Unknown,Transcriptomics,Genomics,Proteomics

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DNA-seq of mitochondrial DNA from liver of OGG1 and MUTYH deficient mice that have been bred for five consecutive generations


ABSTRACT: Studying whether removal of base-excision repair from mitochondria will result into increase in mitochondrial DNA (mtDNA) mutation load. The endogenous genes of OGG1 and MUTYH DNA glycosylases were modified to lack the genomic region encoding for the predicted mitochondrial targeting sequence. The mouse lines used: A mouse line that lacks the region encoding for the mitochondrial targeting sequence (L2 to W23) of OGG1 (Ogg1 dMTS mice). A mouse line that lacks the region encoding the mitochondrial targeting sequence (K2 to P33) of MUTYH (Mutyh dMTS mice). To accumulate mutations to the mitochondrial DNA these mice were bred double homozygous Mutyh dMTS x Ogg1 dMTS mice as a maternal lineage for five consecutive generations and mitochondrial DNA from liver was extracted from the offspring and sequenced with Illumina. OGG1 and MUTYH are involved in repair of 8-oxo-dG from DNA. 8-oxo-dG can be a mutagenic lesion 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): Covaris, NEBNext Ultra II DNA library prep kit, Illumina HiSeq 3000

ORGANISM(S): Mus musculus

SUBMITTER: Nils-Göran Larsson 

PROVIDER: E-MTAB-6532 | 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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