In a new study, Enrique Gonzalez-Duran and Ralph Bock from the Max Planck Institute of Molecular Plant Physiology have revealed how DNA repair mechanisms play a central role in safeguarding plant genomes from unwanted gene insertions. Their research sheds light on endosymbiotic gene transfer (EGT)—a process where DNA from chloroplasts or mitochondria is integrated into the nuclear genome, a key driver of plant evolution but one that carries risks.
Using genetically engineered tobacco plants and a large-scale screening system, the team inactivated two distinct DNA repair pathways and analyzed over 650,000 seedlings. Their findings were striking: when these repair systems were disabled, EGT events increased dramatically—up to 20 times more frequently. The results suggest that under normal conditions, plants rely on rapid DSB repair to seal vulnerable genomic regions before foreign DNA can insert itself, according to a press release.
The researchers propose a model in which the DNA repair machinery acts as a molecular “gatekeeper,” closing off double-strand breaks before organellar DNA can integrate. When one repair pathway fails, slower backup systems leave more time for foreign DNA to enter, leading to increased genome instability.
“The magnitude of the effect suggests that rapid DNA repair is essential for plants to maintain long-term genome stability,” explains Enrique Gonzalez-Duran, first author of the study.
Implications Beyond Plants
Although the work was carried out in tobacco plants, the team believes the mechanism uncovered is likely universal across eukaryotes. “These DNA repair pathways are conserved in animals and fungi,” says Ralph Bock, director of the institute and co-author. “Our findings could explain similar genome instability mechanisms in other organisms, including humans. Further research is needed to clarify this.”
The research opens new avenues for understanding how organellar DNA contributes to mutations in the nuclear genome. It may even have relevance for human health, and in particular to cancer biology, where mitochondrial DNA insertions and genome instability are known molecular triggers of tumor initiation. “Our discovery provides fundamental insights into genome protection and the risks of gene transfer,” adds Gonzalez-Duran. “It reveals how crucial fast DNA repair is — not just to fix damage, but also to defend the integrity of the genome itself.”
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