| First Author | Penzkofer D | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 6 | Pages | e101153 |
| PubMed ID | 24979655 | Mgi Jnum | J:218943 |
| Mgi Id | MGI:5619053 | Doi | 10.1371/journal.pone.0101153 |
| Citation | Penzkofer D, et al. (2014) Phenotypic characterization of miR-92a-/- mice reveals an important function of miR-92a in skeletal development. PLoS One 9(6):e101153 |
| abstractText | MicroRNAs (miRNAs, miRs) emerged as key regulators of gene expression. Germline hemizygous deletion of the gene that encodes the miR-17 approximately 92 miRNA cluster was associated with microcephaly, short stature and digital abnormalities in humans. Mice deficient for the miR-17 approximately 92 cluster phenocopy several features such as growth and skeletal development defects and exhibit impaired B cell development. However, the individual contribution of miR-17 approximately 92 cluster members to this phenotype is unknown. Here we show that germline deletion of miR-92a in mice is not affecting heart development and does not reduce circulating or bone marrow-derived hematopoietic cells, but induces skeletal defects. MiR-92a-/- mice are born at a reduced Mendelian ratio, but surviving mice are viable and fertile. However, body weight of miR-92a-/- mice was reduced during embryonic and postnatal development and adulthood. A significantly reduced body and skull length was observed in miR-92a-/- mice compared to wild type littermates. microCT analysis revealed that the length of the 5th mesophalanx to 5th metacarpal bone of the forelimbs was significantly reduced, but bones of the hindlimbs were not altered. Bone density was not affected. These findings demonstrate that deletion of miR-92a is sufficient to induce a developmental skeletal defect. |
