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Cell Death Flashcards

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1
Q

Cell death is the end of a response. True or false

A

No it is the beginning of an immune response

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2
Q

How many cells die a second

A

1 million

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3
Q

3 reasons cell death is used in normal physiology

A

Development/ ageing

Immune system

To protect from pathogens and tissue malfunction

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4
Q

What is modus operandi

A

Over production of excess cells in development to allow cell culling to select fittest cells and remodel

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5
Q

How many neurons dies in new born

A

60%

This is why identical twins aren’t completely identical - their neuronal network is different

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6
Q

Name a structure we are all born with but it only persists in females

What does it form

A

Mullerian duct

Uterus and oviducts

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7
Q

Name a structure we are all born with but it only persists in males

What does it form

A

Wolffian duct

Male reproductive organs

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8
Q

Why is cell death important in the immune system (3)

A

Many T lymphocytes are produced but only functional ones are selected
Those without a productive T cell receptor die by neglect

Faulty T cells that attack self are killed via negative selection

There is also T cell mediated murder (effector cytotoxic T cells initiate cell death in infected cells)
Also during an infection, T cells for that pathogen are in a very high number but after the infection this must decrease so cell death must occur

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9
Q

What is contraction

A

Reducing number of T cells after an infection is over

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10
Q

Cell death is important for homeostasis - Why

A

Balances with new cell production and well as relative fitness sensing

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11
Q

What happens if cell death exceeds new cell production (3)

A

Neurodegeneration

Immunodeficiency

Infertility

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12
Q

What happens if new cell production outweighs cell death

A

Cancer

Autoimmunity

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13
Q

What is relative fitness sensing and how does it relate to cell death

A

Every cell has a certain level of fitness which is cross referenced to the fitness standard of the organ.

If a cell is produced that is viable but doesn’t reach the fitness standard it is destroyed by the surrounding cells

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14
Q

Name a type of cell death that is immunologically silent and one that is immunogenic

A

Apoptosis = silent

Necroptosis = immunogenic

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15
Q

2 key aspects to consider about the cellular context of cell death

A

1) what was the cell death event

2) what were the underlying signalling events -> were inducible DAMPs produced?

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16
Q

What is a DAMP

A

Danger associated signalling event

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17
Q

4 reasons apoptosis is silent

A

The PM remains intact

Caspase dependant

Caspases incapacitate danger signals and ensure neat disposal of dead corpses

No DAMPs

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18
Q

What happens in all lytic cell deaths

A

Pore formation

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19
Q

Where aRe pores formed in a apoptosis

A

Mitochondrial membrane

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20
Q

What is the most common form of cell death

A

Apoptosis

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21
Q

Give the 5 morphological features of apoptosis

A 
Cell shrinkage
Membrane blebbing 
DNA fragmentation 
Apoptotic body formation 
Engulfment by neighbouring cells and phagocytes

MEMBRANE REMAIN INTACT

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22
Q

How long does engulfment take after apoptosis

A

15 mins

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23
Q

Give the structure of caspases

A

Homo dimers

Produced as inactive form and must be activated

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24
Q

Where do caspases cleave

A

After aspartate

Hence the name: cASPases

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25
2 pathways to activate caspases Give the key complex in each
Mitochondrial pathway - intrinsic - the apoptosome | Death receptor - extrinsic - DISC
26
What does DISC stand for
Death Inducing Signalling Complex
27
Which caspases do DISC and apoptosome activate
Apoptosome: 9 DISC: 8
28
2 groups of caspases
Initiator and executioner (these are subunits of initiator caspases)
29
Key differences between initiator and executioner caspases
Initiator: •long pro-domain • monomeric • activated by dimerisation Executioner •obligate dimers • activated by cleavage
30
3 features common to all caspases
Made of Pro enzymes Active as dimers Cys Asp proteases
31
3 targets for initiator caspases
Themselves Effector caspases (Casp-3, and -7) BCL-2 homology 3 (BH3) - BID
32
5 things effector caspases (eg Casp 3,6 and 7) do
* Dismantle cell structures * Phenotypic changes to cell that are characteristic of apoptosis * cleavage of ICAD, which releases CAD * proteolysis at adhesion sites allowing cell detachment and retraction * exposure of PS and other phagocytic signals on the cell surface
33
What does CAD do in cell death
Cut up the DNA CAD = Caspase activates DNA-ase
34
How are initiator caspases activated
Proximity induced dimerisation - certain ligands change the configuration of a death ligand, allowing recruitment of adapter protein with a death domain The death domain brings in 2 Casp 8 molecules which dimerise and activate
35
What does cytochrome c do after it is released from the mitochondria
Binds to an Apaf-1 molecule which binds to other Apaf-1 molecules forming an apoptosome
36
How is Casp 9 activated
It sits on top of the apoptosome and dimerises
37
Why are executioner caspases activates by cleavage
The catalytic cysteine is masked and cleavage unmasks it allowing substrate entry
38
Is cell death assured once caspases are activated
No IAPs (inhibitor of apoptosis proteins) can inhibit caspases
39
Where were IAPs discovered
In viruses
40
What is the point of no return in apoptosis
MOMP
41
What is the anti apoptotic family that inhibits Bak (pore forming proteins)
The BCL-2 family
42
What do bak and bax proteins do
Form pores in the mitochondria
43
What do BH3-only family members do
Suppress BCL-2 family, allowing Bax and thus pore formation in the mitochondria leading to apoptosis
44
How many proteins in a cell can be cleaved by caspases
2000
45
How do extrinsic signals initiate cell death
The death ligand binds to the death receptor, causing it to trimerise
46
What happens after the death domain trimerises when the death ligand binds
FADD (an adapter protein) is recruited which in turn brings casp 8 molecules to be activated
47
How does FADD from the death receptor activate casp 8
There is a proximity induced conformational change that rotates the catalytic centre into an active position
48
What are the 2 different forms of extrinsic induced apoptosis
Type I: activated casp 8 activates casp 3 and 7, directly leading to apoptosis (no MOMP required) Type II: casp 8 cleaves BID, which activates Bak and MOMP for pore formation in the mitochondria
49
What happens to XIAP in Type I and Type II cells in apoptosis What XIAP do
Type I: XIAP rapidly decreases upon activation of death receptor Type II: SMAC is released from mitochondria after pore formation and inhibits XIAP XIAP inhibits apoptosomes and casp 3 and 7, ultimately inhibiting apoptosis
50
What is special about the TNF death receptor
It can send 2 different signals: one for cell survival (the dominant outcome) and one for cell death
51
What molecule is activated by a TNF death receptor to initiate cell death When is this released
RIPK1 If the cell is not fit enough / under stress as TNF tests cells for fitness
52
What do TRADD and RIPK1 recruit What is important about these
TRAF1, cIAP, LUBAC They recruit ubiquitin chains - different chains either determine cell death or gene expression
53
If RIPK1 recruits a ubiquitin chain NOT for cell death, what recognises the ubiquitin chain What about for TRADD What does this eventually lead to
TAB2 NEMO Activation of NF-κB
54
What is the ubiquitin checkpoint
If RIPK1 and TRADD, bound the the TNF death receptor, have a ubiquitin chain not signalling cell death, the complex remains attached the the plasma membrane If the ubiquitin chain signals cell death, the RIPK1 is released and RIPK1 oligomerises and binds to FADD, allowing casp 8 to be activated by proximity. This leads to apoptosis
55
When RIPK1 oligomerises and activates Casp 8, what is this complex called If this is formed, is cell death certain
Complex 2 No - cFLIP can mediate complex 2 activity
56
What is FLIP
A pseudo caspase Like a caspase in structure but with a mutated catalytic centre It can dimerise with casp 8
57
What does FLIP do
Dimerises and tethers casp 8 so it cannot cleave you activate effector caspases
58
What can The dimer of FLIP + casp 8
Cleave RIPK1 and RIPK3 to disable them and allowing survival
59
Does the RIPK1 complex 2 always lead to apoptosis
No it can activate MLKL pathway for necropotosis
60
When virus prevent cell death what do they target
The extrinsic apoptosis pathway, often targeting caspases
61
Which viral proteins attack casp 8
CrmA and vFLIP
62
Which viral proteins attack executioner proteins
vIAP
63
When does necroptosis occur
When caspases like casp 8 are blocked
64
Does necroptosis affect the mitochondria
No it makes holes in the PM instead
65
What is the main trigger of necroptosis
Pathogens Cell stress damage
66
What are the 2 domains of RIPK1
Death domain and kinase domain
67
What is a ripoptosome What inhibits it
The RIPK-FADD complex that can activate either casp 8 or MLKL as well as NF-κΒ for danger signals cIAP1 and 2 XIAP
68
How does MLKL work
It is a pseudo kinase that is activated via phosphorylation by the ripoptosome
69
How does phosphorylation activate MLKL
A 4HB disengages, exposing the domain allowing dimerisation and thus pore formation
70
Other than TNF what can initiate necroptosis (3)
When ZBP1 senses a virus and uses its RHIM domains to bind and activate RIPK3 IFNs initiate necroptosis when FADD is absent LPS binds TLR4 to initiate necroptosis via TRIF
71
What are the 3 outcomes of a death receptor pathway
Survival Apoptosis Necroptosis
72
What is RHIM
RIP homology interact motifs They allow RIPK1 and RIPK3 to interact
73
Give the sequence of events of necroptosis starting with RIPK1 and RIPK3 interaction
RIPK1 and 3 interact through their RHIMs Activated RIPK3 phosphorylates MLKL MLKL undergoes conformational change to allow oligomerisation and then pore formation in PM
74
How does RIPK1 interact with Casp 8
Casp 8 is cleaved and Inactivated
75
Do carnivores have MLKL Why?
No Pathogens have won the race?
76
Is pyroptosis caspase dependant
Yes- it mainly uses casp 1 and 11
77
How does pyroptosis blow up the cell
Gasdermin- D forms pores in the PM and water comes in to swell the cell
78
What does casp 1 activate in pyroptosis
IL-1β and IL-18 It also cleaves DNA so other casp can become active
79
What are always the final 3 steps leading to pyroptosis What is different
ASC activates casp 1 which activates IL-1β and IL-18 Different stresses have different triggers and sensors
80
How is casp 1 activated
NLRP3 oligomises to form an inflammasome and ASC forms filaments which recruit and activate casp 1
81
What is PAMP vs DAMP
PAMP is a pathogen induces danger signal where as DAMP is endogenous
82
What is the back up system for pyroptosis When is it needed
Inflammasome instead drives activation of casp 8 If casp 1 is deactivated
83
What happens if NKRP3 is spontaneously activated
Chronic inflammation etc
84
Give 3 initiator caspases
2 8 9
85
Give 3 executioner caspases
3 6 7
86
What does TNF do
Tests the fitness of cells
87
How does casp 8 block necroptosis What happens if casp 8 is low? When can this also happen?
By cleaving RIPK1 and RIPK3 RIPK1 activates RIPK3 which in turn activates MLKL. This will also happen if IAP is low
88
What is the key effector of necroptosis
MLKL
89
In which form of cell death is nuclear integrity maintained
Pyroptosis
90
How are initiator caspases activated? Why
Dimerisation Can only be properly activated when there are enough present
91
Key casp for pyroptosis
Casp 1
92
What activates casp 1 What do interleukins do
Inflammasome Create Gasdermin D pores
93
Which cell death modality uses lipid peroxidation?
Ferroptosis
94
What is SMAC / DIABLO
Inhibitors of apoptosis
95
What is BH3 present in
BCL-2 (anti apoptotic) But also BID (pro apoptotic)
96
Describe the domains of the Bcl2 family
All anti apoptotic members have all BH domains (1-4) | All pro apoptotic have at least BH3 (BID has only BH3, Bak has several BH domains)

MIMS (12 decks)

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