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MBB342 - Genetics of Cell Growth & Division > Jones - What is mt dynamics and why is it essential for good health? > Flashcards

Jones - What is mt dynamics and why is it essential for good health? Flashcards

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Biology 101 flashcards
1
Q

What are enlarged mt often indicative of?

A
  • disease state
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2
Q

When/where does mt size and shape vary?

A
  • between cell types and w/ cell cycle stage
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3
Q

Do mts exist as separate organelles?

A
  • no, exist as constantly evolving networks w/in cell cyto → can fuse to form these networks
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4
Q

What is mt length determined by?

A
  • balance between fusion and fission
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5
Q

Why are mts considered ‘dynamic’?

A
  • morphologies can change dramatically by a shift in balance of fusion and fission
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6
Q

Why does mt growth need to be dynamic?

A
  • mt can’t be made, have to be inherited
  • accom cell growth
  • ATP gen in oxygen poor regions of cell
  • redistribution of mt w/ cell division (beneficial to break up so this can happen)
  • genetic complementation (some parts might have defect in eg. complex I, so can fuse diff mts to compensate for presence of some mtDNA mutations)
  • important for cell survival
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7
Q

What are the 3 central players in mt dynamics?

A
  • mitofusins
  • OPA1(/Mgm1)
  • Drp1(/Dnm1)
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8
Q

What do mitofusins, OPA1 and Drp1 have in common?

A
  • all GTPases (can hydrolyse GTP) and belong to dynamin superfam
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9
Q

What are each of the 3 central players of mt dynamics responsible for (mitofusins/OPA1/Drp1)?

A 
Mitofusins = responsible for outer mt membrane fusion
OPA1(/Mgm1) = responsible for fusion of inner mt membrane
Drp1(/Dnm1) = responsible for division of outer and inner mt membrane
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10
Q

What were lots of the the 1st experiments into mt fusion done in?

A
  • yeast
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11
Q

How did an experiment in yeast show mt fusion?

A
  • stained w/ 1 of 2 stains
  • 1 selectively localises to mt, by covalently attaching to mem prots
  • other exp in only 1 parental strain, under control of Gal promoter (so only expressed when grown on galactose)
  • can see after fusion of cells, there is almost complete fusion of 2 diff mt networks
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12
Q

How did further experiments in to mt fusion in Drosophila identify a new gene?

A
  • stained images of dev sperm cells
  • as dev get elongation
  • during these processes mt bodies fuse and form big network that is reshaped as sperm reshaped (= dramatic reorg of mt)
  • sterile male flies observed due to failure in mt fusion
  • observed some fertility defects in these sperm
  • fzo gene identified
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13
Q

What does fzo gene encode?

A
  • encodes founding member of conserved mitofusin GTPase family
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14
Q

What did looking at fzo equivalent yeast gene show?

A
  • at restrictive temp 2 pops don’t fuse (ie. no mixing of mt networks)
  • due to Ts fzo1 mutants
  • conclusion: need functional mitofusin for mt fusion to occur
  • in mutant cells have unopposed fission, mt able to divide but cant fuse, there is no conjoined network of mt
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15
Q

What is the result of mitofusin KOs in mammals?

A
  • KO mice lacking Mfn1 and/or Mfn2 die due to placental defects → cells have fragmented mt
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16
Q

What condition results in humans from Mfn2 mutations?

A
  • Charcot Marie Tooth disease type 2a
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17
Q

What is Mgm1/OPA1, and where is it found?

A
  • large GTPase localised to IMM
  • Mgm1 in yeast
  • OPA1 in mammals
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18
Q

How was it discovered experimentally that Mgm1 had a role in IMM fusion, and why is this data not as convincing as it could be?

A
  • Ts mutants tested for fusion in in vitro assay
  • looking at no. of fusion events –> decreased at restrictive temp
  • therefore mgm1 essential for inner mt membrane fusion
  • BUT also decline at permissive temp → not addressed by authors (so not particularly clear data)
  • overall prob is a reduction, but data not as convincing as could be
  • from timelapse images can see fusion of OMM, but IMM doesn’t fuse
  • conclusion: defects in mgm1 mutants specifically relate to problems w/ IMM fusion (and not OMM)
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19
Q

What is the role of mitofusins in docking/tethering?

A
  • mitofusin from 2 membranes come/dock together and tether 2 sections to each other
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20
Q

Why is GTP hydrolysis important in mt fusion?

A
  • allows OMMs of 2 mt bodies fuse
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21
Q

Apart from IMM fusion, what is OPA1/Mgm1 important in?

A
  • important role in maintenance of cristae structure
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22
Q

What is mt fission important for?

A
  • important for remodelling and rearrangement of mt networks, as well as enabling mt seg during cell div
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23
Q

What do mutations to Dnm1 gene result in?

A
  • large nets of mt due to failed mt division
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24
Q

What is the mammalian equivalent of Dnm1 (yeast)?

A
  • Drp1
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25
Q

How does Dnm1/Drp1 perform its role?

A
  • oligomerises and physically assoc w/ other copies of itself in curved structures on outer surface of mt
  • forming a scission machine
  • curved Drp1/Dnm1 structures constrict and pinch off mt using energy from GTP hydrolysis
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26
Q

How was it determined experimentally that fis1 is important in fission?

A
  • ts mutants grown at restrictive temp
  • mt fluorescently labelled
  • looked at WT, fzo1 mutants, fis1 del mutant and dnm1 del mutant
  • if KO dnm1 get huge networks of mt forming through unopposed fusion
  • if KO fzo1 get unopposed fission
  • conclusion: role of fis1 important in fission, as look like other fission mutants
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27
Q

How is Drp1 recruited?

A
  • fis1 bound to OMM and recruits it
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28
Q

How is balance to mt fusion and fission determined?

A
  • levels of mitofusins, OPA1/Mgm1 and Drp1/Dnm1
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29
Q

In what diff ways can reg of balance between fusion and fission be determined, in diff cell contexts?

A
  • protein stability
  • protein cleavage
  • protein conformation
  • changes, eg. phosphorylation, ubiquitination, PTMs
  • protein localisation via assoc w/ binding partners
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30
Q

What is mitophagy?

A
  • autophagy of mt
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31
Q

Why is mitophagy necessary?

A
  • allows cell to get rid of defective sections of mt, so important for maintaining healthy mt pop
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32
Q

What does mitophagy occur in response to?

A
  • changes in mt membrane pot
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33
Q

How can defective mt prots be removed?

A
  • via ubiquitin proteasome system
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34
Q

How are damaged or defective mt destroyed?

A
  • tagged w/ specific kinases and ubiquitin ligases
  • mt fusion disabled
  • destruction by mitophagy
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35
Q

What is the mt life cycle?

A

DIAG

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36
Q

Do mt divide just for cell division?

A
  • no, constantly happening even in normal cell growth
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37
Q

What happens to mt if defective depolarised section?

A
  • fusion not allowed and degrad by mitophagy

- or poss for mem pot to be recovered, if this happens then allowed to rejoin network

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38
Q

Why does there have to be mechanisms so always at least 1 copy of mtDNA

A
  • so after division each section of mt network must contain mtDNA
39
Q

What happens if fission is decreased?

A
  • nucleoids cluster and lose even distribution
40
Q

In what kind of cells has of close prox between nucleoids and mt division sites been observed?

A
  • budding yeast and mammalian cells
41
Q

How is mtDNA organised?

A
  • into nucleoids, nucleoids distrib t/o mt network
42
Q

What did time lapse fluorescence microscopy images show about what happens to mtDNA during mt fusion/fission, and what questions did this raise?

A
  • nucleoids marked at mt division sites
  • by 36s clear division of 2 parts of mt membrane
  • dye showed nucleoids present at these division site
  • present at 80% fission sites (63% at both tips, 37% at 1 tip)
  • do nucleoids move to fission site?
  • or does location of nucleoid determine site of fission?
  • (lots of research ongoing, but don’t know)
43
Q

What is ERMES?

A
  • ER mt encounter structure
44
Q

What was found experimentally about the ERMES complex and mt fission?

A
  • ERMES present at fission sites and partly responsible for fission occurring
  • could be that nucleoid attracts ERMES to site and fission occurs, or ERMES binds and attracts nucleoids to site
  • conclusion: ERMES complex assoc w/ mt fission sites, present at 60% division sites
45
Q

What is the importance of mt fusion/fission for mtDNA integrity?

A
  • mtDNA undergoes freq mutations due to close prox w/ ROS gen site
  • mt dynamics plays important role in compensating for these mutation
  • mammalian cells w/ defects in mt fusion/fission machinery have reduced mtDNA content and an increased rate of mtDNA mutation –> not allowed to fuse back into network, v important to maintain integrity
46
Q

What evidence is there for other protective mechanisms (apart from mt fusion/fission) for mtDNA integrity?

A
  • complementation –> restoration of oxphos function t/ complementation in cybrids, saw signif increase in levels, but not fully returned to normal (suggests some complementation)
  • deletion/repair of mutant mtDNAs –> when mixed mtDNA, either WT pref rep (and mutant diluted out), or WT used as template to repair DNA
  • segregation of mutated mtDNAs –> mechanism to selectively attract all mutated mtDNAs to 1 area o fmt network to be effective, then just eliminate this area through mitophagy
47
Q

What is a cybrid, and how can they be made in the lab?

A
  • cytoplasmic hybrid
  • might make in lab by treating bunch of somatic cells w/ eg. polyethylene glycol, disrupting mem, spin to remove nucleus and left w/ cytoplast, then fuse w/ somatic cells, so have somatic cell nucleus from 1 type and heteroplasmic mtDNA pop
48
Q

What is a cytoplast?

A
  • cyto w/ mt and other components of cyto in it
49
Q

How does fusion/fission balance change at G1/S (inter)phase?

A
  • needs increase in ATP levels to gen biomolecules, to increase efficiency of ATP synthesis mt fuse and elongate
  • so more fusion/less fission
50
Q

How does fusion/fission balance change at mitosis?

A
  • mt fragmentation needed to ensure distrib of mt to daughter cells
  • so more fission
51
Q

What was found about fission of mt networks in mitosis, through confocal microscopy images?

A
  • mt network stained red t/o interphase and diff stages of mitosis
  • in interphase conjoined network
  • rapid fission of network occurs early in mitosis
  • come together at end before cytokinesis
  • conclusion: mt networks mostly tubular during interphase
52
Q

What conclusion was drawn from an experiment using RNAi knockdown of Drp1 in HeLa cells?

A
  • Drp1 essential for mitosis related mt fission
53
Q

How was reg of Drp1 in cell cycle specific manner determined experimentally, and what was found?

A
  • showed Drp1 phos to activate it, by cdk1/cyclinB MPF complex
  • aimed to identify which residue –> identified 4 poss ser residues that could be phos
  • gel shift assay
  • in WT just 1 band, phos causes v small shift in prot, so see v small increase in prot size –> 2 bands of gel for first 3 mutants (so not this site responsible, as mutating this Ser site and still get shift
  • in last one only get 1 band, so mutating this ser site does stop phos –> therefore this is the residue getting phos
54
Q

What did studies in yeast show about what happens to mt when cells divide?

A
  • distrib of mt during asymmetric cell division –> role of cytoskeleton
  • looking at cycle during G1 phase, get actin filaments lining up from potential bud sites, and on these filaments get mt aligning
  • as bud starts to dev, mt start to move to mother cell tip (retrograde movement) or bud cell tip (anterograde movement)
  • before cell splits mt anchored at poles so can make clear break for cell division
55
Q

How is decision between retrograde and anterograde movement made?

A
  • proposed that ‘fitter’ mt more motile and more likely to move to bud –> as takes more energy to move anterograde (could be mechanism to ensure ‘fitter’ mt as req more here than my mother)
  • site specific anchorage retains mt to certain locations
  • mt anchored in bud tip have fewer ROS
56
Q

What do the quality control mechanisms for damaged mt involve?

A
  • mt fusion repairs low functioning mt by intra-organellar complementation
  • firstly try to mend –> molecular chaperones bind and stabilise unfolded prots
  • if can’t be then proteases w/in and outside organelle degrade mt prots
  • mitophagy and mt fusion and fission eliminate mt that are beyond repair
57
Q

What are the 2 important prots involved in mitophagy?

A
  • PINK1 (PTEN induced putative kinase protein 1) = a ST kinase
  • PARKIN (E3 ubiquitin ligase)
58
Q

How does PINK1 and PARKIN differ in healthy and defective mt?

A
  • healthy mt = functional mem pot, PINK1 imported and degraded
  • defective mt = lack of mem pot, PINK1 remains on surface and recruits PARKIN, mt prots ubiquitinated, destruction by mitophagy
59
Q

What disease has PARKIN been assoc w/?

A
  • Parkinson’s Disease
60
Q

What is the hallmark of PD, and what does this result in ?

A
  • degen of dopaminergic neurons in substantia nigra
  • patients have reduced complex I activity in substantia nigra
  • defective mitophagy so mt network can’t stay healthy, reduced OXPHOS capacity, get problems w/ neurons
61
Q

What mt related mutations has familial PD been linked w/?

A
  • PINK1, Parkin and mtDNA
62
Q

How does PD pathophysiology relate to mt?

A
  • roles for mt dynamics, mitophagy and oxidative stress
63
Q

What is autosomal dominant optic atrophy assoc w/, what are the symptoms and what causes it?

A
  • assoc w/ mtDNA depletion
  • degen of optic nerve –> symptoms inc ophthalmoplegia, ataxia, deafness
  • results from reduced OXPHOS capacity
  • largely effects mt encoded complex I subunits
64
Q

What mutation causes autosomal dominant optic atrophy?

A
  • mutation in OPA1 (mammalian inner mt mem fusion prot)
65
Q

What is the most common hereditary peripheral neuropathy?

A
  • Charcot Marie Tooth Type 2A
66
Q

What is CMT2A caused by, and what does it result in?

A
  • most cases involve Mfn2 (OMM fusion prot) mutations, mainly in GTPase dom, can be gain or loss of function
  • defects in mt motility also linked
  • patients have reduced OXPHOS, linked w/ increase in mtDNA deletion
67
Q

What roles do mt play w/in the cell?

A
  • apoptosis via caspase system
  • KC
  • oxphos
  • Ca signalling
68
Q

What was the main finding of a paper investigating effects of Dnm1 del on ageing, in yeast?
(Scheckhuber)

A
  • reducing fission (Dnm1 del) results in increased life span and fitness in 2 fungal ageing models (P. anserina and S. cerevisiae)
69
Q

What did a paper investigating effects of Dnm1 del on ageing, discover about P. anserina yeast, inc diffs in gene exp and morphology between WT and mutant strains?
(Scheckhuber)

A
  • older cells had higher levels of Dnm1 than juvenile
  • juvenile and mature WT cells had filamentous mt
  • mutants juvenile and mature cells had elongated mt
  • senescent cells (both mutant and WT) had fragmented mt
  • therefore Dnm1p exp more w/ age and fragmentation increases w/ age
  • mean lifespan in WT lower
  • as less fragmentation leads to longer lifespan
70
Q

What did a Dnm1 del prevent in a paper investigating effects of Dnm1 del on ageing?
(Scheckhuber)

A
  • mtDNA reorg in old yeast
  • delayed H2O2 release
    etc. ..
71
Q

What did a paper investigating effects of Dnm1 del on ageing, discover when reprod Dnm1 mutants in S. cerevisiae yeast?
(Scheckhuber et al)

A
  • similar results to P. anserina
  • deletion of Dnm1 counteracted age related fragmentation of mt, by forming nets of densely packed mitochondrial tubules
  • similar mem pot in mutant to WT, so not reg by ETC
  • both Dnm1 and fis1 del mutants increased lifespan and fitness of cells, comp to WT
72
Q

What did a study into OPA1s roles find, by exp a prot in bacteria and yeast?
(Ban et al)

A
  • OPA1 essential for fusion of IMM
  • interaction of OPA1 w/ mems can stim higher order assembly, enhance GTP hydrolysis and lead to mem deformation in tubules
  • mutant OPA1 results in fragmented mt morphology, preventing fusion
73
Q

In a study into the role of OPA1, what was found out about the effects of lipid on OPA1 behaviour?
(Ban et al)

A
  • assocs w/ -vely charged phospholipids (not w/ neutral)
  • OPA1 + neutral phospholipids = basal level of GTP hydrolysis
  • OPA1 + negative phospholipids = enhanced GTP hydrolysis
  • w/ cardiolipin, higher order oligomers of OPA can form
  • cardiolipin is in high conc in IMM, so prob binds OPA1, enhancing GTP hydrolysis and releasing more energy for IMM fusion
74
Q

What can liposomes be used as a model for?

A
  • mt mem
75
Q

What were the findings of a study into the roles of OPA1, on mem tubulation and fusion?
(Ban et al)

A
  • OPA1 alone responsible for tubulation
  • GTP hydrolysis not req, just reg fusion activity by controlling interactions of OPA w/ IMM
  • OPA1 facilitates fusion of mt mems
76
Q

How is OPA1 disruption implicated in disease alleles?

A
  • OPA1 disrupted in DOA (dominant optic atrophy)
  • mutation causes loss of tubular mt, so loss of fusion activity
  • DOA mutations affect liposome binding and GTPase activity –> and OPA1 is involved in lipid binding, reg of GTP hydrolysis and mem tubulation
77
Q

What phenotype did a study of zebrafish find loss of MFN2 function could lead to?
(Chapman et al)

A
  • CMT2A like phenotype
78
Q

Why were zebrafish (and not mice) used for a study of MFN2 KOs?
(Chapman et al)

A
  • MFN2 KO leads to placental defects –> lethal to mice

- but zebrafish dont req placenta

79
Q

What is the effect of MFN2 mutation on mt morphology, and how was this visualised?
(Chapman et al)

A
  • mutations cause fusion failure
  • visualised by staining mt
  • applied model to humans, supporting theory that MFN2 mutations lead to abnormal mt morphology, leading to eg. CMT
80
Q

How was it investigated whether MFN2 loss of function lead to loss of motor function?
(Chapman et al)

A
  • investigated swimming behaviour (indicator of motor function)
  • comp WT to heterozygotes and homozygous mutants
  • loss of MFN2 function shown to be assoc w/ progressive motor defects in adult zebrafish
81
Q

Is loss of MFN2 function assoc w/ defects in distal axon and abnormal NMJ pathology?
(Chapman et al)

A
  • area of pre and postsynaptic compartments signif reduced

- showed alt swimming in MFN2 del zebrafish is assoc w/ defects at NMJ

82
Q

What was found when looked at MFN2 mutations and mt distrib along the axon?, and how did this relate to CMT2A
(Chapman et al)

A
  • looked at muscle biopsies
  • MFN2 mutations lead to alt mt distrib along the axons
  • CMT2A patients have irregular distrib of mt in axons of muscle cells
  • signif reduction in mt density and increase in inter mt distance in the proximal (ie. mt are further apart), but not the distal axon
  • so MFN2 mutation can affect retrograde transport and leads to alt distrib along axon
83
Q

What is the role of Pink1, according to a study in Drosophila?
(Yang et al)

A
  • interacts w/ mt fission/fusion machinery and modulates mt dynamics, linked to familial PD
84
Q

How were the genetic interactions of Pink1 w/ mt fusion/fission pathways investigated?
(Yang et al)

A
  • Drp1 overexp and Opa1 like heterozygosity restored dopamine levels
  • so Pink1 may play role in reg dopaminergic physiology
  • then overexp Pink1 in dopamine neurons
  • -> induced mt clustering and changed mt morphology, may be caused by excessive fission
  • -> supports Pink1 promoting mt fission
85
Q

What is the relationship between Pink1 and Drp1 and how was this investigated?
(Yang et al)

A
  • single and double knockdowns
  • caused perinuclear aggregation of mt
  • some cells from double knockdown had long continuous threads of mt (extreme fusion)
  • disruption of mt function alone does not lead to extreme mt fusion
  • interaction between Pink1 and Drp1 is specific for reg mt morphology
86
Q

What prots are conserved as +ve regulators of mt fission?

Yang et al

A
  • Pink1
  • Fis1
  • Drp1
87
Q

What is the relationship between Pink1, Fis1 and Drp1 in mammals?

A
  • Drp1 may act ds of Pink1

- Drp1 and Fis1 epistatic to Pink1

88
Q

How do levels of fusion and fission prots (and eg.s of each) differ in HD patients?
(Reddy et al)

A
  • high levels of fission prots (Drp1, Fis1) and low levels of fusion prots (MFN1, MFN2, OPA1) in HD patients
89
Q

What is mutant Htt assoc w/ in affected brain regions of HD patients?
(Reddy et al)

A
  • mt imbalance and mt dynamics impairs axonal transport of mt
  • decreases mt function
  • damages neurons
90
Q

What is the effect of Htt on mt encoded genes?

Reddy et al

A
  • increased exp of mt encoded genes in complexes I, III, IV, V in patients
  • may be compensation for loss of mt function caused by mutant Htt
  • related to this loss of neurons mt function
91
Q

What is the result of the fact that HD patients have lower no. neurons?
(Reddy et al)

A
  • mt function lower
92
Q

What was the result of determining oxidative DNA damage was present in HD patients?
(Reddy et al)

A
  • may be due to increased assoc of mutant Htt w/ mt in neurons
  • mutant Htt overexp involved in oxidative damage during disease progression
93
Q

What did a study about the balancing of mt dynamics find about its effects on mt fitness, in S. cerevisiae?
(Bernhardt et al)

A
  • made double Mgm1/Dnm1 mutant, had same morphotype as WT due to complementation
  • assessed replicative lifespan of mutants –> mean lifespan of double mutant and Mgm1 mutant much shorter than Dnm1 mutant, as more sensitive to stress conditions
  • reduced lifespan when Mgm1 del, so has role in responding to exogenous stressors
  • energy metabolism analysis: single Dnm1 mutant not signif diff to WT in terms of resp capacity, but double mutant had signif lower ETC capacity and basic resp capacity comp to WT
  • analysed mt mass and quality:
  • -> Mgm1 del has all small colonies
  • -> also Dnm1 del had more small colonies, double mutant had even more
  • impairment in mt fission and fusion leads to reduction in mitophagy
  • overall reduction of mitophagy key to giving rise to specific characteristics of double mutant

MBB342 - Genetics of Cell Growth & Division (3 decks)

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