Replication-stress response shapes Leishmania genome plasticity through non-equivalent RAD9 and HUS1 functions.
Genome plasticity, manifested as gene copy-number variation and mosaic aneuploidy, enables adaptation in Leishmania , yet how genome-surveillance pathways shape this variation remains unclear. Here we show that partial depletion of HUS1 or RAD9, subunits of the conserved 9-1-1 checkpoint clamp, produces opposing replication-stress responses and contrasting patterns of genome remodelling in…
We haven't written up this one. bioRxiv has the full story — the link below goes straight to it.
