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Significance In this study, Kim et al. identifyDrosophila CFTR (dCFTR ) and show that knockdown ofdCFTR in the adult intestine disrupts osmotic homeostasis and displays CF-like phenotypes that lead to intestinal stem cell hyperplasia. They show that expression of wild-type humanCFTR , but not mutated forms of CFTR that affect protein production or transport, rescues the mutant phenotypes ofdCFTR . Furthermore, global transcriptomic analysis ofdCFTR fly intestine identified a mucin gene that is required for proper intestinal barrier protection. Altogether, their findings suggest thatDrosophila can be a powerful model organism for studying CF pathophysiology.

Drosophila as a model for studying cystic fibrosis pathophysiology of the gastrointestinal system