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Serum factors and v-src control two complementary mitogenic pathways in quail neuroretinal cells in culture

Authors :
Gillet, G.
Michel, D.
Crisanti, P.
Guerin, M.
Herault, Y.
Pessac, B.
Calothy, G.
Brun, G.
Volovitch, M.
Institut de biologie et chimie des protéines [Lyon] (IBCP)
Université Claude Bernard Lyon 1 (UCBL)
Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)
Deleage, Gilbert
Source :
Oncogene, Oncogene, Nature Publishing Group, 1993, 8, pp.565-574
Publication Year :
1993
Publisher :
HAL CCSD, 1993.

Abstract

International audience; 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.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.

Details

Language :
English
ISSN :
09509232 and 14765594
Database :
OpenAIRE
Journal :
Oncogene, Oncogene, Nature Publishing Group, 1993, 8, pp.565-574
Accession number :
edsair.pmid.dedup....68e4566eea51b047409b5469898f329c