Disease relevance of Nlgn1

• We show that deletion mutant mice lacking neuroligin expression die shortly after birth due to respiratory failure [1].

High impact information on Nlgn1

• Oligomerization of neuroligin is required for its function, and we find that beta-neurexin clustering is sufficient to trigger the recruitment of synaptic vesicles through interactions that require the cytoplasmic domain of neurexin [2].
• It is thought to be triggered by members of the neuroligin family of postsynaptic cell adhesion proteins, which may form transsynaptic contacts with presynaptic alpha- and beta-neurexins and have been implicated in the etiology of autism [1].
• Here we show that the postsynaptic density (PSD) proteins PSD-95 and neuroligin-1 (NLG) are critical for dictating the ratio of excitatory-to-inhibitory synaptic contacts [3].
• Down-regulation of neuroligin isoform expression by RNA interference results in a loss of excitatory and inhibitory synapses [4].

Other interactions of Nlgn1

• A balance between excitatory and inhibitory synapses is controlled by PSD-95 and neuroligin [3].

References