MB2014 mitochrondrial in ageing

[MB14]Michael Breitenbach2014, mitochondria in ageing

MB14 showed H2O2 can fragment mitochondrial network and this fragment is reversible. Fragmentation of mitochondrail network in aged yeast cells are irreversible.

MB14 cite Gottschling's paper, arguing that heterophasmic nature of mitochrondrail genotypes in mother cells. Daughters cells start with homoplasmic state of mitochondria genotype (only one mitochondria genotype).

MB14 show some metabolite are prone to oxidation, and form 'underground metabolism" to the ageing process.

Replicative ageing ~ gradual decline of inner mito membrane potential (Lai 2002). In non-plant cells, mitochondria is the only place where Fe-Sulure clusters are formed. Low mito membrane potential -> low Iron intake, and hence low Fe-Sulfur clusters.  DNA replication machinery contain protein with iron sulfur clusters. Hence, low mito membrane potential can lead to genomic instablity (Veatch 2009). We 2011 showed that mito genome mutation ~ decline of mito membrane potential.

Fe4-S4 cluster can be oxidized by superoxide anions to Fe2+, which can lead to more ROS through fenton reacion. (Gardner 2002)

Figure 2 presented a small gene network with different lifespan painted in colors. A good idea. 

Spermine and spermidine are ROS scavengers and decline during aging. Supplemetion of spermind/spemidine extends yeast RLS (Eisenberg 2009, Morselli 2009)

Fig 3 is a nice summary figure, compare mito poential change between health and old cells.