Objective Neuronal connections between the hemispheres are considered important for organisms to organize information to adapt to variable environments.In central complex split flies, the locomotor activity and the visual learning and memory are defect.Axon midline crossing is an event that requires many components to regulate each other.The study is aimed to find the genes that affect the formation of central complex.Methods Histochemistry with antibody nc82 was used to observe the shape of central complex.Western blot with antivsd specific antibodies were used to study the characteristic of the protein.Results (1) Nonsense mutation in the extracellular domain of VSD contributed to the central complex defect.(2) VSD can be cleaved by an unknown protease and release the intracellular domain from the membrane.(3) Overexpression the extracellular domain of NRG can partially rescue the mutant phenotype caused by knockdown of vsd.Conclusion Transmembrane protein VSD (visual system disorganization) is essential for the formation of the central complex and NRG cooperates with VSD to regulate the axon midline crossing.