CFTR 
0 rnin. 4 min. 13 min 
CFTRAF508 
Chloride channel function in lung cells from a cystic fibrosis patient returns to normal following 
insertion of a normal gene. The gene for cystic fibrosis transmembrane conductance regulator 
( CFTR) is mutated in patients with CP, and defective function of chloride channels is the hall- 
mark of the disease. The top row shows fluorescence from a cystic fibrosis cell that is expressing 
normal CFTR; the bottom row shows a cell that is expressing mutated CFTR. Fluorescence indi- 
cates chloride channel activity, with yellow and red indicating high fluorescence and blue and 
green low fluorescence. Fluorescence increases faster in cells expressing the normal CFTR gene 
( top ). The difference between cells expressing the normal gene and the mutated gene is most 
noticeable at the 4 min point. 
Research of Michael f. Welsh. 
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