Active and passive contributions to cell shape change and rearrangements can be distinguished from observed cell geometry, revealing the self-organization mechanisms underlying internally-driven epithelial convergent extension.

An excess of novel non-canonical subtypes of parvalbumin+ interneurons in a mouse model of classical lissencephaly, which possess non-fast-spiking physiological properties, may contribute to network hyperexcitability common in this model.

The human Fibrodysplasia-Ossificans-Progressiva BMP-receptor mutant signals in zebrafish in the absence of ligand-binding, displays BMP ligand-responsive hyperactivity, neither requiring other type-I-BMP receptors, unlike wild-type, challenging views of the pathological mechanism.

In adult mouse hippocampus, neural stem cell and their progeny communicate via Lunatic Fringe mediated Notch signaling to regulate stem cell quiescence, division, and fate.

Type XVII collagen, a transmembranous protein in basal keratinocytes, suppresses interfollicular epidermal proliferation in neonatal and aged skin, and helps rejuvenate epidermis.

A cryo-electron microscopy model of the active human apoptosome illuminates how this "wheel of death" binds the protease procaspase-9 to initiate programmed cell death.

A 5'-UTR SNP of FGF13 impairs PTBP2 interacting with FGF13 mRNA, leading to reduced FGF13 translation and deficits in brain development and cognitive functions.

The combination of juxtacellular recordings with optogenetics in freely moving mice enables the targeting of genetically defined cell classes for high-resolution, single-cell structure–function analysis.

Single-cell sequencing combined with in situ hybridizations reveal dynamic patterns of differentially expressed genes throughout the ventricular and subventricular zone of the embryonic mouse brain, which likely play important roles in cell fate determination.

Kruppel-like factor 9 (Klf9) is a transcriptional regulator of neural stem cell expansion in the adult hippocampus.