Hunter_2010_Dis.Model.Mech_3_366

Reference

Title : Neuroligin-deficient mutants of C. elegans have sensory processing deficits and are hypersensitive to oxidative stress and mercury toxicity - Hunter_2010_Dis.Model.Mech_3_366
Author(s) : Hunter JW , Mullen GP , McManus JR , Heatherly JM , Duke A , Rand JB
Ref : Dis Model Mech , 3 :366 , 2010
Abstract :

Neuroligins are postsynaptic cell adhesion proteins that bind specifically to presynaptic membrane proteins called neurexins. Mutations in human neuroligin genes are associated with autism spectrum disorders in some families. The nematode Caenorhabditis elegans has a single neuroligin gene (nlg-1), and approximately a sixth of C. elegans neurons, including some sensory neurons, interneurons and a subset of cholinergic motor neurons, express a neuroligin transcriptional reporter. Neuroligin-deficient mutants of C. elegans are viable, and they do not appear deficient in any major motor functions. However, neuroligin mutants are defective in a subset of sensory behaviors and sensory processing, and are hypersensitive to oxidative stress and mercury compounds; the behavioral deficits are strikingly similar to traits frequently associated with autism spectrum disorders. Our results suggest a possible link between genetic defects in synapse formation or function, and sensitivity to environmental factors in the development of autism spectrum disorders.

PubMedSearch : Hunter_2010_Dis.Model.Mech_3_366
PubMedID: 20083577
Gene_locus related to this paper: caeel-NLGN1

Related information

Gene_locus caeel-NLGN1

Citations formats

Hunter JW, Mullen GP, McManus JR, Heatherly JM, Duke A, Rand JB (2010)
Neuroligin-deficient mutants of C. elegans have sensory processing deficits and are hypersensitive to oxidative stress and mercury toxicity
Dis Model Mech 3 :366

Hunter JW, Mullen GP, McManus JR, Heatherly JM, Duke A, Rand JB (2010)
Dis Model Mech 3 :366