Unknown,Transcriptomics,Genomics,Proteomics

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DNA-seq of mitochondrial DNA from mouse heart that is both heart SOD2 knockout and deficient for mitochondrial DNA repair


ABSTRACT: To study whether increase in mitochondrial oxidative stress (SOD2 removal) and decrease in mitochondrial DNA repair (Ogg1 dMTS) results into increase in mitochondrial DNA mutation load. Oxidative stress has been suggested to induce mutations in mtDNA. To verify this, we extracted and sequenced (Illumina) mitochondrial DNA from heart Sod2 knockout animals that were also deficient for mitochondrial base-excision repair. The repair deficiency was induced by removing the genomic region encoding for the predicted mitochondrial targeting sequence from endogenous OGG1 (L2 to W23) called Ogg1 dMTS mice, thus excluding the protein from mitochondria. OGG1 is a DNA glycosylase that recognizes and repairs 8-oxo-dG damage from DNA. Oxidative stress can induce 8-oxo-dG lesions, thus we removed the mitochondrial matrix localized superoxide dismutase (SOD2) from these mice to increase the level of oxidative stress. 8-oxo-dG lesion can be mutagenic because some DNA repair polymerases are known to erroneously incorporate adenosine opposite to 8-oxo-dG during replication leading to GC>TA transversion mutations.

INSTRUMENT(S): Illumina HiSeq 3000

ORGANISM(S): Mus musculus

SUBMITTER: Nils-Göran Larsson 

PROVIDER: E-MTAB-6533 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Base-excision repair deficiency alone or combined with increased oxidative stress does not increase mtDNA point mutations in mice.

Kauppila Johanna H K JHK   Bonekamp Nina A NA   Mourier Arnaud A   Isokallio Marita A MA   Just Alexandra A   Kauppila Timo E S TES   Stewart James B JB   Larsson Nils-Göran NG  

Nucleic acids research 20180701 13


Mitochondrial DNA (mtDNA) mutations become more prevalent with age and are postulated to contribute to the ageing process. Point mutations of mtDNA have been suggested to originate from two main sources, i.e. replicative errors and oxidative damage, but the contribution of each of these processes is much discussed. To elucidate the origin of mtDNA mutations, we measured point mutation load in mice with deficient mitochondrial base-excision repair (BER) caused by knockout alleles preventing mitoc  ...[more]

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