Neuronal development articles from across Nature Portfolio

A conserved gene regulatory network involving SOX4, SOX11 and TFAP2D shapes the development of excitatory neurons in ventrolateral pallium and their connectivity with the prefrontal cortex.

Microglia are proposed to have a role in brain development through synaptic engulfment and paracrine signaling. O’Keeffe et al. show that certain neurodevelopmental processes attributed to microglia can proceed normally even in the absence of these cells.

Deafness is the most common form of sensory impairment in humans and frequently caused by defects in hair cells of the inner ear. Here authors demonstrate that in a mouse model for recessive non-syndromic deafness (DFNB6), inactivation of Tmie in hair cells disrupts gene expression in the neurons that innervate them, suggesting treatment modalities for deafness may require restoration of the function of both hair cells and neurons.

Mutations reducing the function of MYT1L, a neuron-specific transcription factor, are associated with a syndromic neurodevelopmental disorder, yet it remains unclear which cell types are most impacted by MYT1L loss. Here authors use single-nuclei RNA sequencing to profile the forebrains of MYT1L-deficient mice at three developmental stages and reveal MYT1L deficiency disrupts cortical neuron proportions and gene expression, primarily affecting excitatory neuron maturation programs.

Fang et al. show that EAT-17 and BICD-1 function in the endocytic degradation pathway to suppress excessive dendrite branching, via down-regulating the level of SAX-7, a dendrite branching ligand, on the C. elegans epidermal plasma membranes.

Genome-wide analysis of miRNA co-expression and co-targeting networks at distinct developmental stages sheds light into the regulatory role of miRNAs in shaping the development of the embryonic cerebral cortex.

A study finds that microglia depletion has no effect on experience-dependent maturation of visual cortex circuitry in mice.

The centrosome is crucial for the microtubule dynamics that underlie the radial migration of developing rodent neurons but is not required for axon growth.

Preventing transient defects in postnatal cortical circuit function limits disease progression in a mouse model of Huntington disease.

Androgen signalling during development may represent the mechanism underpinning some observed sex-differences in adult human brain size.

Study demonstrates that the ion channel KCNN2 has an important role in motor skill learning deficiencies resulting from fetal alcohol exposure in mice.