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Publication : The growth arrest genes gas5, gas6, and CHOP-10 (gadd153) are expressed in the mouse preimplantation embryo.

First Author  Fleming JV Year  1997
Journal  Mol Reprod Dev Volume  48
Issue  3 Pages  310-6
PubMed ID  9322241 Mgi Jnum  J:43320
Mgi Id  MGI:1097500 Doi  10.1002/(SICI)1098-2795(199711)48:3<310::AID-MRD2>3.0.CO;2-U
Citation  Fleming JV, et al. (1997) The growth arrest genes gas5, gas6, and CHOP-10 (gadd153) are expressed in the mouse preimplantation embryo. Mol Reprod Dev 48(3):310-6
abstractText  The gas and gadd family of genes, known collectively as the growth arrest genes, are associated with the negative control of mammalian cell growth. The steady-state levels of their mRNAs are increased by three to fivefold when exponentially multiplying cells are exposed to a variety of stresses including inadequate nutrition or the removal of serum. Reverse transcription-polymerase chain reaction (RT-PCR) has been used to analyze growth arrest gene expression in the preimplantation mouse embryo. The gas5, gas6, and CHOP-10 (gadd153, Ddit3) genes were expressed from the eight-cell stage onward. The gas2 and gas3 genes associated with apoptosis were not expressed. Embryos were cultured in kSOM medium and a semiquantitative RT-PCR method was used to measure the relative gene expression using beta-actin mRNA as a reference. The ratio of gas5 to beta-actin mRNA was high at the eight-cell stage and fell three to fivefold during development. The decline in the gas5:beta-actin ratio corresponded to the activation of true cell growth (cytokinesis). The gas6:beta-actin ratio was low at the eight-cell stage and increased by twofold as the blastocyst formed. CHOP-10 was expressed at a constant level throughout development. Embryos that had developed in vivo were compared with the equivalent blastocyst-stage embryos cultured in kSOM medium. There were no significant differences in the ratio of CHOP-10, gas5, or gas6 mRNAs relative to beta-actin. These results suggest that these genes are expressed as part of normal early embryonic development. The potential roles of the growth arrest genes are discussed.
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