mir-278 microRNA precursor family
| mir-278 | |
|---|---|
| Identifiers | |
| Symbol | mir-278 |
| Rfam | RF00729 |
| miRBase family | 3 |
| Other data | |
| RNA type | microRNA |
| Domain(s) | Eukaryota; |
| PDB structures | PDBe |
In molecular biology mir-278 microRNA is a short RNA molecule belonging to a class of molecules referred to as microRNAs. These function to regulate the expression levels of other genes by several mechanisms, primarily binding to their target at its 3'UTR.
Mis- and altered expression in Drosophila
miR-278 affects energy metabolism in the Drosophila melanogaster species. Elevated insulin production has been observed in miR-278 mutants, due to insulin resistance in the absence of this microRNA. miR-278 is now known to act through regulation of the expanded gene transcript, and most likely through further miR-278 targets as well.[1]
Misexpression in the developing eye has been found to result in overgrowth, partially through apoptotic inhibition.[2] There is a single base substitution which blocks the gain-of-function phenotype, indicating the acquisition of novel functions by misexpressed miRNAs which bring about unscheduled cell proliferation in vivo. This is reflective of a microRNA potential in the promotion of tumour formation.
See also
References
- ^ Teleman AA, Maitra S, Cohen SM (2006). "Drosophila lacking microRNA miR-278 are defective in energy homeostasis". Genes Dev. 20 (4): 417–22. doi:10.1101/gad.374406. PMC 1369043. PMID 16481470.
- ^ Nairz K, Rottig C, Rintelen F, Zdobnov E, Moser M, Hafen E (2006). "Overgrowth caused by misexpression of a microRNA with dispensable wild-type function". Dev Biol. 291 (2): 314–24. doi:10.1016/j.ydbio.2005.11.047. PMID 16443211.
Further reading
- Yu, J. -Y.; Reynolds, S. H.; Hatfield, S. D.; Shcherbata, H. R.; Fischer, K. A.; Ward, E. J.; Long, D.; Ding, Y.; Ruohola-Baker, H. (2009). "Dicer-1-dependent Dacapo suppression acts downstream of Insulin receptor in regulating cell division of Drosophila germline stem cells". Development. 136 (9): 1497–1507. doi:10.1242/dev.025999. PMC 2674257. PMID 19336466.
External links
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