Table 2.

Summary of phenotypes observed in Drosophila Neurexin and Neuroligin mutants

Gene	Nature of mutation	Animal Behaviour	Synaptic Physiology	Other	Reference
Neuroligin	dnl1 deletion	Not tested	Decreased stimulus evoked transmitter release, no change in quantal size	Decrease in number of synaptic boutons, immature postsynaptic apparatus, misalignment of pre- and postsynaptic specialisation	[34]
	dnl2 deletion	Reduced larval locomotion	Increased stimulus evoked transmitter release, decreased paired pulse plasticity, no change in quantal size	Decrease in number of synaptic boutons, increased density of active zones per bouton, immature postsynaptic apparatus, decrease in GluR density, increase in ratio of A-type to B-type GluRs, increased length of PSD	[35]
Neurexin	dnrx deletion	Reduced larval locomotion, defect in associative learning in larvae, shortened life span	Decreased stimulus evoked transmitter release, decreased synaptic vesicle recycling, defective calcium sensitivity of evoked transmitter release	Reduced synapse number in CNS and at NMJ, increased density of active zones per bouton at NMJ, increased size of PSD, increase ratio of A-type to B-type GluR receptors in embryonic NMJs	[26, 27, 70, 91]
Neurexin–neuroligin double mutants	dnrx/dnl1	Not tested	Not tested	Defects in synaptic boutons no worse than in dnl1 mutants, dnl1 D356R rescued phenotype in dnl1 mutant background but does not show dominant negative phenotype like wild type when overexpressed	[34]
	dnrx/dnl2	More severe defect in locomotion than either dnl2 or dnrx	Not tested	Lethal at late 2nd instar larval stage. More severe defect in NMJ morphology in both double homozygous early 2nd instar larvae, and hemizygous 3rd instar larvae. Dnl2 shown to exist in complex with Dnrx in vivo	[35]