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Cell Growth & Differentiation, Vol 6, Issue 12 1541-1547, Copyright © 1995 by American Association of Cancer Research
ARTICLES |
EC Shugart, AS Levenson, CM Constance and RM Umek
Department of Biology, University of Virginia, Charlottesville 22903, USA.
The characterization of growth arrest-associated genes has revealed that cells actively suppress mitotic growth in response to extracellular signals. Mouse 3T3-L1 cells growth arrest at multiple distinct points during terminal differentiation to adipocytes. We examined the expression of growth arrest-specific (gas) and growth arrest- and DNA damage-inducible (gadd) genes as a function of 3T3-L1 growth arrest and adipocyte development. These growth arrest-associated genes are differentially expressed throughout adipocyte development. Some of the gas/gadd genes are preferentially expressed in a subset of growth arrest states. In contrast, gas1 and gas3 are expressed in serum-starved adipoblasts, contact-inhibited adipoblasts, and post-mitotic adipocytes. However, in post-mitotic adipocytes, gas1 and gas3 are induced in response to nutrient deprivation, not altered growth status. gas6 is an exception to the general concordance of mitotic growth arrest and gas/gadd expression in that gas6 is preferentially expressed during the clonal expansion of postconfluent adipoblasts. Combined, the expression patterns indicate that growth arrest-associated genes are regulated by numerous signal transduction pathways throughout a discrete developmental transition.
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