期刊
NATURE STRUCTURAL & MOLECULAR BIOLOGY
卷 13, 期 1, 页码 13-21出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nsmb1041
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资金
- NCI NIH HHS [P01 CA072765, P01 CA072765-050002] Funding Source: Medline
- NHLBI NIH HHS [R01 HL070045-04, R01 HL070045] Funding Source: Medline
- NIGMS NIH HHS [R01 GM040536, R01 GM040536-15] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P01CA072765] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL070045] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM040536] Funding Source: NIH RePORTER
Adenosine deaminases acting on RNA (ADARs) are involved in editing of adenosine residues to inosine in double-stranded RNA ( dsRNA). Although this editing recodes and alters functions of several mammalian genes, its most common targets are noncoding repeat sequences, indicating the involvement of this editing system in currently unknown functions other than recoding of protein sequences. Here we show that specific adenosine residues of certain microRNA ( miRNA) precursors are edited by ADAR1 and ADAR2. Editing of pri - miR-142, the precursor of miRNA-142, expressed in hematopoietic tissues, resulted in suppression of its processing by Drosha. The edited pri - miR- 142 was degraded by Tudor-SN, a component of RISC and also a ribonuclease specific to inosine-containing dsRNAs. Consequently, mature miRNA-142 expression levels increased substantially in ADAR1 null or ADAR2 null mice. Our results demonstrate a new function of RNA editing in the control of miRNA biogenesis.
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