Lmo4 specifies two neuron subclasses in the mouse neocortex by promoting postnatal co-expression of the transcription factors Ctip2 and Satb2 via chromatin remodelling in a time and area-specific manner.

The miR-34/449 family is abundantly expressed in the central nervous system, and fine-tunes optimal numbers of spinal interneurons to ensure sensory-motor circuit outputs.

The Timothy syndrome mutation in Ca_v1.2 gives rise to defects in neuronal differentiation by preventing a developmental switch in channel splicing and elevating calcium signaling in differentiating cells.

Competition between neurons for postsynaptic ephrin-B3 controls distribution of a limited pool of synapses and defines a novel trans-synaptic mechanism enabling neurons to set the number of synapses they receive.

Mid-gestational exposure to maternal immune activation drives a sequence of transcriptional signatures and developmental pathology in embryonic mouse cortex, culminating in altered lamination and cellular lineage specification.

Aberrant ERK/MAPK signaling in cortical pyramidal neurons leads to selective disruption of layer 5 circuit development and generalized changes in neuronal excitability.

Upon injury, the regeneration of the adult axolotl brain rebuilds neuronal diversity, but alters the original long-distance circuitry and tissue architecture.

A novel 2D-to-3D human brain organoid protocol reveals the pivotal role of FGF8 signaling in driving regional patterning and cellular diversity, while also modulating genes crucial for both normal and pathological neural development.

The genome-organizer Satb2 has a key role in memory formation by modulating availability of miRNAs that control the function of synapses.

Primary-cilia-mediated processing of the Gli3 transcription factor enables the formation of subtypes of projection neurons in appropriate numbers during the development of the cerebral cortex.