Many cellular mRNAs contain internal ribosomal entry sites (IRES) that become functional under conditions of cellular stress, when the rate of protein synthesis for most cellular mRNA is reduced. Internal ribosomal entry increases in response to hypoxia, cell differentiation, apoptosis, γ irradiation, and heat shock. Heat shock is the principal cellular stress in which general cap-dependent translation is inhibited. On the other hand, heat shock induces the preferential translation of a small class of mRNA, called heat shock protein (HSP) mRNAs, which probably occurs because little or no eIF4F activity is required for their translation. In this study, we found that continuous heat stress enhances expression of the heat shock protein BiP at the level of translation. Interestingly, heat stress also enhanced the viral IRES-dependent translation of encephalomyocarditis virus and hepatitis C virus but not poliovirus. Although several BiP inducers increased BiP protein expression, BiP IRES-dependent translation was enhanced only during heat shock, suggesting that heat shock is a specific inducer for BiP IRES-dependent translation. Taken together, these results indicate that the mechanism of IRES-dependent translation can be used during heat shock and suggest that this translational mechanism may be critical to the survival and proliferation of cells under stress.
|Number of pages
|Biochemical and biophysical research communications
|Published - 2002
Bibliographical noteFunding Information:
We are indebted to Dr. Peter Sarnow at Stanford University for kindly providing us with the plasmid pSK(+)/BiP-CAT. This work was supported in part by the G7, NRL, and the Molecular Medicine Research Group Programs of MOST and by a grant from the PNRC of KOSEF.
Copyright 2008 Elsevier B.V., All rights reserved.
- Heat shock
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology