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Health 31 > Mitochondria > Flashcards

Mitochondria Flashcards

1
Q

why are mitochondria referred to as powerhouses of the cell?

A

as provide most energy for cell function

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2
Q

what 5 parts form the structure of mitochondria?

A

outer mitochondrial membrane,
intermembrane space,
inner mitochondrial membrane,
cristae
matrix

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3
Q

What is found within the outer mitochondrial membrane? 2

A
  • porins: small permeable molecules
  • outer translocases TOMs: selective transport proteins
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4
Q

What is found within the intermembrane space of the mitochondria? 3

A

small molecules,
peptides
cytochrome C

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5
Q

what is cytochrome C (found in intermembrane space of the mitochondria)

A

protein essential for funtion of electron transport by transfer e- between complexes 3+4

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6
Q

what part of mitochondria is similar to cytosol in solute composition?

A

intermemb space

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7
Q

What is found within the inner mitochondrial membrane of the mitochondria?

A
  • small IMpermeable molecules (selective transport)
  • inner translocases TIMs: selective transport proteins
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8
Q

is the inner mitochondrial membrane impermeable or permeable to most small molecules?

A

impermeable

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9
Q

where can we find OXPHOS (electron transport complexes for oxidative phosphorylation)?

A

cristae

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10
Q

What is found within the matrix of the mitochondria?

A
  • mtDNA
  • mtRNA
  • proteins
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11
Q

What is the structure of mitochondrial DNA (mtDNA)?

A
  • circular double strand
  • no introns
  • packed in protein-DNA aggregates
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12
Q

How many copies of mtDNA exist in a mitochondrion?

A

multiple

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13
Q

what is meant by no introns? mtDNA

A

most of mtDNA encodes for a protein or a ribosome

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14
Q

most proteins for structure and function are encoded in the nuclear DNA and are imported via?

A

TOMs and TIMs

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15
Q

mitochondrial DNA has limited repair and is highly prone to damage (oxidative stress) and?

A

mutations

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16
Q

mtDNA is packed in nucleoids. What are nucleoids?

A

protein DNA aggregates

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17
Q

How many genes are within the mtDNA and what do they code for?

A
  • 37 genes:
  • 13 proteins for proteins of ETC, rRNA + all tRNAs
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18
Q

what is the role of TFAM (mitochondrial transcription factor A) ?

A

coats and stabilises mtDNA
regulates transcription/ replication

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19
Q

what is the specific replicative machinery of mtDNA known as?

A

replisome

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20
Q

the replisome of mitochondria is comprised of Twinkle, POLG…
what are these?

A

Twinkle: DNA helicase

POLG: DNA polymerase gamma

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21
Q

where is mtDNA replication primarily initiated?

A

D loop region non coding

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22
Q

role of Twinkle?

A

open the 2 strands of mtDNA
(DNA helicase)

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23
Q

what are the 3 safeguards of mitochondrial health for cell homeostasis?

A

mitochondrial dynamics, mitochondrial biogenesis and mitophagy

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24
Q

whats mitochondrial dynamics?

A

fusion and fission

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25
Q

whats mitochondrial biogenesis

A

de novo synthesis (generation of new) of mitochondria

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26
Q

whats mitophagy?

A

removal of mitochondria in lysosomes by autophagy

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27
Q

Why are mitochondria said to be very dynamic organelles?

A

undergo fusion and fission

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28
Q

What molecules are involved in mitochondria dynamics?

A

Mitofusins, OPA1, Fis1, Drp1….

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29
Q

How are mitochondria dynamics related to bioenergetics status of cell?

A
  • Fusion: more efficient for OXPHOS
  • Fission: less efficient for OXPHOS - may be indicative of mitochondrial stress
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30
Q

what process can occur v quickly and can induce to cell stress and death?

A

mitoc. oxidation

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31
Q

What is the master regulator of mitochondrial biogenesis?

A

PGC-1a
(a TF that can be activated by diff molecular pathways e.g. AMPK)

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32
Q

How does PGC-1a regulate mitochondrial biogenesis?

A
  • it translocates to cell nucleus to activate TFAM expression
  • TFAM essential to coordinate mitochondrial biogenesis through mtDNA transcription/replication
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33
Q

What triggers mitophagy?

A

mitochondria being dysfunctional or damaged

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34
Q

mitophagy is primarily initiated in dysunctional mitochondria. What stabilizes at the OMM before parkin is activated?

A

PINK1

35
Q

mitochondria is primed for degradation through autophagy and occurs in the?

A

lysosome
–> engulfed form autophagosomes + removes fusion w lysosomes

36
Q

give one condition where mitophagy may be initiated in non damaged mitochondria via pink1 independant mechanisms?

A

hypoxia (BNIP3L/NIX pathway)

37
Q

Why is coordination of biogenesis and mitophagy essential?

A
  • self-repair: replace damaged mitochondria by new healthy units
  • adjust mitochondrial mass to cope w cellular demands

to keep an appropriate turnover of healthy mitochon.

38
Q

mitochondria are essential for cellular homeostasis. Give one thing that is produced and one thing that is regulated?

A

production of ATP via oxidative phosphorylation (OXPHOS)
regulation of central metabolic pathways

39
Q

production of ATP via oxidative phosphorylation (OXPHOS) involves transfer of e- from where through where?

A

NADH + FADH through mitochon. complexes… to make ATP

40
Q

true or false, mitochondrial mass can be adjusted to satisfy energetic demands?

A

true

41
Q

does fusion or fission support oxidative phosphorylation?

A

fusion
fission more linked w glycolysis

42
Q

what are the functions of mitochondria?
(all)

A
  • regulation of cellular bioenergetics and metabolism
  • Control of cell death
  • Generation of Reactive oxygen species (ROS)
  • Cell differentiation/reprogramming
  • Cellular ageing (senescence)
  • Calcium Transport
  • Steroid synthesis
  • Hormonal signalling
    …
43
Q

Describe the process of cell death control in a mitochondria.

A
  • intrinsic cell death signals activate BAK and BAX in cytosol
  • triggers OMM permeabilisation via formation of pore complexes
  • cytochrome C released into cytosol
  • binds to Apaf-1 (apoptosome)
  • caspase(s) activate and apoptosis occurs
44
Q

mitochondria can generate ROS (reactive oxygen species), how might this occur during OXPHOS?

A

fraction of e- leaks and reacts with O2 to produce superoxide + H2O2

45
Q

ROS production is excerabted in damaged mitochondria, true or false?

A

true

46
Q

What mitochondria antioxidant systems exist to scavenge ROS?

(detox. superoxide-> less damaging forms)

A
  • Manganese Superoxide dismutase (MnSOD )
  • Thioredoxin 2 (Trx2)
47
Q

What can ROS damage?

A

cell components:proteins, DNA and lipids

48
Q

What exists to maintain balanced mitochondrial redox key for cell signalling?

A
  • Posttranslational modifications of proteins
  • Action on signal transduction
49
Q

How do mitochondria cause cell differentiation/reprogramming?

A

mitophagy facilitates the process by switching from OXPHOS to glycolysis

50
Q

What are examples of cell differentiation/reprogramming that the mitochondria play a role in?

A

Differentiation of:
- neuroblasts into Retinal Ganglion cells
- Stem cells into various lineages (erythrocytes, myotubes…)

Macrophage polarization

51
Q

What is cellular ageing (senescence)?

A

permanent arrest of cell proliferation

52
Q

What are the causes of senescence?

A
  • stress
  • oncogene activation
  • telomere shortening (ageing)
53
Q

What unique phenotype accompanies cell senescence and what does it do?

A
  • senescence-associated secretory phenotype SASP
  • causes secretion of inflammatory cytokines
54
Q

How do we know mitochondria play a role in cell senescence?

A
  • senescent cells show high mitochondrial mass
  • removing mitochondria prevents senescence
55
Q

What aspects of inflammation do mitochondria play a role in?

A
  • Polarization/ reprogramming of immune cells
  • Antiviral responses
  • Immune responses to DAMPs
56
Q

What T-cells do mitochondria reprogramme?

A
  • naïve
  • T-effector
  • T-memory
57
Q

How do mitochondria affect naïve T cells?

A

mature and exit the thymus primarily relying on OXPHOS

58
Q

How do mitochondria affect T-effector cells?

A

Glycolytic metabolism

59
Q

How do mitochondria affect T-memory Tm cells?

A

OXPHOS

60
Q

once naive T cells mature + exit thymus, they can be primed by what to become T-effector Te cells?

A

antigen presenting cells

61
Q

why can we taregted mitochondria dynamics ?

A

as novel approach to reprogram T cells

62
Q

What does reinforcing mitochondria fusion in T-effector cells cause?

A
  • it imposes T-memory cell features (remember mitochondrial fusion favours OXPHOS)
  • increased OXPHOS
  • increased cell half-life
63
Q

What are the two types of macrophages?

A

M1 and M2

64
Q

What types of cytokines do M1 macrophages secrete? Name examples.

A

pro-inflammatory:

  • iNOS
  • IL-1β
  • TNF-α, etc
65
Q

What mitochondrial dynamic characterises the release of pro-inflammatory cytokines from M1 macrophages?

A

Mitochondrial fission:

  • glucose used for aerobic glycolysis, broken in krebs cycle
    -> high levels of succinate and mtROS
  • stabilisation of HIF-1a
  • expression of pro-inflammatory cytokines
66
Q

What types of cytokines do M2 macrophages secrete? Name examples.

A

tissue repair/angiogenesis:

  • IL10
  • TGF-β
  • ECM deposition, etc
67
Q

What mitochondrial dynamic characterises the release of tissue repair/angiogenesis cytokines from M2 macrophages?

A

mitochondrial fusion:

  • OXPHOS
  • intact Krebs cycle
68
Q

Apart from helping to release cytokines, how else do mitochondria affect macrophages?

A

key for macrophage polarisation by blocking mitophagy during M1 polarisation

69
Q

results/ effects of macrophages: blocking mitophagy during M1 polarisation

A

inc mitochon mass
dec glycolytic gene expression
reduced expression of pro-inflamm factors

70
Q

how can antiviral responses be intiated at the mitochondria?

A

viral dsRNA recognised by RIGI,
assembly of MAVS at outer mitochondrial membrane,
antiviral interferon 1 responses–>

  • inhibition of rna translation,
  • degradation of RNAs
  • inhibition of viral assembly
71
Q

what does antiviral interferon-I bind to, to interfere with viral replication?

A

memb receptors of the non-infected adjacent cells

72
Q

how does the induction of mitochondrial fission of mitochondrial viral evasion help protect against viruses?

A

get collapse of mitochondrial function to facilitate their removal and viral factors directly induce mitophagy

73
Q

whata are the 2 mechanisms of mitochon viral evasion?

A

induction of mito fission -> mitophagy (Hep B,C, HPV3, CVB..)

disruption of MAVS signalling (SARS-Cov1)

74
Q

how does the disruption of MAVS signalling such as in the case of SARS cov 2 lead to mitochondiral viral evasion?

A

targets mitochondria,
disrupts MAVs and triggers its degradation, reduced IFNI responses
promotes mitochondrial fusion through DRP1 degredation,

keeps host cells happy (almost all lung cells rely on OXPHOS)

75
Q

what is the term given to molecules with physiological function inside the cell that alert about danger when released, intra or extra cellular?

A

DAMPs
damage associated molecular patterns

76
Q

damps trigger innate immune responses via recruitment of what 3 cell types?

A

macrophages, neutrophils and dcs

77
Q

mitochondria are major sources for damps, what are these damps known as?

A

mitodamps

78
Q

what cells involved in immune cell activation + underlying mechanism from studies of bacterial DNA: that activates TLR9 by recognising unmethylated CpGsequences (immunostimulant)

A

mitodamps

79
Q

what is the endosymbiant theory?

A

mitochondria thought to evolve from saprophytic bacteria
I
mtDNA also rich in CpG sequences
I
activates TLR9 receptors

80
Q

mitoDAMPs: once immune activation as extracellular signal, -> neutrophil activation (TLR9), adhesion and transmigration leading to what?

A

distal organ inflammation

81
Q

in COVID19 px, are circulation levels of mtDNA high/low?

A

high.
associated w circulating levels of inflamm factors

82
Q

therefore, what can levels of mtDNA/ inflamm factors in COVID19 px predict?

A

risk of
- mortality
- ICU
- intubation
- fatal organ dysfunction

83
Q

what can high circulation level of mtDNA also be used as a prognosis factor for?

A

traumatic brain injury
AIA
acute liver failure
cancer
diabetes
aging

84
Q

immune activation as intracellular signal can ‘ignit’ inflammasome activation (NLRP3, AIM2) when released in cytosol. what will this release?

A

pro-inflamm IL-1b and IL-18

normally occur due to mitochondrial damage, highlights need of competent mitophagy to remove dysfunctional mitochondria

Health 31 (16 decks)

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