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Explaining the Origin of Basal Eukaryotic Traits

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Covers the Eukaryotic Traits lecture from Energy and Evolution with extra reading

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  • April 6, 2016
  • 11
  • 2014/2015
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Explaining the origin of basal Eukaryotic Traits

(Lane, 2011) Summary of previous lecture…

 Mitochondria are essential to complex life – all eukaryotes possess mitochondria or
did at one point then lost them
 It was not aerobic respiration, protection against oxygen or compartmentalisation
that mitochondria contribute – as prokaryotes can do all three
Complexity resides for bioenergetics reasons in the mitochondria themselves –
specifically the genome
 All eukaryotes capable of oxidative phosphorylation independently retained a similar
core mtDNA genome – mostly encoding for respiratory chain subunits
Conserved pattern: genes strictly required for the maintenance of inner membrane
potential
Membrane potential  have field strength of 30 million V/m – distinguishes
mitochondria from other endomembrane systems
Endosymbiosis has unique ability to place the right genes in the right place to
maintain membrane potential while eliminating redundant genes by reductive
evolution and gene transfer to nucleus
 Protein synthesis requires a lot of energy – total amount of protein-coding DNA lost
from all the endosymbionts equates to the amount of protein-coding DNA that could
be supported energetically, in the nucleus
Streamlining and specialistion of mtDNA enabled the evolution, maintenance and
expression of many thousands of new genes in the nucleus
Massively expanded genome capacity key to evolution of multicellular organisms, and
was strictly dependent on reductive evolution of mitochondria
Possessing thousands of mitochondria enabled eukaryotic cells to generate
thousands of times the energy of a bacterium at a fraction of their total running
costs = consequence of bioenergetics specialisation
Genetic asymmetry  giant nuclear genomes supported energetically by multiple
tiny mitochondrial genomes


Requirement of Local Genome Outposts…

 Cybrid – cytoplasmic hybrid  host cell and
transplant mitochondria from different places
(nuclear background same in each case, mtDNA
different)
 Low-ROS cybrid: ATP synthesis is normal, low ROS
leak, little copies of mtDNA

,  High-ROS cybrid: ROS leak doubles, mtDNA doubles – lot more effort required to
generate same amount of DNA
 High-ROS cybrid but removing ROS leak (adding antioxidants): ROS leak reduced,
but mtDNA copies are also reduced, ATP synthesis decreased – ROS seems to be
some sort of signal to locally optimise ATP synthesis (relationship between ROS
leak and mtDNA copy number)

Rate of respiration depends on mtDNA copy number (Rocher et al., 2008)

 Genes are needed in the mitochondria –
penalty of failure is greater than in other
organelles (eg. apoptosis, cell loss) and
timeline is shorter – minutes
 NDS transcript levels fall within 30 min of
hypoxia – Half-life of hypoxia-inducible
fator, HIF-1a, is 2 minutes – speed
important

Where do free radicals/ROS come from?

Free radical: atom or molecule with an unpaired electron

 Main sites of FR leak  high saturation of
FeS clusters in the early complexes
(particularly I, less so for III) which are
highly reducing, low reduction potential – more
likely to pass electrons singly to oxygen
 Most biologically relevant FRs: oxygen FRs
(eg. mildly reactive superoxide radical O2.-,
extremely reactive hydroxyl radical OH.),
nitrogen FRs (eg. NO)
- Oxygen FRs important as highly reducing
complexes of respiratory chain, especially FeS clusters in complex I, react
directly with O2 to release superoxide FRs
- Superoxide is usually reduced further by superoxide dismutase (SOD) to
hydrogen peroxide – also reactive but not a free radical  reactive oxygen
species (ROS)
- Interactions of FeS and oxygen is an issue that only arose in an oxygenated
world




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