High-throughput single-cell functional elucidation of neurodevelopmental disease-associated genes reveals convergent mechanisms altering neuronal differentiation.
Molecular Mechanisms
Neural stem cells direct axon guidance via their radial fiber scaffold.
Exponential-family embedding with application to cell developmental trajectories for single-cell RNA-seq data.
De novo missense variants disrupting protein-protein interactions affect risk for autism through gene co-expression and protein networks in neuronal cell types.
Inflammation of the embryonic choroid plexus barrier following maternal immune activation.
Regulation of neural gene expression by estrogen receptor alpha.
Human cerebral organoids reveal early spatiotemporal dynamics and pharmacological responses of UBE3A.
Chd8 haploinsufficiency impairs early brain development and protein homeostasis later in life.
How do neurexins promote presynaptic development?
Neurexins constitute a family of presynaptic transmembrane molecules that are encoded by three distinct genes, and mutations in all three genes are associated with risk for autism spectrum. In mammals, neurexins are expressed as thousands of different splice isoforms, all containing an invariant intracellular domain responsible for an as yet uncharacterized downstream signaling pathway. In the current project, Peri Kurshan and colleagues plan to use the simpler in vivo system afforded by the nematode C. elegans, along with a recently developed proteomics approach, to identify the proteins responsible for neurexin’s downstream signaling pathway(s).
FMRP sustains presynaptic function via control of activity-dependent bulk endocytosis.
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