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Although autism is typically characterized by differences in language, social interaction and restrictive, repetitive behaviors, it is becoming more well known in the field that alterations in energy metabolism and mitochondrial function are comorbid disorders in autism. The synaptic cell adhesion molecule,  neurexin -1 ( NRXN1 ), has previously been implicated in autism, and here we show that in  Drosophila melanogaster,  the homologue of  NRXN1,  called  Nrx-1,  regulates energy metabolism and nutrient homeostasis. First, we show that  Nrx-1- null flies exhibit decreased resistance to nutrient deprivation and heat stress compared to controls. Additionally,  Nrx-1  mutants exhibit a significantly altered metabolic profile characterized by decreased lipid and carbohydrate stores.  Nrx-1- null  Drosophila  also exhibit diminished levels of nicotinamide adenine dinucleotide (NAD + ), an important coenzyme in major energy metabolism pathways. Moreover, loss of  Nrx-1  resulted in striking abnormalities in mitochondrial morphology in the flight muscle of  Nrx-1- null  Drosophila  and impaired flight ability in these flies. Further, following a mechanical shock  Nrx-1- null flies exhibited seizure-like activity, a phenotype previously linked to defects in mitochondrial metabolism and a common symptom of patients with  NRXN1  deletions. The current studies indicate a novel role for  NRXN1  in the regulation of energy metabolism and uncover a clinically relevant seizure phenotype in  Drosophila  lacking  Nrx-1 .

Loss of neurexin-1 in Drosophila melanogaster results in altered energy metabolism and increased seizure susceptibility