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MBB342 - Genetics of Cell Growth & Division > Jones - How do organisms preserve the integrity of their mt genome? > Flashcards

Jones - How do organisms preserve the integrity of their mt genome? Flashcards

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1
Q

What is the structure of mtDNA?

A
  • ds closed circle
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2
Q

What does human mtDNA encode and how big is it?

A
  • 13 polypeptides
  • 22 tRNAs
  • 2 rRNAs
  • 16.6kb size
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3
Q

What do the features of mtDNA inc?

A
  • D loop = displacement loop (or control region)
  • HSP = heavy strand promoter region
  • LSP = light strand promoter region
  • OH = H strnad origin of rep
  • OL = L strand origin of rep
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4
Q

Does mammalian mtDNA have non coding DNA?

A
  • no introns

- but some area of non coding DNA, eg. D loop, OL

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5
Q

How do mts increase SA, and why is this needed?

A
  • cristae

- for oxphos

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6
Q

Do mts always act independently, why?

A
  • fuse together to form diverse networks t/o cell

- do this at diff stages t/o cell cycle

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7
Q

What is meant by intergenomic communication?

A
  • transcrip and translation of mtDNA is dependant of effective interaction with nucleus
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8
Q

How much does mt genome vary in size between species?

A
  • 16-18kb in mammals
  • 75kb in yeast
  • up to 400kb in plants
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9
Q

Why does mt genome size vary between species?

A
  • presence and sizes of introns
  • also considerable difference in genes encoded, reflecting many changes since endosymbiotic event (movement of genes/loss of genes if redundant etc.)
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10
Q

Why does mtDNA have a v variable copy no?

A
  • multiple genomes per organelle, multiple organelles per cell
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11
Q

How does copy no. vary between somatic and germline cells?

A
  • 20-200 in somatic cells

- over 200,000 in mature oocyte

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12
Q

Where does mtDNA originate from, what is the evidence from this?

A
  • bacterial origins
  • mt ribosomes differ
  • variation in triplet code (eg. UGA usually stop, but in mtDNA encodes Trp)
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13
Q

What are the diff complexes of ETC?

A
  • Complex I = NADH deHase
  • Complex II = succinate deHase
  • Complex III = cytochrome c reductase
  • Complex IV = cytochrome c oxidase
  • Complex V = ATP synthase
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14
Q

Are any of the ETC complexes entirely nuclear encoded?

A
  • only complex II
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15
Q

What is the consequence of the fact that vital cellular apparatus is encoded by 2 genomes?

A
  • need effective communication between them for normal cellular function
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16
Q

What are the features of mtDNA rep?

A
  • 2 origins of rep: OH and OL –> most genes encoded by H, few by L
  • transcrip commences from HSP and LSP
    mtDNA rep, dep on transcrip of short section from LSP
  • TFs, cofactor and pols all nuclear encoded → need these factors to come together and interact for effective rep
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17
Q

What is TFAM?

A
  • essential mt transcrip factor
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18
Q

What is special about POLG?

A
  • DNA pol that is only mitochondrial
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19
Q

What was an experiment which showed TFAM was essential for maintaining mtDNA copy no. and for ETC function?

A
  • actin is control
  • w/o TFAM mtDNA can’t be maintained (in homozygous KO) –> shown by PCR
  • levels TFAM less in heterozygote
  • TFAM +/- = reduced mtDNA copy no., reduced mtDNA transcript and ETC dysfunction in heart
  • TFAM -/- = severe mtDNA depletion, abolished OP, enlarged mt, growth retardation, die prior to embryonic day E10.5
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20
Q

How does TFAM reg mtDNA rep?

A
  • binds LSP
  • together w/ complex of other factors enables transcrip of entire copy of L stand and short primer for rep (both from LSP)
  • get transition from RNA to DNA, POLG recruited
  • rep of H strand –> need TFAM to bind before mt rep
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21
Q

What are the roles of TFAM?

A
  • req for transcrip from LSP and HSP –> so essential for mtDNA rep
  • levels may directly control mtDNA copy no.
  • also important packaging role and most abundant prot in mt nucleoids (another is mtSSB, a mt ss DNA BP)
  • nucleoid prots reg stability, rep, transcrip and segregation of mtDNA
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22
Q

What is the structure of TFAM?

A
  • high mobility group box A and B joined by linker dom
  • short C-ter dom attached to HMG-box B
  • binding recognition site upstream of HSP and LSP
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23
Q

How does TFAM binding to LSP and HSP affect the structure of mtDNA, and why is this important?

A
  • forces mtDNA into U shape

- structurally important for activation of transcrip from these 2 sites

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24
Q

Why might there be problems if have mt and nDNA from diff source (/species) and how might this affect OP?

A
  • if changes in seq (recognition/binding sites) then wont get same binding (more/less effective) → so more/less trancrip
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25
Q

How does nuclear and mtDNA interplay?

A
  • nuclear encoded enz req for mtDNA transcrip and rep
  • co-assembly of nuclear encoded and mtDNA encoded subunits of resp chain complexes
  • majority of prots that function in mt are nuclear encoded
  • over 1000 nuclear encoded products are essential to mt function
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26
Q

What is the effect of crosses between diff species on mtDNA?

A
  • more diverse species = more problems
  • some level of cross species compatibility → resp chain defects when crossed mice with rats, but diff species of mouse were fine
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27
Q

How is mtDNA inherited in humans (and most organisms)?

A
  • maternally (or uniparentally) inherited
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28
Q

How are yeast able to survive loss of mt function, and how is there mtDNA inherited?

A
  • facultative anaerobes, so can gen energy through glycolysis
  • inherit mtDNA from both parental cells and therefore have heteroplasmic mtDNA pop → but reversion to homoplasmy w/in 20 cell divisions
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29
Q

What causes variation in mtDNA?

A
  • no recomb of parental alleles, unlike nDNA
  • faster mutation rate than nDNA = at least 10x
  • high level of variation in D loop as non encoding so fewer consequences, known as hypervariable region
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30
Q

Why does mtDNA have a faster mutation rate then nDNA?

A
  • as no protective histones
  • lack of proofreading by POLG
  • decreased level of repair in mtDNA
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31
Q

What are the sources of heteroplasmy?

A
  • age related muts
  • inheritance of germline mut
  • introd of foreign mt to reconstructed embryos
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32
Q

What is the mtDNA bottleneck, and what suggests its existence?

A
  • next gen has quite diff pop, so must be taking small no. from parent
  • so must be dramatic reduction in no. mtDNA copies at some point in oogenesis to allow these changes to occur
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33
Q

What are the 3 theories for the mtDNA bottleneck?

A

1) passive reduction of mtDNA
2) packaging into homoplasmic clusters
3) focal rep of mtDNA

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34
Q

What would a passive reduction of mtDNA involve (a mtDNA bottleneck theory)?

A
  • huge copy no. in oocyte, fertilised, then reduced no. copies after each cell division
  • so by chance segregating in diff way to cells that spawn next gen
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35
Q

What would packaging into homoplasmic clusters involve (a mtDNA bottleneck theory)?

A
  • passive reduction not enough

- mt genomes cluster in nucleoids or multiple nucliods cluster, and get segregation of nucleoids/groups of nucleoids

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36
Q

What would a focal rep of mtDNA involve (a mtDNA bottleneck theory)?

A

= segregation then selective amp of certain mtDNA mols

  • random segregation v early in dev
  • so genomes distrib at random to each of cells, so cells of next gen have much lower mtDNA copy no.
  • after puberty get selective amp
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37
Q

What evidence is there for a focal rep of mtDNA?

A
  • study visualised replicating mtDNA in vivo
  • after 2 hours not much new mtDNA being made even though lots of TFAM, probs lots of mtDNA just not all being replicated → selective amp of certain mtDNAs during oocyte maturation, so heteroplasmy levels can change dramatically between gens
38
Q

Why do we not know which theory of mtDNA bottleneck is correct?

A
  • conflicting data on extent of mtDNA copy no. decline in PGCs
  • plenty of evidence to show lack of mtDNA rep during early embryogenesis
  • multiple sources of experimental evidence that show selection of beneficial mtDNA variants over mutants
  • combo of models most likely to be correct
39
Q

Why is elimination of paternal mtDNA needed?

A
  • to protect subsequent gens from heteroplasmy
40
Q

What is the dilution effect?

A
  • copy no. of mtDNA in sperm approx 20, comp to 20,000 in oocyte
  • reduced during spermatogenesis
41
Q

What evidence is there for the involvement of TFAM in elimination of paternal mtDNA?

A
  • TFAM and mtDNA levels decline during maturation
  • WB data shows that in comp to other tissues testes have lower levels TFAM, and declines t/o puberty → therefore levels of mtDNA are much reduced in mature sperm than spermatogonia and reduction of sperm TFAM levels t/o dev
42
Q

What mechanism is in place to deal w/ paternal mtDNA that still enters oocyte?

A
  • active degrad of paternal mtDNA in fertilised oocyte
43
Q

Is homoplasmy ‘normal’?

A
  • yes, it’s the desired state
44
Q

Is heteroplasmy rare, and when is it more common?

A
  • heteroplasmy not uncommon

- increases w/in indivs w/ age and assoc w/ ageing effects and numerous diseases

45
Q

How many people carry known disease causing point mutation, comp to those w/ mt disease?

A
  • 1 in 200 carry known disease causing point mutation

- only 1 in 5000 have mt disease

46
Q

Can mt diseases arise from a nuclear mutation?

A
  • yes, if impairs mt function
47
Q

What do threshold levels mean in relation to mt disease

A
  • certain level of genomes must be mutated before disease evident (can be up to 90%, if 10% encode enough normal polypeptides for normal levels of oxphos to occur)
48
Q

How can heteroplasmy lead to homoplasmy through mitotic segregation?

A
  • genomes randomly segregated to each daughter cell → so heteroplasmic cell can prod homoplasmic daughter
  • DIAG*
49
Q

When does random segregation of mtDNA variants occur?

A
  • PGCs made early in dev
  • have certain mtDNA pop
  • undergo mitosis and meiosis before get mature oocytes
  • during cell divisions get random segregation of mutant genomes so eventual pool of oocytes can have v variable mutant load
50
Q

What do PGCs (primordial germline cells) become?

A
  • sperm/egg cells
51
Q

How do levels of mutant mtDNAs affect the outcome, and what is the consequence of this?

A
  • low levels mutant mt unlikely to suffer
  • high levels more likely to
  • so can see how severity of disease can shift rapidly from 1 gen to next and can vary a lot between siblings
52
Q

Why is there pref rep of normal mtDNA?

A
  • need protective mechanism acting at this point to prevent selective rep of mutated genomes
53
Q

How was a cell specific oxphos req shown experimentally?

A
  • looked at patients w/ mutation in EFG1 (mt translation factor)
  • ran WB against diff ETC complexes
  • muscle and heart cells had much higher levels of prot (logical as energy intensive tissues)
  • patients had gen less prot than control
  • complex II was control, as all nuclear encoded
  • so dep on tissue, a mutant load of eg. 90% may/may not be important
54
Q

How is mt disease spread out across genome?

A
  • every mtDNA encoded subunit of ETC is assoc w/ at least 1 known disease causing mutation
55
Q

Where is mt disease shown?

A
  • energy intensive tissues
56
Q

What can mt disease result from?

A
  • mutations in mtDNA, nuclear genes encoding OXPHOS subunits, or proteins req for their translation or assembly
57
Q

What kind of inheritance do mt disorders caused by nuclear mutations show?

A
  • mendelian
58
Q

What inheritance pattern do mt disorders caused by mtDNA mutations show?

A
  • maternally inherited

- but follow laws of pop dynamics

59
Q

What did a study looking a whether disease severity correlated w/ levels of heteroplasmy find?

A
  • looked at A>G mutation in 12S rRNA gene of mtDNA, that causes hearing loss
  • age of onset and symptom severity varied
  • measured heteroplasmy levels in all in pedigree, by direct seq analysis
  • risk of deafness increased w/ increased mutant load, BUT levels of heteroplasmy did not correlate w/ disease severity
  • so mutant load v important in determining phenotype, but not only variable
60
Q

What type of mutations can happen to POLG, and what is most common?

A
  • 94% missense
  • low no. fs/dels
  • CAG repeats
61
Q

How can POLG mutations be inherited?

A
  • majority autosomal recessive

- except autosomal dominant progressive external ophthalmoplegia (adPEO)

62
Q

What do POLG mutations result in?

A
  • array of 2° mtDNA mutations
  • deletions (no rep)
  • mtDNA depletion
63
Q

POLG mutations are clinically what?

A
  • heterogeneous
64
Q

Are mt functions conserved between humans and yeast?

A
  • yes, highly conserved between humans and S. cerevisiae
65
Q

Why are yeast models used to study mt disease?

A
  • poss to undertake large scale screens
  • genetic manipulations easy
  • biochemical analyses well established
  • facultative anaerobes, so can survive on fermentable C sources in absence of mt function
  • growth phenotype simple to assess
  • become homoplasmic w/in few gens, so could set up series of mutants w/ diff nuclear background against 1 mt background (or opp)
66
Q

How was it shown experimentally than 2° nuclear mutations can impact on phenotype?

A
  • looked at growth dynamics under resp conditions for interspecific hybrids
  • looked at effects of 4 diff nuclear contexts on growth phenotype of particular mutation
  • serial dilutions of yeast cells harbouring single mt mutation, looking at growth of glycerol (no growth suggests OXPHOS not working)
67
Q

What are 3 methods of assisted reproductive tech?

A

1) mt supplementation to treat infertility (cyto transfer)
2) mt supplementation/replacement to treat mt diseases caused by mt defects
3) somatic cell nuclear transfer to gen stem cells

68
Q

What kind of patients is cytoplasmic transfer used to treat?

A
  • infertile
69
Q

How does cytoplasmic transfer work?

A
  • threshold no. copies of mtDNA genomes for egg to be fertile
  • so take some extra ooplasm from another of patients eggs or donor egg and supplement/ transfer some in, so no. mt genomes above threshold, allowing egg to become fertile
70
Q

Is cytoplasmic transfer successful?

A
  • was initially

- then banned due to safety concerns

71
Q

Who is mt replacement therapy used for?

A
  • women carrying mt disease, to allow them to have baby w/o disease
72
Q

What 2 methods can be used to carry out mt replacement therapy?

A
  • PNT (pro nuclear transfer)

- spindle trasnfer

73
Q

How is spindle transfer carried out?

A
  • start w/ unfertilised patients egg w/ abnormal mt and unfertilised donor egg w/ normal mt
  • at fert eggs arrested at metaphase 2 (don’t complete meiosis till after fert) → so all chromosomes clustered on metaphase spindle
  • spindle and assoc chromosomes removed as karyoplast from both eggs → discarded from donor egg and patients spindle fused into “enucleated” donor egg (so have donor ooplasm and mtDNA w/ patients chromosomes)
  • reconstituted egg fertilised w/ sperm
74
Q

How is PNT carried out?

A
  • patients and donors egg fertilised and form zygote

- take out pronuclei from donor egg and insert pronuclei from patient egg

75
Q

What happens to mutant mtDNA pop during mt replacement therapy?

A
  • mt cluster around metaphase 2 spindle
  • so in spindle transfer although trying to just take chromosomes and leave all mutant mt, prob transfer of some mutant genomes into final reconstructed oocyte
  • do they get diluted out/is there persistence/is there rep?
76
Q

How could pref rep of mutant mtDNAs be a problem?

A
  • some of children born of cytoplasmic transfer analysed and shown to harbour heteroplasmy
  • if ending up w/ eg. 1% of mutant mtDNA genomes, what happens if prefrep and segregate into diff tissues, might go into oocyte and rapidly increase over gens to cause mt disease
  • part of debate was whether to only allow for male embryos, but didn’t due to problem of gender selection
77
Q

What is the reported contrib of donor mtDNA in somatic cell nuclear transfer, and what does this mean?

A
  • 0-63% in embryos
  • 0-59% in offspring
  • so must be pref rep of donor mtDNA
78
Q

When is pref rep more likely?

A
  • if species more divergent → less likely to pref rep if species same/more similar
79
Q

How is persistence overcome in somatic cell nuclear transfer, and what is the problem w/ this?

A
  • mtDNA depletion of donor cells

- prob not approp for oocyte as would be damaging

80
Q

What did a paper studying small fish discover about how elimination of sperm mtDNA was achieved - main findings?
(Nishimura)

A
  • happened through gradual decrease in no.s of mt nucleoids during spermatogenesis
  • and rapid digestion of sperm mtDNA just after fertilisation, achieved by complete destruction of mt structure (poss to avoid transmission of pot deleterious sperm mtDNA to offspring)
81
Q

What did a paper studying small fish discover about how elimination of sperm mtDNA was achieved - experiments/explanations?
(Nishimura)

A
  • mtDNA nucleoids present in living sperm at every stage during dev (through staining to visualise mtDNA)
  • no. nucleoids and copy no. of mtDNA per nucleoid changes during spermatogenesis
    (staining to visualise DNA) → 5 fold decrease in no. nucleoids per nucleus, but same mtDNA copy no., so although amount of mtDNA decreases a lot, mtDNA composition of each nucleoid is conserved
  • active digestion of male mtDNA in natural fertilisation → diluted paternal mtDNA in initial oocyte, but actively degrad before 2 cell stage
  • removal of sperm mtDNA in egg and sperm after fertilisation
    → microinjection of sperm mtDNA into egg, stained mtDNA, then used optical tweezers to remove single sperm w/ or w/o mtDNA and analysed w/ PCR
    → saw decrease in levels of mtDNA in sperm after fertilisation
    → saw polymorphism from maternal mtDNA always present in cases where sperm mtDNA may/may not be (shows inheritance of mtDNA only from mother)
82
Q

What did a paper studying drosophila discover about elimination of sperm mtDNA before fertilisation - main findings?
(DeLuca)

A
  • 2 mechanisms to avoid transmission of sperm mtDNA to zygote
    1) endonucleases G degrades nucleoids in sperm, thus removing mtDNA in mt
    2) back up mech: actin containing investment cone sweeps all nucleoids
83
Q

What did a paper studying drosophila discover about elimination of sperm mtDNA before fertilisation - experiments/explanations?
(DeLuca)

A
  • qPCR to quantify paternal mtDNA
    → not detected in zygote immed after fertilisation = less than 1 male mtDNA per egg
    → so mtDNA removed prior to sperm maturation, so none/v little transferred to egg
  • mtDNA levels followed t/o spermatogenesis and found nucleoids eliminated in coord w/ the sperm elongation phase
  • characterising the mechanism through informatics screen for nucleases → found 5 homologous genes (inc EndoG) w/ predicted mt targeting signals, only EndoG mutations prevented nucleoid elimination
84
Q

What did a paper studying contrib of paternal mtDNA to the next gen in mice find - main findings?
(Rojansky)

A
  • paternal mt doesn’t contrib to next gen and is degrad by mitophagy
  • MUL1 and PARKIN have roles in this
85
Q

What did a paper studying contrib of paternal mtDNA to the next gen in mice find - experiments/explanations?
(Rojansky)

A
  • tracked paternal mt in early mouse embryo, by fluorescence microscopy → after 84 hrs paternal mt almost completely lost, no reduction of maternal mt
  • identified mitophagy genes, as exp increased in oxphos inducing conditions → 3 genes identified
    oxphos req for paternal mt to be lost
  • knockdown experiments to identify roles of PINK1, PARKIN and MUL1
    → MUL1 compensated for PARKIN
    → knockdown of both reduced ubiquitination of mt
    → PINK1 knockdown alone reduced ubiquitination
  • paternal mt deleted through mitophagy → knockdown of mitophagy genes, these genes were req for elimination of paternal mt
  • looked at whether paternal and maternal mt fuse, paternal mt didn’t fuse w/ other mt and segregation of paternal mt important for degrad
86
Q

What did a paper studying the role of autophagy in sperm mtDNA degrad in C. elegans find - main findings?
(Sato)

A
  • autophagy involved in degrad sperm mt immed after fertilisation, so only maternal inheritance of mtDNA
87
Q

What did a paper studying the role of autophagy in sperm mtDNA degrad in C. elegans find - experiments/explanations?
(Sato)

A
  • measured disappearance of paternal mt and saw male mt initially enter embryo, but degrad by 4 cell stage
  • monitored autophagosome formation, induced in 1 cell stage embryo, most disappeared by 16 cell stage, then some reappeared around 32 and 64 cell stage, before disappearing again in late embryo dev → shows dynamic reg of genes involved in autophagosome formation
  • induction of autophagosomes dep on fertilisation
    → used Ts mutants against fertilisation, embryogenesis
    → mutants in fertilisation prevented induction of autophagosomes
    → mutants in embryogenesis, but not affecting fertilisation still had induction of autophagosomes around paternal mtDNA
  • autophagosomes degrade mt → autophagosome and paternal mtDNA signals disappear at same time, so is degrading paternal mtDNA
88
Q

What did a paper looking at mutations in prot coding genes of mtDNA in mice find - main findings?
(Stewart)

A
  • purifying selection against non-synonymous mutations in prot-coding genes of mtDNA
89
Q

What did a paper looking at mutations in prot coding genes of mtDNA in mice find - experiments/explanations?
(Stewart)

A
  • looked at ratio of nonsynonymous to synonymous mutations, found purifying selection against nonsynonymous changes in prot coding genes and selection for silent mutations
  • comp mutations in 1st and 2nd codon position, to 3rd, decrease in 1st/2nd position as likely to cause change in AA, less likely in 3rd, due to degenerate nature = hallmark of purifying selection
  • comp to human mtDNA seq data and saw conserved in humans
90
Q

What did a paper looking at homoplasmic state in mice find - main findings?
(Sharpley)

A
  • homoplasmic state gen beneficial for the mouse, therefore may have evolved to be pref homoplasmic
91
Q

What did a paper looking at homoplasmic state in mice find - main findings?
(Sharpley)

A
  • looked at 2 pops of mtDNA: NZB and 129 → prop of NZB pref reduced and 129 pref amp during oogenesis
  • detailed analysis of mtDNA pops → higher levels of maternal heteroplasmy resulted in increased chance of NZB mtDNA reduction
  • demonstrated selection of 1 mtDNA variant over another in female germline
  • observed diff between hetero and homplasmic mice → heteroplasmic mice had reduced activity and cognitive impairment, comp to both homoplasmic strains

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

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