期刊
NEURON
卷 25, 期 1, 页码 139-149出版社
CELL PRESS
DOI: 10.1016/S0896-6273(00)80878-8
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资金
- NIGMS NIH HHS [GM43100] Funding Source: Medline
- NINDS NIH HHS [NS15390] Funding Source: Medline
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM043100] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS015390] Funding Source: NIH RePORTER
The mle(napts) mutation causes temperature-de pendent blockade of action potentials resulting from decreased abundance of para-encoded Na+ channels. Although maleless (mle) encodes a double-stranded RNA (dsRNA) helicase, exactly how mle(napts) affects para expression remained uncertain. Here, we show that para transcripts undergo adenosine-to-inosine (A-to-I) RNA editing via a mechanism that apparently requires dsRNA secondary structure formation encompassing the edited exon and the downstream intron. In an mle(napts) background, >80% of para transcripts are aberrant, owing to internal deletions that include the edited exon. We propose that the Mle helicase is required to resolve the dsRNA structure and that failure to do so in an mle(napts) background causes exon skipping because the normal splice donor is occluded. These results explain how mle(napts) affects Na+ channel expression and provide new insights into the mechanism of RNA editing.
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