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The neuroanatomical and functional analysis of genetically-identified motoneurons controlling all major steps of Drosophila proboscis extension provides new insights into the architecture of a motor circuitry controlling a reaching-like behavior.

Constitutive deficiency of AP2γ transcription factor impairs hippocampal glutamatergic neurogenesis and induces alterations on limbic-cortical connectivity that contribute to anxiety-like behavior and cumulative memory deficits in mice from juvenile to adult periods.

A muscle-derived Wnt signal promotes dendritic branching of somatosensory neurons in response to a concurrent deficiency in vitamins, minerals, and cholesterol.

Genetic and optogenetic analyses in Drosophila neurons reveal calcium as one of the key regulators of nucleocytoplasmic localization of TDP-43 via Calpain-A and Importin α3.

Extended biochemical and functional analyses in primary neurons show that early neuronal morphogenesis critically relies on cooperation of the actin nucleator Cobl and its ancestor Cobl-like and uncover their cooperative mechanisms at dendritic branch initiation sites.

Different Purkinje cell subpopulations show distinct developmental profiles of physiological activity, climbing fiber inputs and axonal and dendritic morphology, matching different timelines of cerebellum-dependent behaviors.

Detailed SYNGAP1 splice variant characterization uncovers distinct isoform functions and biochemical properties contributing to critical aspects of neurodevelopment, providing previously unknown isoform-level insight into SYNGAP1-related cognitive disorders.

The m⁶A reader YTHDF2 negatively regulates retinal ganglion cell dendrite branching through destabilizing its m⁶A-modified target mRNAs which control dendrite development and maintenance, and Ythdf2 conditional knockout in retina improves visual acuity and alleviates acute ocular hypertension-induced glaucoma in mice.

Expanded repeat RNAs associated with human neurodegenerative diseases can become incorporated into transported granules in neurons, perturbing their function to cause neuritic branching defects.

A minus-end-binding stabilizes minus-end-out microtubules in dendrites, which are required for dendrite-specific pruning during neuronal remodelling.