Gillet G, Michel D, Crisanti P, Guérin M, Herault Y, Pessac B, Calothy G, Brun G, Volovitch M
Laboratoire de Biologie Moléculaire et Cellulaire, UMR 49 CNRS, ENS Lyon, France.
Oncogene. 1993 Mar;8(3):565-74.
Quail neuroretinal cells (QNR cells) from 7-day-old embryos do not proliferate even in the presence of 8% fetal calf serum. After infection by the Rous sarcoma virus (RSV) they proliferate actively and exhibit a transformed phenotype; this effect is mediated by the oncoprotein pp60v-src. Secondary cultures infected by the thermosensitive strain tsNY68 of RSV are blocked in G0 either by thermal inactivation of pp60v-src at 41.5 degrees C or by serum deprivation at the permissive temperature (36.5 degrees C). Cell division is reinduced either by pp60v-src thermal renaturation or by subsequent serum addition. Our results indicate that v-src and serum control two synergic pathways leading to G0/G1 transition in QNR cells. In order to characterize genes related to the mitogenic and transforming effects of v-src in nerve cells, we have constructed a cDNA library from QNR cells transformed by tsNY68. We report the properties of five molecular clones isolated by differential screening of this library. Unlike immediate-early genes like c-fos, they are induced in mid and late G1. Four of them correspond to unknown mRNAs and the last one codes for nucleolin. This set of v-src-regulated genes is likely to code for functions deficient in terminally differentiated QNR cells and necessary for the progression in G1.
来自7日龄胚胎的鹌鹑神经视网膜细胞(QNR细胞)即使在含有8%胎牛血清的情况下也不会增殖。感染劳氏肉瘤病毒(RSV)后,它们会积极增殖并呈现转化表型;这种效应由癌蛋白pp60v-src介导。被RSV的温度敏感株tsNY68感染的传代培养细胞,在41.5℃时通过pp60v-src的热失活或在允许温度(36.5℃)下通过血清剥夺而被阻断在G0期。细胞分裂可通过pp60v-src的热复性或随后添加血清来重新诱导。我们的结果表明,v-src和血清控制着导致QNR细胞从G0期向G1期转变的两条协同途径。为了鉴定与v-src在神经细胞中的促有丝分裂和转化作用相关的基因,我们构建了一个由tsNY68转化的QNR细胞的cDNA文库。我们报告了通过对该文库进行差异筛选分离出的五个分子克隆的特性。与c-fos等即早基因不同,它们在G1期中期和后期被诱导。其中四个对应于未知的mRNA,最后一个编码核仁素。这一组受v-src调控的基因可能编码终末分化的QNR细胞中缺乏且对G1期进展必需的功能。