| First Author | Ito M | Year | 2015 |
| Journal | Development | Volume | 142 |
| Issue | 14 | Pages | 2425-30 |
| PubMed ID | 26138477 | Mgi Jnum | J:224145 |
| Mgi Id | MGI:5661605 | Doi | 10.1242/dev.121996 |
| Citation | Ito M, et al. (2015) A trans-homologue interaction between reciprocally imprinted miR-127 and Rtl1 regulates placenta development. Development 142(14):2425-30 |
| abstractText | The paternally expressed imprinted retrotransposon-like 1 (Rtl1) is a retrotransposon-derived gene that has evolved a function in eutherian placentation. Seven miRNAs, including miR-127, are processed from a maternally expressed antisense Rtl1 transcript (Rtl1as) and regulate Rtl1 levels through RNAi-mediated post-transcriptional degradation. To determine the relative functional role of Rtl1as miRNAs in Rtl1 dosage, we generated a mouse specifically deleted for miR-127. The miR-127 knockout mice exhibit placentomegaly with specific defects within the labyrinthine zone involved in maternal-fetal nutrient transfer. Although fetal weight is unaltered, specific Rtl1 transcripts and protein levels are increased in both the fetus and placenta. Phenotypic analysis of single (DeltamiR-127/Rtl1 or miR-127/DeltaRtl1) and double (DeltamiR-127/DeltaRtl1) heterozygous miR-127- and Rtl1-deficient mice indicate that Rtl1 is the main target gene of miR-127 in placental development. Our results demonstrate that miR-127 is an essential regulator of Rtl1, mediated by a trans-homologue interaction between reciprocally imprinted genes on the maternally and paternally inherited chromosomes. |
