Post-transcriptional control by YTHDC2 is required to turn off the mitotic proliferation program and facilitate proper expression of the meiotic program to allow a clean cell fate transition in the germline stem cell lineage.
The condensin I subunit Cap-G is expressed in post-mitotic neurons and its removal, especially from less mature neurons, results in gene expression changes, reduced survival and behavioural defects in Drosophila.
In contrast to other transcription factors, CTCF and Esrrb rapidly regain binding after replication and remain bound to their targets during mitosis, preserving local nucleosome organization throughout the cell cycle.
In humans, specific sequence features can predict whether meiotic recombination occurs at sites bound by the protein PRDM9, whose DNA-binding zinc-finger domain can unexpectedly bind to gene promoters and to other copies of PRDM9.
The INM protein LAP1B, an activator of Torsin ATPases, is a chromatin-binding factor that erroneously persists on mitotic chromatin if Torsin functionality is compromised, inducing chromosome segregation defects and binucleation.