Autophagy Flashcards

1
Q

cytological EM

A

vesicles containing cytoplasm adjacent to vacuole

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2
Q

cytological light microscopy

A

autophagic-cytoplasm containing bodies on vacuole

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3
Q

TOR

A
  • Ser/Thr kinase
  • master regulator
  • suppresses autophagy and regulates 26SP
  • ATG13 phosphorylation
  • no ATG1 kinase assembly
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4
Q

Cytology

A
  • ATG8 and 12 UBLs are PAS
  • TOR inactivation: activated ATG1 kinase phosphorylates ATG4, ATG9
  • small ATG9 vesicles localise to PIS
  • ATG9 lipidates ATG8
  • isolation membrane forms at or near ER
  • thins (direct transfer of lipids via small vesicles by ATG8-PE), expands, curves (stabilised by actin sandwich, ATG8-PE binds ATG12-5-16), becomes spherical (requires COPII-ATG2 recruitment)
  • pore closes (ATG9, ESCRT-mediated fission)
  • autophagosome
  • lysosome/vacuole translocation
  • outer membrane fusion (v and t snares)
  • hydrolase degradation and recycling
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5
Q

IM

A
  • phagophore
  • small, flattened
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6
Q

autophagosome

A

double-membrane bound

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7
Q

ATG1 kinase

A

multiple complices assembles to form an autophagosomal assembly platform

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8
Q

ATG9

A
  • phosphorylated by ATG1 kinase
  • multi-spanning membrane protein
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9
Q

ATG4 protease

A

catalyses ATG8-PE delipidation

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10
Q

In vitro liposomes

A

tethering, hemifusion and fusion

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11
Q

microautophagy

A

direct invagination

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12
Q

chaperone-mediated

A

Hsc70

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13
Q

selective autophagy

A
  • autophagy receptors bypass TOR
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14
Q

ATG8-interacting-motif (AIM)

A
  • short, 4 residue core sequences in hydrophobic patch
  • ## phosphorylation activation
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15
Q

Ub in selective autophagy

A
  • labels cargo and bind to ATG8
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16
Q

Mitophagy

A
  • E3 = Parkin
  • PINK1
17
Q

No parkinsons

A
  • PINK goes through TOM translocon into mitochondria for degradation
  • auto-inhibited Parkin
18
Q

Feedforward in PARKIN

A

PINK1 phosphorylation creates more Parkin binding sites on MOM

19
Q

Chlorophagy

A
  • dark treatment, leaf senescence, photo damage
20
Q

chloroplast recycling

A

rubisco containing bodies

21
Q

neurodegeneration

A

insoluble aggregate neutralisation declines w age

22
Q

amyloid-beta, alpha-synuclein and huntingtin

A

affect 26SP and autophagy