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Mutations in the gene  CLN3  are responsible for the neurodegenerative disorder juvenile neuronal ceroid lipofuscinosis or Batten disease.  CLN3  encodes a multi-spanning and hydrophobic transmembrane protein whose function is unclear. As a consequence, the cell biology that underlies the pathology of the disease is not well understood. We have developed a genetic gain-of-function system in  Drosophila  to identify functional pathways and interactions for  CLN3 . We have identified previously unknown interactions between  CLN3  and the Notch and Jun N-terminal kinase signalling pathways and have uncovered a potential role for the RNA splicing and localization machinery in regulating CLN3 function.

Interactions between the juvenile Batten disease gene, CLN3 , and the Notch and JNK signalling pathways