| Autor: |
Mitsuteru Ito, Sferruzzi-Perri, Amanda N., Edwards, Carol A., Adalsteinsson, Bjorn T., Allen, Sarah E., Tsui-Han Loo, Kitazawa, Moe, Tomoko Kaneko-Ishino, Fumitoshi Ishino, Stewart, Colin L., Ferguson-Smith, Anne C. |
| Předmět: |
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| Zdroj: |
Development (09501991); Jul2015, Vol. 142 Issue 14, preceding p2425-2430, 22p |
| Abstrakt: |
The paternally expressed imprinted retrotransposon-like 1 (Rtl1)isa 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 (ΔmiR-127/Rtl1 or miR-127/ ΔRtl1) and double (ΔmiR-127/ΔRtl1) 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 miR127 is an essential regulator of Rtl1, mediated by a trans-homologue interaction between reciprocally imprinted genes on the maternally and paternally inherited chromosomes. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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