Oehler, J., Morrow, C. A., & Whitby, M. C. Gene duplication and deletion caused by over
replication at a fork barrier. Nat. Commun. 14, 7730;
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10676400/ (2023).

Oehler et al. hypothesized that stalling a replication fork at a specific locus during cellular DNA
replication can induce gene duplication-deletion rearrangements. This duplication-deletion
rearrangement is characterized by the duplication of a specific gene to be added at a different
site, while the original gene is deleted due to the whole duplication being moved.
Experimentally, they used a fission yeast, a strong polar replication fork barrier, a hygromycin
resistance gene, and a ura4 gene required for uracil synthesis. They placed the fork barrier
(RTS1) on chromosome 3 which replicates unidirectionally. Their experiment yielded a 100%
duplication-deletion rearrangement ratio of the correctly oriented RTS1, with 3 uniquely noted
classes of dup-del.
The research team then compared their work with RST1 to previous work of theirs that
delayed fork convergence by deleting a strong centromere-proximal replication origin.
Combining the two methods provided an experimental ~6-fold increase in the RST1 induced
recombinants with the ori deleted.
They also found that downstream of RTS1, RDR can create a larger amount of replicated
DNA, with varying replicability. To determine how common such an occurrence is, they
modified the experiment. The results of this showed that after the dup-del is initiated, the RDR
has the capability of extending the leading strand of the collapsed replication fork beyond the
initial barrier.