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m2mweek6 > M2MWeek6NotecardsSet8 > Flashcards

M2MWeek6NotecardsSet8 Flashcards

1
Q

What are the three main types of autophagy?

A

macroautophagy and chaperone-mediated autophagy. And microautophagy

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2
Q

Describe chaperone-mediated autophagy. What makes it unique?

A

Chaperone-mediated involves a chaperone protein (HSC70) that specifically targets certain proteins (must have KFERQ in them). Unique because of selectivity of proteins and direct shuttling of these proteins across the lysosomal membrane without the requirement for formation of additional vesicle.

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3
Q

Compare chaperone-mediated to macroautophagy

A

Macroautophagy involves a double-membrane made around what is to be degraded. Thought to be more of a bulk/unregulated process; although this is probably not true

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4
Q

Why do mice without Atg7 (autophagy gene) die right after birth?

A

Suggests that autophagy is a very important part in surviving nutrient starvation (autophagy keeps you alive between meals)

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5
Q

What are functions of macroautophagy?

A

Recycle proteins et al during nutrient deprivation. Recycle mitochondira and peroxisomes. Allow cell suvival under stress conditions. Present antigens to MHC system. Neuro-protection. Remove intracellular pathogens. Involved in agin process (can extend life). Tumor suppression AND tumor promotion? Regulates apoptosis

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6
Q

What are Atg genes?

A

Regulate autophagy but also do other things (Atg1 =protein kinase; Atg12 = ubiquitin-like Atg6 = “scaffold”). First identified in yeast- highly conserved. Because these are enzymes they are potentially “druggable.”

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7
Q

What is Atg6 AKA? What does it form a part of?

A

AKA Beclin-1. Scaffold that forms part of Type III PI3 kinase complex

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8
Q

What is the 7 step process for macroautophagy?

A
  1. Induction 2. Vesicle Nucleation (phagophore) 3. Vesicle Expansion (omegasome) 4. Cargo Targeting (LC3II and p62) 5. Vesicle Closure (now an autophagosome) 6. Vesicle Fusion with endosome (now an amphisome) 7. vesicle fusion with lysososome (now autolysosome)
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9
Q

What does activation of PI3K complex do?

A

allows nucleation of a membrane that will eventually form autophagosome

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10
Q

Autophagy signaling often converges on which pathway?

A

mTOR

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11
Q

What are some things that regulate autophagy?

A

Amino acids. Growth factors. Lipids. Everything that regulates the PI3 kinase pathway. Other protein kinases. Tumore suppresors like p53. Mutated oncogenes like RAS. Drugs

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12
Q

What does rapamycin do with respect to autophagy? How does this show that autophagy is protective against neurodegeneration?

A

Rapamycin promotes autophagy and also protects against Huntington’s disease. Shows decreasing neurodegeneration is related to increased autophagy

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13
Q

What specifically does autophagy do with respect to Huntington’s?

A

Autophagy will degrade the aggregate-prone proteins (the expanded stretches of glutamine residues) that cause neuronal cell death

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14
Q

What do capsases do with respect to Beclin 1?

A

Cleave it

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15
Q

What happens to autophagy and apoptosis when Beclin 1 is cleaved or bound to?

A

Inhibits autophagy; increases apoptosis

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16
Q

What to Bcl2 and Bcl-xL do?

A

Bind to BH3 domains on Beclin 1. Inhibits autophagy

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17
Q

What does cytochrome c do once it is released from the mitochondria?

A

Helps to activate capsases (proteolytic enzymes); which cleaves Beclin1. Autophagy is inhibited and apoptosis is induced

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18
Q

What happens to autophagy and apoptosis after cytochrome c is released from mitochondria?

A

Autophagy is inhibited. Increases apoptosis

19
Q

Why can it be difficult to interpret results of therapeutic interventions that target Bcl-2 and other proteins?

A

Many of these proteins regulate apoptosis but also control autophagy. How do you tell which caused the results?

20
Q

Which organelle is stressed first in necrosis?

A

Mitochondria

21
Q

What happens to the mitochondria when it is starved for oxygen?

A

Begins to swell. At “high-amplitude swelling” it can no longer maintain its ionic gradients or oxidative phosphorylation and the cell runs out of energy.

22
Q

What happens to the rest of the cell once mitochondria are no longer producing ATP?

A

The plasma membrane’s ion pumps fail and water floods in. The cell swells and bursts. Lysis releases the cell�s intracellular contents into the extracellular space

23
Q

What happens to the body when after lysis of cells?

A

The body can tell when internal lipids and molecules are in the extracellular space and this induces an intense proinflammatory reaction. Many white cells (mostly macrophages) are drawn to the area of damage. This is usually good as it leads to debris removal and injury resolution

24
Q

What is the difference between necrosis and apoptosis?

A

Necrosis implies death of cells that are not supposed to die. Apoptosis is used in cells for whih death was normal and predictable.

25
Q

What is the general process of apoptosis?

A

Begins with collapse of the nucleus: chromatin is fragmented and supercondensed. Cells shrink and then tear themselves into smaller apoptotic bodies. These are recognized by macrophages and are soon phagocytosed

26
Q

What is phosphatidylserine (PS)?

A

A phospholipid that is normally confined to the inner surface of the membrane. When a cell commits to apoptosis PS is exposed on the outter surface and signals to macrophages and dendrites to consume the cell.

27
Q

What does the enzyme flippase do?

A

Ensures than any PS molecules that stray to the outer surface of the membrane are quickly returned

28
Q

What does the enzyme scramblase do?

A

Soon after apoptosis begins; scramblase makes sure PS is on both sides of the membrane via a “scrambling” mechanism

29
Q

Does apoptosis trigger an immune response?

A

No because the apoptotic cells are consumed before they lyse. This is a good thing

30
Q

What is morphogenetic death?

A

Determines the final shape of body parts and organs. EX in limbs the death by apoptosis of cells between the digits gives the final form to fingers and toes

31
Q

Describe the signaling of internal apoptosis pathway

A

Involves outer membrane of the mitohondria. Nomally; the membrane is guarded by anti-apoptotic proteins. When cell receives signal the pro-apoptotic proteins replace their anti-apoptotic family members. This allows other members of the family to act on the membrane so it is permeable and releases cytochrome C. Cty C activates a cytoplasmic protein that starts a signaling cascade.

32
Q

What are the anti-apoptotic members of the Bcl-2 protein family?

A

Bcl-2 and Bcl-XL

33
Q

What are the pro-apoptotic members of the Bcl-2 protein family?

A

Bim and PUMA

34
Q

What are the names of the proteins that act on the membrane of the mitochondria to make it permeable?

A

Bax and Bak

35
Q

What is the name of the cytoplasmic protein that is activated by cytochrome C?

A

Apaf-1

36
Q

What protein does Apaf-1 activate? What does it do?

A

Activates caspase-9 which is the signal caspase. Caspase-9 activates caspase-3 (the executioner)

37
Q

What does caspase-3 do?

A

Cleaves many substrates; eventually resulting in the classic appearance of apoptosis

38
Q

Describe the signaling of the external apoptosis pathway

A

Cytotoxic T cells (CTLs) survey surface of all body cells. If there is a mutation or infection the CTL expresses a surface molecule which binds to the abnormal cell’s surface. This binding then sends a signal to the cell’s interior; which activates a cascade of signaling to trigger apoptosis.

39
Q

What is the name of the surface molecule that CTL cells express when an abnormal cell is found? What do they bind to?

A

Could be one of two. Either Fas ligand (FasL) or CD95 ligand (CD95L). These ligands bind to either Fas or CD95 on the abnormal cell’s surface

40
Q

What molecule is recruited to CD95 (or Fas?)? What does that molecule do?

A

CD95 sends a signal which recruits FADD. FADD activates caspase-8. Caspase-8 is a signaling caspase (like caspase-9 in the intrinsic pathway) and it activates caspase-3

41
Q

What is mutated in children with the condition called autoimmune lymphoproliferative syndrome (ALPS)?

A

Either Fas or FasL (their malignancy starts because not enough cells die; not because of uncontrolled proliferation)

42
Q

What is a FLIP? How does it relate to some pathogens?

A

FLIP is a competitor with caspase-8 for binding to FADD. When FLIP is bound to FADD it inhibits apoptosis signaling. There are viral FLIPs (v-FLIPs) which use anti-apoptotic genes to keep the cell alive until they can finish their replicative cycle

43
Q

What is another CTL mechanism?

A

The CTL secretes enzymes (granzymes) and a pore-making protein (perforin) that together deliver apoptosis-inducing molecules to its intended target

m2mweek6 (8 decks)

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