This week’s articles highlight interactions between astrocytes and neurons that influence both cell types’ form and function; a genetic basis for individual variation in aging; and the mechanism by which an E3 ubiquitin ligase adaptor affects synaptic transmission.
NEUROSCIENCE
Astrocyte-neuron contacts
Stogsdill et al. show that the interaction between astrocyte neuroligins and neuronal neurexins controls both astrocyte morphology and synaptogenesis.
Natural variation and aging
Yin et al. report that polymorphisms in a neuropeptide-encoding gene underlie differences in aging between individual nematodes (see also McGrath).
Degrading RhoA for synaptic transmission
Escamilla et al. demonstrate that loss of the E3 ubiquitin ligase adaptor KCTD13 reduces synaptic transmission by increasing the accumulation of the small GTPase RhoA. Copy number variations in Kctd13 have been linked to neuropsychiatric and neurodevelopmental disorders, suggesting RhoA as a potential therapeutic target for treating disorders in which Kctd13 is deleted.