PUBLICATION
Numerous microRNPs in neuronal cells containing novel microRNAs
- Authors
- Dostie, J., Mourelatos, Z., Yang, M., Sharma, A., and Dreyfuss, G.
- ID
- ZDB-PUB-041229-3
- Date
- 2003
- Source
- RNA (New York, N.Y.) 9(2): 180-186 (Journal)
- Registered Authors
- Keywords
- Gemin3; miRNAs; SMA; motor neurons
- MeSH Terms
-
- Animals
- DEAD Box Protein 20
- DEAD-box RNA Helicases
- Humans
- Mice
- MicroRNAs*
- Neurons/metabolism*
- RNA Helicases/genetics
- RNA Helicases/metabolism
- Ribonucleoproteins/genetics*
- PubMed
- 12554860 Full text @ RNA
Citation
Dostie, J., Mourelatos, Z., Yang, M., Sharma, A., and Dreyfuss, G. (2003) Numerous microRNPs in neuronal cells containing novel microRNAs. RNA (New York, N.Y.). 9(2):180-186.
Abstract
Spinal muscular atrophy (SMA) is a common neurodegenerative disease that is caused by deletions or loss-of-function mutations in the Survival of Motor Neuron (SMN) protein. SMN is part of a large complex that functions in the assembly/restructuring of ribonucleoprotein (RNP) complexes. We recently showed in HeLa cells that two components of the SMN complex, Gemin3 and Gemin4, together with the argonaute protein eIF2C2, also associate with microRNAs (miRNAs) as part of a novel class of RNPs termed miRNPs. Here we report on miRNPs isolated from neuronal cell lines of mouse and human, and describe 53 novel miRNAs. Several of these miRNAs are conserved in divergent organisms, including rat, zebrafish, pufferfish, and the nematode Caenorhabditis elegans. The chromosomal locations of most of the novel miRNAs were identified and indicate some phylogenetic conservation of the likely precursor structures. Interestingly the gene locus of one miRNA, miR-175, is a candidate region for two neurologic diseases: early-onset parkinsonism (Waisman syndrome) and X-linked mental retardation (MRX3). Also, several miRNAs identified as part of miRNPs in these cells appear to constitute two distinct subfamilies. These subfamilies comprise multiple copies of miRNAs on different chromosomes, suggesting an important function in the regulation of gene expression.
Errata / Notes
Erratum in: RNA. 2003 May;9(5):631-2.We wish to revise the designation of the microRNAs (miRNAs)reported in Tables 1 and 2 of the original manuscript. The simultaneous publication of numerous new miRNA sequences in the same issue of RNA (Lagos-Quintanas, M., Rauhut, R., Meyer, J., Borkhardt, A., and Tuschl, T. 2003. New microRNAs from mouse and human. RNA 9: 175–179), and the report of several miRNA sequences which were not available at the time of submission of our manuscript resulted in an extensive overlap in the designation of many of the miRNAs we reported. To rectify this, we changed the designations of many of the miRNAs included in Tables 1 and 2 and adopted the designation used by others. The novel miRNAs—those not included in publications by others—are numbered sequentially beginning with miRNA 224. In addition, many of the miRNAs we reported do not, in the absence of additional data, fulfill the stringent criteria suggested as guidelines for classification of newly discovered RNAs as miRNAs as was recently published (Ambros, V., Bartel, B., Bartel, D.P., Burge, C.B., Carrington, J.C., Chen, X., Dreyfuss, G., Eddy, S.R., Griffiths-Jones, S., Marshall, M., et al. 2003. A uniform system for microRNA annotation. RNA 9: 277–279). However, we are confident in the authenticity of these RNAs as assessed by co-immunoprecipitation with anti-Gemin3 antibodies and sequence determination often from multiple clones. In light of this, we refer to these RNAs as miRNA-like (miRNA-Lk-#) in the revised Tables. Four RNAs—miR-173, miR-196a, miR-196b, and miR-196c—were deleted from the Tables because their relevance to the corresponding genome could not be confirmed by additional criteria. The new designations of the novel miRNAs will be corrected in the NCBI database. We regret any potential confusion in nomenclature that our original publication may have caused. All the conclusions of the paper remain.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping