AI Article Synopsis
- Control of cell proliferation is crucial for forming a multi-cellular organism, and while much is known about cell cycle regulators, the growth arrest state (G0) is less understood.
- Following serum starvation, six growth arrest-related genes (Gas1 to Gas6) were identified, with Gas1 being unique in its ability to induce growth arrest in cultured cells.
- This study reveals Gas1's expression patterns during mouse embryogenesis, indicating it might play additional roles beyond just inhibiting cell proliferation, along with findings from cloning the chick GAS1 gene and comparing expression patterns across species.
Article Abstract
Control of cell proliferation is essential to generate the defined form of a multi-cellular organism. While much is known about the regulators for cell cycle progression, relatively little is known about the state of growth arrest. Growth arrest (G0) is defined as a cell in a metabolically active but proliferation-quiescent state (reviewed in Baserga (1985) The Biology of Cell Reproduction), typically induced by serum starvation in vitro. Using subtractive hybridization, Schneider et al. (Cell 54 (1988) 787) identified six genes (Gas1 through Gas6) whose expressions are upregulated in serum-deprived NIH3T3 cells. Among the Gas genes, Gas1 is the only one that can cause growth arrest when expressed in cultured cell (Cell 70 (1995) 595; Int. J. Cancer 9 (1998) 569). Here, we describe for the first time the expression pattern of Gas1 during mouse embryogenesis. Our data reveal that Gas1 is expressed in many regions that the cells are actively proliferating and suggest that it may have other roles during development than negatively regulating cell proliferation. Furthermore, we have cloned the chick GAS1 gene and documented the similarity and divergence of Gas1 gene expression patterns between the two species.
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| http://dx.doi.org/10.1016/s0925-4773(01)00283-0 | DOI Listing |
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