mir-6 microRNA precursor

mir-6 microRNA precursor
Identifiers
Symbol mir-6
Rfam RF00143
miRBase MI0000124
miRBase family MIPF0000119
Other data
RNA type Gene; miRNA
Domain(s) Eukaryota
GO 0035195 0035068
SO 0001244
PDB structures PDBe

The mir-6 microRNA precursor is a precursor microRNA specific to Drosophila species. In Drosophila melanogaster there are three mir-6 paralogs called dme-mir-6-1, dme-mir-6-2, dme-mir-6-3, which are clustered together in the genome. The extents of these hairpin precursors are estimated based on hairpin prediction. Each precursor is generated following the cleavage of a longer primary transcript in the nucleus, and is exported in the cytoplasm. In the cytoplasm, precursors are further processed by the enzyme Dicer, generating ~22 nucleotide products from each arm of the hairpin. The products generated from the 3' arm of each mir-6 precursor have identical sequences. Both 5' and 3' mature products are experimentally validated. Experimental data suggests that the mature products of mir-6 hairpins are expressed in the early embryo of Drosophila and target apoptotic genes such as hid, grim and rpr.[1]

Near perfect complementarity has been observed between miR-5 and miR-6 at 20/21 nucleotides.[2] However, miR-5 is only related on a minor level to any of the three respective miR-6 sequences. miR-6 genes reside in a gene cluster containing other non-K-box family miRNAs, including miRNAs-3 and-309, and the Brd box family gene mir-4. Alignment has shown miR-6 to share the same family motif as miR-11 and miR-2b, together making up the mir-2 clan. There is, however, little similarity in the 3' ends between these clan members.

Apoptotic regulation

mir-6 plays a key role in the regulation of early apoptosis. Indeed, there is a much increased apoptotic rate in miR-6-depleted embryos compared with control embryos, indicating that mir-6 acts to suppress apoptosis. The pro-apoptotic factor Hid is controlled solely by miR-6, which sees its regulation at a post-transcriptional level. miR-6-depleted embryos have been found to show the strongest phenotype of all miR-2 family members, explained by their interaction with hid, the pro-apoptotic gene with the broadest expression and strongest proapoptotic effect.[3] Embryos injected with mir-6 antisense failed to differentiate normal internal and external structures, with the number of apoptotic cells much increased compared to wildtype cells.[1] Further work into this with miR-6-depleted blastoderm embryos found pole cell formation at the posterior end of the anteroposterior axis to be disrupted, despite normality of both cellularisation and early pattern formation.[1]

References

  1. 1 2 3 Leaman, Dan; Chen, Po Yu; Fak, John; Yalcin, Abdullah; Pearce, Michael; Unnerstall, Ulrich; Marks, Debora S.; Sander, Chris; et al. (2005). "Antisense-Mediated Depletion Reveals Essential and Specific Functions of MicroRNAs in Drosophila Development". Cell. 121 (7): 1097–108. doi:10.1016/j.cell.2005.04.016. PMID 15989958.
  2. ↑ Su, H; Caldwell, HD (1992). "Immunogenicity of a chimeric peptide corresponding to T helper and B cell epitopes of the Chlamydia trachomatis major outer membrane protein". The Journal of Experimental Medicine. 175 (1): 227–35. doi:10.1084/jem.175.1.227. PMC 2119084. PMID 1370528.
  3. ↑ Figueiras, Ana M.; González-Jaén, M. Teresa; Candela, Milagros; Benito, César (2006). "Genic heterozygosity, chromosomal interchanges and fitness in rye: Any relationship?". Genetica. 128 (1–3): 273–86. doi:10.1007/s10709-005-6242-2. PMID 17028957.

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