The identification of a novel mechanism of chromatin remodeling, including a conserved remodeler domain and regulatory epitopes, provides targets for the design of therapeutics to modulate transcriptional regulation in cells.
STAG1 has been identified as a hardwired genetic dependency of cancer cells harbouring mutations in the cohesin subunit and emerging major tumor suppressor STAG2 holds the promise for the development of selective therapeutics.
Soon after fertilisation, a critical portion of the embryonic genome is switched on through the actions of maternally inherited Stella, in part through controlling the activation of transposable elements.
Heterochromatin is established at nucleation sites associated with open chromatin and RNA transcripts and matures into stable domains if they are found near transposable elements targeted by maternally deposited piRNAs.
Measuring and simulating chromatin dynamics reveals that repositioning of genes to the nuclear pore is neither active nor vectorial, but reduces sub-diffusion and coordinates movement between loci on different chromosomes.