when safety is engaged, Bak can never fire

134
Q

what happens when you take out Bcl2

A

remove safety, when trigger is pulled Bak makes channels –> apoptosis

135
Q

basically what does Bak do

A

pro-apoptotic; forms channels and increases permeability of membrane

136
Q

basically what does Bcl2 do

A

anti-apoptotic; blocks Bak and formation of channel

137
Q

what is 3rd apoptotic regulator protein

A

Bad; pro-apoptotic

138
Q

what does active Bad do

A

inhibits Bcl2

139
Q

what does Bad inhibiting Bcl2

A

inhibits inhibitor of Bak; causes activation of Bak and apoptosis

140
Q

what does PI 3-kinase signaling pathway

A

prevents apoptosis

141
Q

what does trans autophosphorylation of RTK provide

A

docking site for PI 3-kinase

142
Q

what does PI 3 kinase do

A

phosphorylates PI (4,5)P2 into PI(3,4,5)P3; which provides docking site in plasma membrane for downstream kinases PDK1 and AKt

143
Q

what does PDK1 do

A

helps activate Akt

144
Q

what happens when AKt is activated

A

released from plasma membrane, goes into cytoplasm

145
Q

what does Akt phosphorylate

A

Bad

146
Q

what does Bad phosphorylation do

A

releases active apoptosis inhibitory protein

147
Q

what happens when Bad is phosphorylated

A

can’t inhibit the inhibitor Bcl2 (meaning Bcl2 is free to inhibit apoptosis)

148
Q

what happens to Bcl2 when PI 3 Kinase pathway is active

A

Bcl2 can bind to Bak and prevent cytochrome channel from forming (cytochrome can’t go into cytoplasm)

149
Q

describe PI 3 kinase pathway

A

survival pathway; if in right env. cells don’t need to go in apoptosis

150
Q

what happens if survival signal for PI-3-kinase pathway is withdrawn or cell is in wrong place and needs to self-destruct

A

Bad is gonna be de-phosphorylated, can inhibit the inhibitor Bcl2 and allow Bak to trigger apoptosis (thru cytochrome channel formation)

151
Q

what does this survival signaling pathway regulate

A

intrinsic mechanism of apoptosis

152
Q

when do cells stay alive

A

when pathway is active

153
Q

why do we need survival signaling

A

we have more neurons early in dev. than as adult; more cells than the survival factor can keep alive

154
Q

describe abundance of survival signal

A

kinda limited; some cells are gonna die so it leaves cells that remain to enjoy benefits of limiting survival signal

155
Q

what causes apoptosis via PI3-kinase mechanism acting on regulation of intrinsic apoptotic pathway

A

apoptosis adjusts number of nerve cells to size of target; more nerve cells than survival factors released by target cells

bio 211 (18 decks)

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