NDLI: Mouse let-7 miRNA populations exhibit RNA editing that is constrained in the 5'-seed/ cleavage/anchor regions and stabilize predicted mmu-let-7a:mRNA duplexes.

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Mouse let-7 miRNA populations exhibit RNA editing that is constrained in the 5'-seed/ cleavage/anchor regions and stabilize predicted mmu-let-7a:mRNA duplexes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Reid, Jeffrey G. Nagaraja, Ankur K. Lynn, Francis C. Drabek, Rafal B. Muzny, Donna M. Shaw, Chad A. Weiss, Michelle K. Naghavi, Arash O. Khan, Mahjabeen Zhu, Huifeng Tennakoon, Jayantha Gunaratne, Gemunu H. Corry, David B. Miller, Jonathan McManus, Michael T. German, Michael S. Gibbs, Richard A. Matzuk, Martin M. Gunaratne, Preethi H.
Description	Country affiliation: United States Author Affiliation: Reid JG ( Department of Chemistry, University of Houston, Houston, Texas 77204, USA.)
Abstract	Massively parallel sequencing of millions of < 30-nt RNAs expressed in mouse ovary, embryonic pancreas (E14.5), and insulin-secreting beta-cells (betaTC-3) reveals that approximately 50% of the mature miRNAs representing mostly the mmu-let-7 family display internal insertion/deletions and substitutions when compared to precursor miRNA and the mouse genome reference sequences. Approximately, 12%-20% of species associated with mmu-let-7 populations exhibit sequence discrepancies that are dramatically reduced in nucleotides 3-7 (5'-seed) and 10-15 (cleavage and anchor sites). This observation is inconsistent with sequencing error and leads us to propose that the changes arise predominantly from post-transcriptional RNA-editing activity operating on miRNA:target mRNA complexes. Internal nucleotide modifications are most enriched at the ninth nucleotide position. A common ninth base edit of U-to-G results in a significant increase in stability of down-regulated let-7a targets in inhibin-deficient mice (Inha-/-). An excess of U-insertions (14.8%) over U-deletions (1.5%) and the presence of cleaved intermediates suggest that a mammalian TUTase (terminal uridylyl transferase) mediated dUTP-dependent U-insertion/U-deletion cycle may be a possible mechanism. We speculate that mRNA target site-directed editing of mmu-let-7a duplex-bulges stabilizes 'loose' miRNA:mRNA target associations and functions to expand the target repertoire and/or enhance mRNA decay over translational repression. Our results also demonstrate that the systematic study of sequence variation within specific RNA classes in a given cell type from millions of sequences generated by next-generation sequencing (NGS) technologies ('intranomics') can be used broadly to infer functional constraints on specific parts of completely uncharacterized RNAs.
File Format	HTM / HTML
ISSN	10889051
e-ISSN	15495469
DOI	10.1101/gr.078246.108
Journal	Genome Research
Issue Number	10
Volume Number	18
Language	English
Publisher	Cold Spring Harbor Laboratory Press
Publisher Date	2008-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Genetics Discipline Genomics Micrornas Chemistry Metabolism Rna Editing Rna, Messenger Animals Cells, Cultured Deoxyuracil Nucleotides Embryo, Mammalian Mice Genetics Molecular Sequence Data Nucleic Acid Conformation Rna Nucleotidyltransferases Rna Stability Rna, Guide Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Genetics Genetics (clinical)

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Mouse let-7 miRNA populations exhibit RNA editing that is constrained in the 5′-seed/ cleavage/anchor regions and stabilize predicted mmu-let-7a:mRNA duplexes

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Mouse let-7 miRNA populations exhibit RNA editing that is constrained in the 5'-seed/ cleavage/anchor regions and stabilize predicted mmu-let-7a:mRNA duplexes.

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Mouse let-7 miRNA populations exhibit RNA editing that is constrained in the 5′-seed/ cleavage/anchor regions and stabilize predicted mmu-let-7a:mRNA duplexes

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Mouse let-7 miRNA populations exhibit RNA editing that is constrained in the 5'-seed/ cleavage/anchor regions and stabilize predicted mmu-let-7a:mRNA duplexes.