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To check for inconsistencies between the mitochondrial and the nuclear gene mutation rates, we ran analyses using the mitochondrial priors only as well as priors for both the mitochondrial and nuclear genes together.
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Mitochondria were visualized using the mitochondrial matrix marker DsRed2-Mito and the antibody against the outer mitochondrial membrane (OMM) protein TOM20.
Mitochondrial mass was also determined in live cells using the specific mitochondrial probe MitoTracker Green FM.
Prior to multiple sequence alignment, nucleotide sequences of the 12 protein-coding genes were translated to amino acid sequences using the invertebrate mitochondrial genetic code.
The priors were set using the gamma-Dirichlet prior [ 56].
The mitochondrial membrane potential was analyzed using the JC-1 mitochondrial membrane potential detection kit (Biotium).
Mitochondrial superoxide anions were measured using the MitoSOX Red mitochondrial superoxide indicator.
Mitochondrial reads were specifically trimmed using the Amblyomma triguttatum mitochondrial genome.
We report herein that mitochondrial transfection using the MITO-Porter results in mitochondrial transgene expression in G625A fibroblasts obtained from a patient with a mitochondrial disease.
Finally, confirmation of mitochondrial dysfunction using the MTT assay further suggested mitochondrial formation of Fenton reactants.
Sequences were trimmed of low quality and vector sequence, then screened to remove mitochondrial sequences using the SeqMan II software (DNASTAR, Inc ., prior to contig assembly.
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