No abstract

Obesity, defined as an increase in adipose tissue mass, is the most prevalent nutritional disorder in industrialized countries and is a growing problem in developing countries. An increase in adipose tissue mass can be the result of the production of new fat cells through the process of adipogenesis and/or the deposition of increased amounts of cytoplasmic triglyceride per cell. Although much has been learned about the differentiation of adipocytes in vitro, less is known about the molecular basis for the mechanisms regulating adipogenesis in vivo. Here oligonucleotide microarrays have been used to compare the patterns of gene expression in preadipocytes and adipocytes in vitro and in vivo. These data indicate that the cellular programs associated with adipocyte differentiation are considerably more complex than previously appreciated and that a greater number of heretofore uncharacterized gene regulatory events are activated during this process in vitro. In addition, the gene expression changes associated with adipocyte development in vivo and in vitro, while overlapping, are in some respects quite different. These data further suggest that one or more transcriptional programs are activated exclusively in vivo to generate the full adipocyte phenotype. This gene expression survey now sets the stage for further studies to dissect the molecular differences between in vivo and in vitro adipocytes.

No abstract

The brachyury, or T, locus encodes a transcription factor that plays a crucial role in the early development of all animals. In the mouse, animals heterozygous for a null mutation at this locus are born with a characteristic short tail. Expressivity of the short tail phenotype is greatly affected by genetic background. As a genetic entry into the identification of genes that interact with the Brachyury locus, we have performed a QTL analysis for modifiers of this phenotype. Surprisingly, we discovered that the major modifiers uncovered all act in a sex-limited manner. We have identified two QTLs--Brm1 on Chr 9 and Brm2 on Chr 15--that act only in female offspring(N2) from female T/+ parents(F1) and are responsible together for most, or all, of the genetic variance in phenotypic expression observed between C57BL/10 and C3H/HeJ animals.