ArticleNature plants2025
Suppression of plastid-to-nucleus gene transfer by DNA double-strand break repair.
Article in Nature plants, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Plastid genes in motion: mechanisms and physiological implications of endosymbiotic gene transfer.Journal of experimental botany · 2026Article
- A gatekeeper for gene transfers.Nature plants · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plant nuclear genomes contain thousands of genes of mitochondrial and plastid origin as the result of endosymbiotic gene transfer (EGT). EGT is a still-ongoing process, but the molecular mechanisms determining its frequency remain largely unknown. Here we demonstrate that nuclear double-strand break (DSB) repair is a strong suppressor of EGT. Through large-scale genetic screens in tobacco plants, we found that EGT from plastids to the nucleus occurs more frequently in somatic cells when individual DSB repair pathways are inactive. This effect is explained by the expected increase in the number and residence time of DSBs available as integration sites for organellar DNA. We also show that impaired DSB repair causes EGT to increase 5- to 20-fold in the male gametophyte. Together, our data (1) uncover DSB levels as a key determinant of EGT frequency, (2) reveal the strong mutagenic potential of organellar DNA and (3) suggest that changes in DNA repair capacity can impact EGT across evolutionary timescales.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.