An Orphan CpG Island Drives Expression of a let-7 miRNA Precursor with an Important Role in Mouse Development
| Autor: | Jim Selfridge, Joanna Bottomley, Adrian Bird, Ramires-Solis R, Lelliott C, Martha V. Koerner, Skarnes B, Barry Rosen, Mark G. Thomas, David J. Adams, De Sousa D, Shaun Webb, Kashyap Chhatbar, Justyna Cholewa-Waclaw |
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| Přispěvatelé: | Lelliott, Christopher [0000-0001-8087-4530], Apollo - University of Cambridge Repository |
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
Health
Toxicology and Mutagenesis lcsh:Medicine Biology medicine.disease_cause Biochemistry Genetics and Molecular Biology (miscellaneous) Biochemistry 03 medical and health sciences 0302 clinical medicine microRNA Genetics medicine lcsh:QH301-705.5 030304 developmental biology 0303 health sciences Mutation lcsh:R micro-RNA RNA Promoter Let-7 miRNA Embryonic stem cell Let-7 mouse genetics CpG site lcsh:Biology (General) Human genome 030217 neurology & neurosurgery |
| Zdroj: | Koerner, M, Chhatbar, K, Webb, S, Cholewa-Waclaw, J, Selfridge, J, De Sousa, D, Skarnes, B, Rosen, B, Thomas, M, Bottomley, J, Ramires-Solis, R, Lelliott, C, Adams, D & Bird, A 2019, ' An Orphan CpG Island Drives Expression of a let-7 miRNA Precursor with an Important Role in Mouse Development ', Epigenomes, vol. 3, no. 1 . https://doi.org/10.3390/epigenomes3010007 Epigenomes, Vol 3, Iss 1, p 7 (2019) Epigenomes Volume 3 Issue 1 |
| Popis: | Most human genes are associated with promoters embedded in non-methylated, G + C-rich CpG islands (CGIs). Not all CGIs are found at annotated promoters, however, raising the possibility that many serve as promoters for transcripts that do not code for proteins. To test this hypothesis, we searched for novel transcripts in embryonic stem cells (ESCs) that originate within orphan CGIs. Among several candidates, we detected a transcript that included three members of the let-7 micro-RNA family: Let-7a-1, let-7f-1, and let-7d. Deletion of the CGI prevented expression of the precursor RNA and depleted the included miRNAs. Mice homozygous for this mutation were sub-viable and showed growth and other defects. The results suggest that despite the identity of their seed sequences, members of the let-7 miRNA family exert distinct functions that cannot be complemented by other members. |
| Databáze: | OpenAIRE |
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