HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gloger, I. Articles by Panet, A. Search for Related Content PubMed PubMed Citation Articles by Gloger, I. Articles by Panet, A. Agricola Articles by Gloger, I. Articles by Panet, A.

Glutamine Starvation of Murine Leukaemia Virus-infected Cells Inhibits the Readthrough of the gag-pol Genes and Proteolytic Processing of the gag Polyprotein

Department of Virology, The Hebrew University-Hadassah Medical School, Jerusalem, Israel

The production of Moloney murine leukaemia virus from chronically infected cells was inhibited after starvation of glutamine. While the rate of synthesis of the precursor of the core proteins, Pr65^gag, was not affected in the starved cells, its proteolytic processing was blocked. Pulse-chase experiments indicated that glutamine was required during the synthesis of Pr65^gag to facilitate its subsequent processing. In addition, the synthesis of Pr200^gag-pol, the precursor of the protease, reverse transcriptase and endonuclease, was inhibited in the glutamine-starved cells. Starvation for other essential amino acids such as tyrosine and isoleucine affected neither the synthesis nor the processing of the virus proteins. These results suggest that the readthrough mechanism which enables synthesis of the Pr200^gag-pol polyprotein is modulated in the chronically infected cells by glutamine levels. Since the viral protease is part of the pol gene, its synthesis may be inhibited in the glutamine-starved cells and Pr65^gag is therefore not processed.

Keywords: MuLV, readthrough, glutamine starvation

Received 16 January 1986; accepted 1 July 1986.