The specification of a very small number of progenitor cells with competence to adapt their neurogenic output to different probabilistic rules underlies the generation of distinct cortical cytoarchitectures.
The Timothy syndrome mutation in Cav1.2 gives rise to defects in neuronal differentiation by preventing a developmental switch in channel splicing and elevating calcium signaling in differentiating cells.
In neuronal mitophagy, Parkin and OPTN induce efficient sequestration of damaged somal mitochondria into autophagosomes, but slow turnover via lysosomal acidification may be a point of vulnerability for the cell.
Elucidation of the molecular basis of early wound epidermis dependence during salamander limb regeneration reveals midkine as a key modulator of wound epidermis development and wound-healing resolution.
Two new polymorphic structures of recombinant human alpha-synuclein fibrils show striking differences to previous structures, while familial PD mutation sites remain crucial for protofilament interaction and fibril stability.