Hairless emerged as an evolutionarily novel regulatory protein that replaced an ancestral paradigm of direct co-repressor recruitment by Suppressor of Hairless, its partner transcription factor in the Notch signaling pathway.

Hey together with LaminC continuously supervise nuclear organisation and differentiated enterocyte identity, a regulation that is lost upon ageing, resulting in loss of gut homeostasis.

DNA binding site architecture promotes Notch transcription complex degradation to sensitize developmental processes requiring long-duration signaling.

Silencing of stem cell identity genes during progenitor commitment ensures that intermediate progenitors robustly commit to generate differentiated cell types rather than abnormal stem-cell-like cells during indirect neurogenesis.

Depleting Mi-2 in the progeny of neural stem cells prevents normal enhancer decommissioning so that they become sensitive to Notch activity and re-acquire stem cell properties.

Genome-wide recruitment of Mediator and Pol II is reduced in yeast lacking the Med2-Med3-Med15 tail module triad, and Mediator association with gene promoters depends on Pol II, Taf1, and TBP.

A lack of ADAM10-mediated shedding increases prion protein levels at the plasma membrane and promotes the generation of pathological prion proteins, which accelerates prion disease in mice.

Regulatory success operates by goal-consistent increases and decreases of distinct attribute representations in generic neural hubs and in domain-specific brain regions, explaining when and why regulatory success generalizes across domains and contexts.

The protofilaments that curl outward from a disassembling microtubule tip carry a large amount of strain energy and they can drive movement with an efficiency similar to conventional motor proteins.

Cell fates endowed by higher Bicoid concentration require input for longer duration, demonstrating a temporally non-linear morphogen-mediated pattern formation.