Generation of myc/fos transfectant Balb-3T3 cell lines.

M C Armelin, C A Joazeiro, K M Rocha, H A Armelin
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Abstract

Early and transient expression of proto-oncogenes c-fos and c-myc is involved in the mitogenic response to PDGF (platelet-derived growth factor). We used DNA-mediated transfection to approach the role played by these genes in cell growth control by PDGF and in growth deregulation (neoplasia). Cloned pFBJ-2 (v-fos) and glucocorticoid-inducible mouse c-myc were co-transfected with a neo genetic marker to allow a neutral selection on the basis of resistance to the neomycin derivative geneticin G418. pFBJ-2 transfection was found to interfere with the number of G418-resistant (G418r) colonies. By using a v-fos-deleted pFBJ-2 construct, the deleterious effect was attributed to v-fos coding sequences. Cellular fos gene disruption, by homologous recombination with exogenous v-fos, is proposed as the basis for the deleterious effect. Co-transfection with MMTV-H3-c-myc effectively counteracts the negative effects of v-fos. Different from the parental line or single myc or fos transfectants, double myc/fos transfectants are morphologically transformed. Double transfectants still retain the PDGF requirement for growth in monolayer cultures.

myc/fos转染Balb-3T3细胞系的产生。
原癌基因c-fos和c-myc的早期和短暂表达参与了对血小板衍生生长因子(PDGF)的有丝分裂反应。我们使用dna介导的转染来探讨这些基因在PDGF控制细胞生长和生长失调(肿瘤)中所起的作用。克隆的pFBJ-2 (v-fos)和糖皮质激素诱导的小鼠c-myc用一种新的遗传标记共转染,以便在对新霉素衍生物遗传素G418抗性的基础上进行中性选择。发现转染pFBJ-2可干扰g418抗性(G418r)菌落的数量。通过使用v-fos缺失的pFBJ-2结构,将有害效应归因于v-fos编码序列。通过与外源v-fos的同源重组,细胞fos基因被破坏,被认为是有害作用的基础。与MMTV-H3-c-myc共转染可有效抵消v-fos的负面影响。不同于亲本系或单myc或fos转基因,双myc/fos转基因在形态上发生了转化。在单层培养中,双转染仍然保留了生长所需的PDGF。
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