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With regard to the rearrangement of mitochondrial genes, two major categories of mechanisms have been advanced: (1) tandem duplication followed by random or non-random deletion of excess genes [ 51, 52]; and (2) non-homologous recombination [ 53, 54].
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Notably, the highest levels of excess mtDNA deletion compared to controls were found in the dopaminergic neurons of the substantia nigra.
This survival seems highly related to quality control and turnover of mitochondria as shown with mouse models characterized by T cell-specific deletion of Atg5 or Atg7., Moreover, excess of autophagy that is detrimental to T cell survival under IFN-γ stimulation, is tightly regulated by immunity-related GTPase family M proteins in mice.
However, we do observe a few very large events (deletions in excess of 1 Mb), which are likely explained by the presence of dispersed duplicates on the same chromosome arm, chimeric sequences produced during adapter ligation (a problem for all singleton reads), or an inadequacy in our filtering or pipeline.
The single deletion mutant (tet-WT Δ ach1), as well as ACH1 deletion combined with the knockdown of ACS2 (tet-ACS2 Δ ach1), displayed almost comparable levels of excess acetate released from cells.
A terror of excess?
Advertising of excess insurance.
§ 740.3 Advertising of excess insurance.
Accusations of excess have long followed him.
The culture of excess.
See also: Signs of excess.
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