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trophin-associated glycoprotein complex. Although gentamicin did not completely restore dystrophin levels, the level produced was sufficient to protect against contraction-induced injury. This presents a significant first step toward the use of these antibiotics in treating a broad class of genetic diseases resulting from nonsense mutations. Although gentamicin promotes translation read-through of the nonsense codon in dystrophin, it may also interfere with nonsense-mediated mRNA decay (6). All eukaryotic cells eliminate mRNAs that encode prematurely terminated products. This may protect cells from the production of nonfunctional or gain-offunction proteins. mRNAs that contain nonsense mutations more than 50 nucleotides upstream of the 3′-most exon-exon junction are selectively degraded by a process that requires protein synthesis. Stabilization of these mRNAs can occur if the ribosome translates through the termination codon (7, 8). The nonsense mutation in the mdx mouse reduces dystrophin mRNA levels to 10‐15% of normal (9). Therefore, the beneficial effects of gentamicin may result from dystrophin mRNA stabilization. It will be important to study dystrophin mRNA levels in the muscle tissues to determine if these drugs exert their action by stabilizing the nonsensecontaining mRNA. This appears likely, because gentamicin restored CFTR mRNA level in a cystic fibrosis (CF) bronchial epithelial cell line carrying a premature stop codon (3).

Correction of genetic disease by making sense from nonsense