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The neuronal ceroid lipofuscinosis protein, Cln7, regulates neural development from the post-synaptic cell

The neuronal ceroid lipofuscinoses (NCLs) are a group of monogenetic neurodegenerative disorders with an early onset in infancy or childhood. Despite identification of the genes disrupted in each form of the disease, their normal cellular role and how their deficits lead to disease pathology is not fully understood. Cln7, a major facilitator superfamily domain-containing protein, is affected in a late infantile-onset form of NCL. We demonstrate that in Drosophila, Cln7 is required for normal synapse development. In the absence of Cln7 the neuromuscular junction fails to develop fully leading to reduced function and behavioral changes. Cln7 is required in the post-synaptic muscle for appropriate pre-synaptic development suggesting an involvement in regulating trans-synaptic communication. Loss of Cln7 leads to reduced TORC activity, suggesting Cln7 acts as a regulator of TORC activity to influence synaptic development. Summary Cln7, a protein disrupted in an early-onset neurodegenerative disease, is required for normal development of the Drosophila neuromuscular junction. Cln7 functions by regulating TORC signaling in the post-synaptic muscle as part of trans-synaptic communication that matches pre-and post-synaptic development.