Odd-paired (opa) is required for the progression of temporal patterning in Drosophila neural progenitors to regulate temporal identities via an incoherent feed-forward loop.

The homeodomain protein Bsh increases lamina neuron types and visual function.

Parkinson’s disease-associated LRRK2 kinase is recruited to membranes by its Rab GTPase substrates, and LRRK2 is both retained on membranes and further activated there by cooperative interaction with the phosphorylated Rab proteins that it generates.

Perception is proposed to be a dynamic motor-sensory closed-loop process in which information flows through the environment and the brain in continuous loops, converging towards steady-state percepts.

Loss or PTH1R-mediated repression of Zfp467 results in a pathway that increases Pth1r transcription via NFκB1 and thus cellular responsiveness to PTH/PTHrP, ultimately leading to enhanced bone formation.

Mycobacterium tuberculosis exploits an IFN/IL6/CEBP axis linked to monocyte expansion in humans.

Arid1a loss in the pancreas enables an irreversible reprogramming of cell fate that is dependent on both cellular and genetic context.

Lineage-specific regulatory loops involving evolutionarily conserved myogenic Transcription Factors control muscle identity specification in Drosophila.

The identification of key determinants of LSC “stemness” and LSC differentiation that is reversible through an epigenetic mechanism may have considerable implications in understanding leukemia and designing effective therapies.

FOXL2 maintenance of ovarian identity is not solely due to a simple direct repression of Sox9 but to the mobilization of estrogen signalling by FOXL2.