> The research group behind the current study previously showed11 that NHEJ <non-homologous end-joining, an error-prone mechanism of double-strand DNA break (DSB) repair> is essential for NSPC <neural stem/progenitor cells> differentiation, which implies a role for NHEJ-mediated DSB repair during normal brain development. It is possible that subpopulations of cells in the brain display the same types of rearrangements, and that some are positively selected. Similar studies in vivo and in other tissues are needed to test this hypothesis.
> We show that genome-wide maps of endogenous DSBs are highly correlated between experimental replicates up to 10 kilobases (kb) resolution, and that DSBs are non-uniformly distributed along the genome, in all three cell differentiation stages analyzed.
...
> Our datasets and analytical tools represent a valuable resource for exploring genome fragility during human neurogenesis and investigating how this might contribute to the pathogenesis of NDDs. <neurodevelopmental disorders>
> More complex than the immune system?
Possibly. From 2016: https://www.nature.com/articles/nature17316
text in <> are mine.
> The research group behind the current study previously showed11 that NHEJ <non-homologous end-joining, an error-prone mechanism of double-strand DNA break (DSB) repair> is essential for NSPC <neural stem/progenitor cells> differentiation, which implies a role for NHEJ-mediated DSB repair during normal brain development. It is possible that subpopulations of cells in the brain display the same types of rearrangements, and that some are positively selected. Similar studies in vivo and in other tissues are needed to test this hypothesis.
From 2022: https://www.nature.com/articles/s41597-022-01508-x
> We show that genome-wide maps of endogenous DSBs are highly correlated between experimental replicates up to 10 kilobases (kb) resolution, and that DSBs are non-uniformly distributed along the genome, in all three cell differentiation stages analyzed.
...
> Our datasets and analytical tools represent a valuable resource for exploring genome fragility during human neurogenesis and investigating how this might contribute to the pathogenesis of NDDs. <neurodevelopmental disorders>