Neonatal mortality and leanness in mice lacking the ARID transcription factor Mrf-2

Biochem Biophys Res Commun. 2003 Dec 26;312(4):997-1004. doi: 10.1016/j.bbrc.2003.11.026.


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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / metabolism*
  • Adipose Tissue / pathology*
  • Aging / physiology
  • Animals
  • Animals, Newborn
  • Body Constitution / physiology
  • Body Weight / physiology
  • DNA-Binding Proteins / deficiency*
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Dietary Fats / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Myogenic Regulatory Factors / genetics*
  • Phenotype
  • Sex Factors
  • Structure-Activity Relationship
  • Survival Rate
  • Thinness / genetics
  • Thinness / metabolism*
  • Transcription Factors


  • Arid5b protein, mouse
  • DNA-Binding Proteins
  • Dietary Fats
  • Myogenic Regulatory Factors
  • Transcription Factors