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BMS 2 > Mito Genome > Flashcards

Mito Genome Flashcards

1
Q

Outer mito membrane

A

Permeable to sm molecules

Impermeable large molecules, transport systems

Contains signalling receptors

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2
Q

Intermembrane space

A

Apoptotic proteins

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3
Q

Inner mito membrane

A

Transporter proteins

ETC

ATP synthesizing complex

Impermeable to small/large molecules

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4
Q

Mito matrix

A

Proteins for TCA cycle, lipid oxidation, transamination, mtDNA, mind protein synthesis machinery

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5
Q

What does metabolizing require to occur

A

Require oxygen and generate ATP

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6
Q

Endosymbiosis

A

Mito provide ATP, host does all else

Very similar replication to proks

Two genomes-13 polypeptides from mito

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7
Q

2 pathways to mitochondric protein production

and where do proteins go?

A

from nucleus, rna in cyto, precursor protein, inmported protien

organllele DNA, to rna, to organelle syn protein

Used as inner mito membrane proteins (among other things)

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8
Q

Mito division

A

Fission and fusion

Similar to bacteria

Change under different physiological conditions

Increasing by double everytime cell divides

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9
Q

Human mito genome

A

2 rRNA
22 tRNA
13 protein-coding seqs

Can have many copies of DNA
-occurs out of phase of cell cycle

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10
Q

Mito membrane subunits

A

Most subunits encoded by nuclear DNA%%%%%

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11
Q

mtDNA replisome

A

Individual mtDNA can replicate individual of cell cylcle

D loop-site of mito dna rep initiation
-also site of transcription promoters

Replication and integrity maintance-nuclear DNA

DNA poly, exonuclease/proofreading, lyase activity (enzymatic DNA repair)

Twinkle-DNA helicase, also acts as primase

DNA pol gamma

Both have mutations that lead to mito disease

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12
Q

tDNA genetic features

A

very high mutation rate

Maternal inheritance

Bottle neck

Replicative (random) segregation of mito and tDNA

threshold efect

changes with age

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13
Q

High mutation rate

A

CLose to reactive O2 species

DNA poly has proofreading errores

No introns-all mutations in coding region

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14
Q

Bottleneck effect

A

Primoridal germ cell has heteroplastic mtDNA mutation

During oogenesis, reduction in ant of mtDNA present

Random samping tells if going to have mutated mito or not mutated

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15
Q

Random/replicative set of mito and mtDNA

A

mito fusion and fission leads to random dist of mito and mtDNA

Can have mixtures of mutant and normal tDNA in same cell
(different than homoplasmy-all normal or all mutant tDNA)

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16
Q

Threshold effect

A

Need a certain threshold of ox phos for cell to function (which is different or each cell)

Also need certain amount of mutated mitos to show expression (50%?)

17
Q

mt changes with age

A

levels of ox phosphorylation decline

ATP syn drop below threshold, problems result

mutations occur much more rapidly as get older

18
Q

Mito inhericance

A

All females with homosplassmic mutation will pass it down, males with homoplasmic will not

Heteroplasmic pt/dups depends on threshold/ bottleneck
-deletions generally not heritable

Different numbers of mutant mito per dif tissues-diseases can vary tremendously-variable expression

19
Q

2 mechs of mito disease

A

impair mito protein synthesis

protein coding gene mutation

20
Q

Mutations in mtDNA are from

A

Heridary-from mom

Somatic-can be spontaneous in oocyte or early embryo

Can result in free radical damage or from defective mtDNA replication due to mutation in DNA poly gamma

21
Q

Mito DNA poly?

A

DNA poly gamma

22
Q

Mito DNA disease symptoms (4)

A

Build up of lactic acid if defect is oxidative phosphorylation

Matneral inheritance

Late onset due to accumulation of mtDNA mutations leading to inefficient ox phos

Varability in tissues and among family members (random seg and heteroplasmy)

23
Q

Leber’s hereditary optic neuropathy

A

Maternal inheritance (no affected male transmits disease)

Sudden death of optic nerve

80/90% is threshold

mtDNA coded disease

24
Q

mtTRAnscription

A

polycistronic precursor mRNA
-codes for ribo RNA and tRNA

2 ribo proteins
most are prob from DNA

25
Q

mtTRANSLATION

A

normal codon/anticodon pairing rules are relaxed

  • many tRNA molecules don’t even bother with third position DNA
  • fewer tRNA needed

Proteins come in and help start/stop translation

Only two ribosomal proteins are made by mito genes-but all tRNA is made from mito genes

Proteins needed for translation-nucelarly encoded

26
Q

oxphos proteins

A

Mostly by nuclear DNA

27
Q

Mito gamma polyermase mutations

A

MANY DISEASES

28
Q

Diseases with no RRFs vs with RRF

A

Leigh Syndrome and Leber sydrome
-problems with energy metabolism

CPEO, KSS, MELAS, MERRF

  • ataxia, short, dementia
  • —CNS problems

RRF are actually mitochondria
HALL MARK OF MITO DISORDERS (only 1/3 of all mito diseases)

29
Q

Succinate dehydrogenase and cytochrome d oxidase

A

RRF proteins

BMS 2 (41 decks)

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