Evidence for a Regulatory Protein Involved in the Increased Activity of System A for Neutral Amino Acid Transport in Osmotically Stressed Mammalian Cells

System A for neutral amino acid transport is increased by hypertonic shock in NBL-1 cells previously induced to express system A activity by amino acid starvation. The hypertonicity-mediated effect can be blocked by cycloheximide but is insensitive to tunicamycin. The activity induced may be inactiv...

Full description

Saved in:
Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1994-09, Vol.91 (20), p.9569-9573
Main Authors: Ruiz-Montasell, Bonaventura, Gómez-Angelats, Mireia, Casado, Francisco J., Felipe, Antonio, McGivan, John D., Pastor-Anglada, Marçal
Format: Article
Language:English
Subjects:
Actinomycin
Amino acids
Amino Acids - metabolism
Animals
Biochemistry
Biological Transport - drug effects
Cattle
Cell culture techniques
Cell Line
Cell lines
Cell membranes
CHO Cells
Clone Cells
Cricetinae
Culture Media
Cultured cells
Dactinomycin - pharmacology
Epithelial cells
Epithelium - metabolism
Genes
Genes, Regulator
Hypertonic Solutions
Hypertonicity
Kidney
Kinetics
Mammals
Models, Biological
Proteins
RNA, Messenger - metabolism
Somatic cells
Starvation
Sucrose - pharmacology
Tunicamycin - pharmacology
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:System A for neutral amino acid transport is increased by hypertonic shock in NBL-1 cells previously induced to express system A activity by amino acid starvation. The hypertonicity-mediated effect can be blocked by cycloheximide but is insensitive to tunicamycin. The activity induced may be inactivated irreversibly by the addition of system A substrates, by a rapid mechanism insensitive to cycloheximide. In CHO-K1 cells, hypertonicity increases system A activity, as has been shown in NBL-1 cells. This effect is additive to the activity produced by derepression of system A by amino acid starvation and is insensitive to tunicamycin. Furthermore, the alanine-resistant mutant CHO-K1 alar4, which bears a mutation affecting the regulatory gene R1, involved in the derepression of system A activity after amino acid starvation, is still able to respond to the hypertonic shock by increasing system A activity to a level similar to that described in hypertonicity-induced derepressed CHO-K1 (wild type) cells. These results suggest (i) that the hypertonicity-mediated increase of system A activity occurs through a mechanism other than that involved in system A derepression and (ii) that a regulatory protein coded by an osmotically sensitive gene is responsible for further activation of preexisting A carriers.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.91.20.9569