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adv mol cell > autophagy > Flashcards

autophagy Flashcards

1
Q

what is macro autophagy

A

→ a mechanism to digest intracellular material
-> exchange in cytosol → engulfs into cell

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2
Q

why do cells need degredation

A
  • homeostasis - was to rid of damaged components
  • signalling - changing protein composition
  • reprogramming cells
  • removing damaged components
  • recycling nutrients
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3
Q

ubiquitin system of degredation

A
  • proteosome - certain proteins in cytosol that target degradation
  • proteosome recognises cargo protein → degradation
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4
Q

different types of autophagy

A
  • macroautophagy
  • chaperone autophagy
  • microautophagy
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5
Q

chaperone autophagy

A

receptor on surface of lysosome that recognise target proteins with spectific amino acids

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6
Q

microautophagy

A

direct engulfment of cytoplasmic cargo at a boundary membrane by autophagic tubes, which mediate both invagination and vesicle scission into the lumen

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7
Q

compare proteasome, macroautophagy and chaperone mediated autophagy

A

proteasome = no lysosomes and targets individual proteins
macroA = targets many proteins simultaneously
chaperone mediated = lower capacity, targets one protein at a time, specific subset targets

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8
Q

functions of macroautophagy

A

nutrient recycling
- upregulated during cell starvation -> smaller

cellular remodelling
- erythropoisis = loss of nucleus/other organelles
- remove sperm-derived mitochondria = rid of male mito = so dont have double

removal of damaged components
- mitochon, induction of autophagosomes etc

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9
Q

dietary restriction hypothesis

A

eating less -> live longer?
constant diet = yes e.g eat2 inhibition
fall off = no

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10
Q

how can autophagy target bacteria

A

trap bacteria in cytosol as a back up mechanism

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11
Q

how can autophagy be used in disease

A
  • cancer - inhibit autophagy
  • aging - boost autophagy
  • pathogens - mechanisms for survival
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12
Q

how to make an autophagosome

A
  • yeast - useful model organism
    • one vacuole inside cell
    • take mtuant where you dont have enough proteases - degradation activity is compromised - vacuole fills with vesicles - autophagosomes form
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13
Q

use of identifying the Atg genes

A
  • disruption of autophagy to investigate its functions
  • start on dissecting how the machinery works
  • observed of autophagy in live cells
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14
Q

groups of autophagy machinery

A
  • kinase - turns process on and off
  • P13K
    • defines where phagosomes form
  • complex module
    • addition of new lipids
    • fuse with vesicles
    • expand membrane
  • snares
    • recognise autophagosomes and allows fusion
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15
Q

what is selective autophagy

A
  1. ubiquitin tag
  2. adaptor proteins
    • scafolding
    • ubuqitn binding domain and atg8 protein domain (lipidated and encorporated into the membrane)
    • adaptors → bind ubuiqitn and agt8 and drag into the membrane
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16
Q

Functions of autophagy:

A
  • recycling nutrients
  • damaged protein
  • cellular remodelling
  • intracellular pathogen removal
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16
Q

Functions of autophagy:

A
  • recycling nutrients
  • damaged protein
  • cellular remodelling
  • intracellular pathogen removal
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16
Q

Functions of autophagy:

A
  • recycling nutrients
  • damaged protein
  • cellular remodelling
  • intracellular pathogen removal
17
Q

proteinopathies in neurodegeneration

A
  • huntington and parkinsons diseases have ubuquitin aggregates found in brain
18
Q

cause of huntingtons disease

A
  • monogenic
  • polyglutamine (polyQ) expansion in Huntingtin protein = amplification of gene, causing protein aggregation
  • more glutamines = earlier onset
19
Q

function of huntington protein

A
  • protein/neurone maintenance
  • accumulation of protein = forms aggresomes = clump
20
Q

mechanisms of toxicity during protein misfolding

A
  • loss of normal function
  • toxic oligomer
  • aggresomes
  • adapter sequestration
  • proteosomal damage
21
Q

what is parkinsons

A
  • affects dopaminergic neurones
  • Main neuropathology is aggregates of α-synuclein (Lewy Bodies)
22
Q

mutation causing parkinsons

A

a-synuclein mutations
-> α-syn normally degraded by chaperone-mediated autophagy, if not it accumulates in cytosol and blocks lysosomes from degrading

23
Q

how can mitochondrial dysfunction contribute to parkinsons

A
  • parkinsons may be caused by mitochondrial-derived oxidative damage
  • damaged mitochondria can accumulate
  • mitochondria are the main source of Reactive Oxygen Species (ROS)
  • ROS damages cellular components
24
Q

enzymes regulating mitophagy

A

PINK1
- mitochondrial kinase
- LOF
- linked with early onset

PARKIN
- Cytosolic E3 ubiquitin ligase = adds ubiquitin
- AR
- early onset

25
Q

function of mitochondrial enzymes

A
  • kinase and u ligase allow targeting of damaged mitochondria to allow autophagy
  • without these enzymes you accumulate damaged organelles and products
  • ROS:
    Oxidative damage
    Protein misfolding
    Damaged organelles
26
Q

role of autophagy in cancer

A
  • autophagy is tumour suppressive and prevents dna damage in cells
  • Autophagy is unregulated in hypoxic, nutrient-poor tumour regions
  • blocking autophagy causes necrosis / apoptosis
27
Q

beclin1 (Atg6) gene role

A
  • important gene for autophagy
  • gene that is monoallellically deleted in 40-75% of ovarian, breast and prostate carcinomas
28
Q

what does unregulated autophagy cause

A

Autophagy is unregulated in hypoxic, nutrient-poor tumour regions

29
Q

what does blocking autophagy cause

A

necrosis / apoptosis

30
Q

effect of beclin 2 on surface of mitochondria

A

inhibition of apoptosis and interacts with beclin 1 = death

31
Q

effect of beclin 1

A

autophagosome formation -> survival

32
Q

what genes are linked to tumour survival via autophagosome formation

A

vps34 and UVRAG

33
Q

list 2 strategies for autophatic therapy

A

inhibition of authophagy = increases apoptosis = prevent tumour growth in cancers

34
Q

how does autophagy inhibit apoptosis

A

Bcl-2 inhibits apoptosis by blocking activation of Bax (and Bak) to prevent MOMP and subsequent release of cytochrome c and other apoptogenic proteins from the mitochondria

35
Q

what affects autophagy activation

A

genes
beclin and bcl2
membrane permeabilisaiton/caspase activation

36
Q

anti-oncogenic autophagy processes

A

cell homeostasis
damage removal
reduced ROS/genotoxicity
reducing inflammation

37
Q

pro-oncogenic autophagy processes

A

survival during oxygen/nutrient shortage
prevention of apoptosis
survival during chemotherapy

38
Q

how do issues with autophagy cause neurodegeneration

A

impaired autophagosome formation
disrupted cargo recognition
disrupted lysosomal function
autophagic cargo
inhibited autolysosome formation
autolysosome secretion

39
Q

how does mitophagy contribute to neurodegeneration

A

ROS, ocidative damage, protein misfolding, damaged organelles -> inhibits mitophagy and ubuquitination of mitochondria => damaged mitochondria accumulate

40
Q

how is autophagy tumour suppressive

A

decreased damaged organelles, protein toxicity, ROS = less oxidative stress, DNA damage, tumourigenesis

41
Q

how can autophagy be manipulated in huntingtons treatment

A

induction of autophagy in HD cells cales accelerated breakdown of huntintin aggregates -> neuroprotection

42
Q

how is a-syn normally degraded

A

chaperone-mediated autophagy

adv mol cell (15 decks)

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