Continuous heat shock enhances translational initiation directed by internal ribosomal entry site

被引:52
作者
Kim, YK [1 ]
Jang, SK [1 ]
机构
[1] Pohang Univ Sci & Technol, Dept Life Sci, Div Mol & Life Sci, NRL, Pohang 790784, Kyungbuk, South Korea
关键词
heat shock; translation; IRES; BiP; HCV;
D O I
10.1016/S0006-291X(02)02154-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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, gamma 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. (C) 2002 Elsevier Science (USA). All rights reserved.
引用
收藏
页码:224 / 231
页数:8
相关论文
共 47 条
  • [1] Ali N, 2000, J BIOL CHEM, V275, P27531
  • [2] La autoantigen is cleaved in the COOH terminus and loses the nuclear localization signal during apoptosis
    Ayukawa, K
    Taniguchi, S
    Masumoto, J
    Hashimoto, S
    Sarvotham, H
    Hara, A
    Aoyama, T
    Sagara, J
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (44) : 34465 - 34470
  • [3] Bernstein J, 1997, J BIOL CHEM, V272, P9356
  • [4] Requirement of Poly(rC) binding protein 2 for translation of poliovirus RNA
    Blyn, LB
    Towner, JS
    Semler, BL
    Ehrenfeld, E
    [J]. JOURNAL OF VIROLOGY, 1997, 71 (08) : 6243 - 6246
  • [5] POSTTRANSLATIONAL ASSOCIATION OF IMMUNOGLOBULIN HEAVY-CHAIN BINDING-PROTEIN WITH NASCENT HEAVY-CHAINS IN NONSECRETING AND SECRETING HYBRIDOMAS
    BOLE, DG
    HENDERSHOT, LM
    KEARNEY, JF
    [J]. JOURNAL OF CELL BIOLOGY, 1986, 102 (05) : 1558 - 1566
  • [6] Brostrom CO, 1998, PROG NUCLEIC ACID RE, V58, P79
  • [7] Burdon R H, 1987, Symp Soc Exp Biol, V41, P113
  • [8] Initiation of Apaf-1 translation by internal ribosome entry
    Coldwell, MJ
    Mitchell, SA
    Stoneley, M
    MacFarlane, M
    Willis, AE
    [J]. ONCOGENE, 2000, 19 (07) : 899 - 905
  • [9] Sequences within a small yeast RNA required for inhibition of internal initiation of translation: Interaction with la and other cellular proteins influences its inhibitory activity
    Das, S
    Kenan, DJ
    Bocskai, D
    Keene, JD
    Dasgupta, A
    [J]. JOURNAL OF VIROLOGY, 1996, 70 (03) : 1624 - 1632
  • [10] PROTEIN-SYNTHESIS AND PROTEIN-PHOSPHORYLATION DURING HEAT-STRESS, RECOVERY, AND ADAPTATION
    DUNCAN, RF
    HERSHEY, JWB
    [J]. JOURNAL OF CELL BIOLOGY, 1989, 109 (04) : 1467 - 1481