| First Author | Whitson RH | Year | 2003 |
| Journal | Biochem Biophys Res Commun | Volume | 312 |
| Issue | 4 | Pages | 997-1004 |
| PubMed ID | 14651970 | Mgi Jnum | J:130390 |
| Mgi Id | MGI:3771609 | Doi | 10.1016/j.bbrc.2003.11.026 |
| Citation | Whitson RH, et al. (2003) Neonatal mortality and leanness in mice lacking the ARID transcription factor Mrf-2. Biochem Biophys Res Commun 312(4):997-1004 |
| abstractText | Proteins containing the ARID (AT-rich interaction domain) DNA-binding motif regulate gene expression and differentiation in fungi, plants, and animals. This report describes phenotypes resulting from targeted disruption of the ARID gene Mrf-2. Homozygous loss of Mrf-2 resulted in a high rate of neonatal mortality that was partially strain-dependent: survival of Mrf-2(-/-) pups ranged from 6.4% on the 129S1 genetic background to 38% on a mixed 129S1.C57Bl/6J background. Loss of Mrf-2 expression did not affect embryonic survival, embryonic growth or birth weight. Lipid accumulation was severely reduced in brown adipose of Mrf-2(-/-) neonates at 24h of age, however, and Mrf-2(-/-) mice weighed significantly less than controls from postnatal day five onward. Adult Mrf-2(-/-) mice were lean, with significant reductions in brown and white adipose tissues, and in the percentage of body fat. Mrf-2(-/-) and Mrf-2(+/-) mice were also resistant to weight gains and obesity when maintained on high-fat diets. These phenotypes suggest that Mrf-2 is essential for accumulation of lipid stores in postnatal life. |
