Run-on transcription as a method for the analysis of mitochondrial genome expression

Belozerova, N. S.; Пожидаева, Е. С.; Шугаев, А. Г.; Kusnetsov, V. V.

doi:10.1134/s1021443711010031

Cited by 5 publications

(2 citation statements)

References 9 publications

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“…In the A. thaliana mtDNA, we see slightly elevated XR-seq coverage of the CDS compared to the intergenic regions of the genome, but rRNA and tRNA genes, which are typically expressed more highly than CDS regions ( Belozerova et al 2011 ; Pérez Di Giorgio et al 2019 ), have XR-seq coverage below or near the level of intergenic sequence ( Supplementary Fig. 18 , top left panel).…”

Section: Resultsmentioning

confidence: 95%

UV damage induces production of mitochondrial DNA fragments with specific length profiles

Waneka,

Stewart,

Anderson

et al. 2024

Genetics

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UV light is a potent mutagen that induces bulky DNA damage in the form of cyclobutane pyrimidine dimers (CPDs). Photodamage and other bulky lesions occurring in nuclear genomes can be repaired through nucleotide excision repair (NER), where incisions on both sides of a damaged site precede the removal of a single-stranded oligonucleotide containing the damage. Mitochondrial genomes (mtDNAs) are also susceptible to damage from UV light, but current evidence suggests that the only way to eliminate bulky mtDNA damage is through mtDNA degradation. Damage-containing oligonucleotides excised during NER can be captured with anti-damage antibodies and sequenced (XR-seq) to produce high resolution maps of active repair locations following UV exposure. We analyzed previously published datasets from Arabidopsis thaliana, Saccharomyces cerevisiae, and Drosophila melanogaster to identify reads originating from the mtDNA (and plastid genome in A. thaliana). In A. thaliana and S. cerevisiae, the mtDNA-mapping reads have unique length distributions compared to the nuclear-mapping reads. The dominant fragment size was 26 nt in S. cerevisiae and 28 nt in A. thaliana with distinct secondary peaks occurring in regular intervals. These reads also show a nonrandom distribution of di-pyrimidines (the substrate for CPD formation) with TT enrichment at positions 7-8 of the reads. Therefore, UV damage to mtDNA appears to result in production of DNA fragments of characteristic lengths and positions relative to the damaged location. The mechanisms producing these fragments are unclear, but we hypothesize that they result from a previously uncharacterized DNA degradation pathway or repair mechanism in mitochondria.

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Section: Resultsmentioning

confidence: 95%

UV damage induces production of mitochondrial DNA fragments with specific length profiles

Waneka,

Stewart,

Anderson

et al. 2024

Genetics

View full text Add to dashboard Cite

show abstract

“…In the A. thaliana mtDNA, we see slightly elevated XR-seq coverage of the CDS compared to the intergenic regions of the genome, but rRNA and tRNA genes, which are typically expressed more highly than CDS regions (82,83), have XR-seq coverage below or near the level of intergenic sequence (Figure S18, top left panel). This suggests that increases in expression may not correlate with increased levels of of incisions or repair activity as is observed in the A. thaliana nucDNA due to TC-NER (53).…”

Section: Variation In the Distribution Of Xr-seq Reads Among Genomic ...mentioning

confidence: 99%

UV damage induces production of mitochondrial DNA fragments with specific length profiles

Waneka,

Stewart,

Anderson

et al. 2023

Preprint

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UV light is a potent mutagen that induces bulky DNA damage in the form of cyclobutane pyrimidine dimers (CPDs). In eukaryotic cells, photodamage and other bulky lesions occurring in nuclear genomes (nucDNAs) can be repaired through nucleotide excision repair (NER), where dual incisions on both sides of a damaged site precede the removal of a single-stranded oligonucleotide containing the damage. Mitochondrial genomes (mtDNAs) are also susceptible to damage from UV light, but current views hold that the only way to eliminate bulky DNA damage in mtDNAs is through mtDNA degradation. Damage-containing oligonucleotides excised during NER can be captured with anti-damage antibodies and sequenced (XR-seq) to produce high resolution maps of active repair locations following UV exposure. We analyzed previously published datasets fromArabidopsis thaliana, Saccharomyces cerevisiae, andDrosophila melanogasterto identify reads originating from the mtDNA (and plastid genome inA. thaliana). InA. thalianaandS. cerevisiae, the mtDNA-mapping reads have unique length distributions compared to the nuclear-mapping reads. The dominant fragment size was 26 nt inS. cerevisiaeand 28 nt inA. thalianawith distinct secondary peaks occurring in 2-nt (S. cerevisiae) or 4-nt (A. thaliana) intervals. These reads also show a nonrandom distribution of di-pyrimidines (the substrate for CPD formation) with TT enrichment at positions 7-8 of the reads. Therefore, UV damage to mtDNA appears to result in production of DNA fragments of characteristic lengths and positions relative to the damaged location. We hypothesize that these fragments may reflect the outcome of a previously uncharacterized mechanism of NER-like repair in mitochondria or a programmed mtDNA degradation pathway.

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Effect of salicylic acid on the alternative pathway of yellow lupine respiration

Belozerova

Baik

Буцанец

et al. 2013

Russ J Plant Physiol

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Run-on transcription as a method for the analysis of mitochondrial genome expression

Cited by 5 publications

References 9 publications

UV damage induces production of mitochondrial DNA fragments with specific length profiles

UV damage induces production of mitochondrial DNA fragments with specific length profiles

UV damage induces production of mitochondrial DNA fragments with specific length profiles

Effect of salicylic acid on the alternative pathway of yellow lupine respiration

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