scholarly journals Transcriptional activation and subsequent control of the human heat shock gene during adenovirus infection.

1983 ◽  
Vol 3 (11) ◽  
pp. 2058-2065 ◽  
Author(s):  
H T Kao ◽  
J R Nevins
Keyword(s):  
Heat Shock ◽  
Transcriptional Activation ◽  
Peak Level ◽  
Heat Shock Gene ◽  
Adenovirus Infection ◽  
Wild Type ◽  
Rapid Turnover ◽  
Transformed Cell Line ◽  
Shock Gene ◽  
E1a Gene

A cDNA copy of the major human heat shock mRNA was cloned. The clone is complementary to the mRNA encoding the major 70-kilodalton heat shock protein as shown by hybrid arrest translation. We utilized the cloned DNA to measure induction of the gene during adenovirus infection. The mRNA increases in abundance approximately 100-fold during a wild-type adenovirus infection but does not increase more than 2-fold during an infection in which there is no E1A gene function [high multiplicity of infection of an E1A (-) mutant]. Furthermore, by measuring transcription in isolated nuclei, we found that the induction was transcriptional and was mediated by the E1A gene product. The induction was not maintained, however. After a peak level was obtained, transcription returned to preinfection levels. This decline was also reflected in the cytoplasmic mRNA abundance indicating a rapid turnover of the heat shock mRNA. This rapid turnover of the heat shock mRNA appears to be induced by the viral infection since the heat shock mRNA was found to be stable when synthesized in an adenovirus-transformed cell line.

Transcriptional activation and subsequent control of the human heat shock gene during adenovirus infection

1983 ◽  
Vol 3 (11) ◽  
pp. 2058-2065 ◽  
Author(s):  
H T Kao ◽  
J R Nevins
Keyword(s):  
Heat Shock ◽  
Transcriptional Activation ◽  
Peak Level ◽  
Heat Shock Gene ◽  
Adenovirus Infection ◽  
Wild Type ◽  
Rapid Turnover ◽  
Transformed Cell Line ◽  
Shock Gene ◽  
E1a Gene

A cDNA copy of the major human heat shock mRNA was cloned. The clone is complementary to the mRNA encoding the major 70-kilodalton heat shock protein as shown by hybrid arrest translation. We utilized the cloned DNA to measure induction of the gene during adenovirus infection. The mRNA increases in abundance approximately 100-fold during a wild-type adenovirus infection but does not increase more than 2-fold during an infection in which there is no E1A gene function [high multiplicity of infection of an E1A (-) mutant]. Furthermore, by measuring transcription in isolated nuclei, we found that the induction was transcriptional and was mediated by the E1A gene product. The induction was not maintained, however. After a peak level was obtained, transcription returned to preinfection levels. This decline was also reflected in the cytoplasmic mRNA abundance indicating a rapid turnover of the heat shock mRNA. This rapid turnover of the heat shock mRNA appears to be induced by the viral infection since the heat shock mRNA was found to be stable when synthesized in an adenovirus-transformed cell line.

scholarly journals The Heat Shock Protein YbeY Is Required for Optimal Activity of the 30S Ribosomal Subunit

2010 ◽  
Vol 192 (18) ◽  
pp. 4592-4596 ◽  
Author(s):  
Aviram Rasouly ◽  
Chen Davidovich ◽  
Eliora Z. Ron
Keyword(s):  
Heat Shock ◽  
Ribosomal Subunit ◽  
Heat Shock Gene ◽  
Wild Type ◽  
Lower Efficiency ◽  
Ribosomal Subunits ◽  
Translation Machinery ◽  
Shock Gene

ABSTRACT The highly conserved bacterial ybeY gene is a heat shock gene whose function is not fully understood. Previously, we showed that the YbeY protein is involved in protein synthesis, as Escherichia coli mutants with ybeY deleted exhibit severe translational defects in vivo. Here we show that the in vitro activity of the translation machinery of ybeY deletion mutants is significantly lower than that of the wild type. We also show that the lower efficiency of the translation machinery is due to impaired 30S small ribosomal subunits.

scholarly journals Common control of the heat shock gene and early adenovirus genes: evidence for a cellular E1A-like activity.

1984 ◽  
Vol 4 (5) ◽  
pp. 867-874 ◽  
Author(s):  
M J Imperiale ◽  
H T Kao ◽  
L T Feldman ◽  
J R Nevins ◽  
S Strickland
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Gene Product ◽  
Hela Cells ◽  
Heat Shock Gene ◽  
Viral Gene ◽  
Teratocarcinoma Cell ◽  
Shock Gene ◽  
E1a Gene

We have employed an antiserum specific to the 70-kilodalton human heat shock protein and a cDNA clone specific to the mRNA for this protein to analyze the expression of the gene under noninducing conditions. Expression of the heat shock gene can be detected in the absence of heat induction, and this uninduced level of expression depends greatly on the particular cell type. For instance, the basal expression of the heat shock gene is at least 50 times higher in HeLa cells than in WI38 cells at both the mRNA and protein levels. We have previously shown that the inducer of transcription of the early adenovirus genes, the E1A gene product, also induces the heat shock gene, suggesting that these genes may be subject to the same regulation. We have, therefore, investigated the control of the adenovirus genes in relation to the cellular control of the heat shock gene. We find that human cells that allow a high level of uninduced expression of the heat shock gene (i.e., HeLa cells) also allow expression of the early adenovirus genes in the absence of the E1A inducer. The same is also true for the mouse F9 teratocarcinoma cell line. F9 stem cells, which constitutively express the heat shock protein, allow early adenovirus gene expression in the absence of E1A; upon differentiation induced by retinoic acid and cyclic AMP, the cells become restrictive and early viral gene expression requires the E1A gene product. Coordinately, upon differentiation there is also a loss of heat shock protein expression.

Common control of the heat shock gene and early adenovirus genes: evidence for a cellular E1A-like activity

1984 ◽  
Vol 4 (5) ◽  
pp. 867-874 ◽  
Author(s):  
M J Imperiale ◽  
H T Kao ◽  
L T Feldman ◽  
J R Nevins ◽  
S Strickland
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Gene Product ◽  
Hela Cells ◽  
Heat Shock Gene ◽  
Viral Gene ◽  
Teratocarcinoma Cell ◽  
Shock Gene ◽  
E1a Gene

We have employed an antiserum specific to the 70-kilodalton human heat shock protein and a cDNA clone specific to the mRNA for this protein to analyze the expression of the gene under noninducing conditions. Expression of the heat shock gene can be detected in the absence of heat induction, and this uninduced level of expression depends greatly on the particular cell type. For instance, the basal expression of the heat shock gene is at least 50 times higher in HeLa cells than in WI38 cells at both the mRNA and protein levels. We have previously shown that the inducer of transcription of the early adenovirus genes, the E1A gene product, also induces the heat shock gene, suggesting that these genes may be subject to the same regulation. We have, therefore, investigated the control of the adenovirus genes in relation to the cellular control of the heat shock gene. We find that human cells that allow a high level of uninduced expression of the heat shock gene (i.e., HeLa cells) also allow expression of the early adenovirus genes in the absence of the E1A inducer. The same is also true for the mouse F9 teratocarcinoma cell line. F9 stem cells, which constitutively express the heat shock protein, allow early adenovirus gene expression in the absence of E1A; upon differentiation induced by retinoic acid and cyclic AMP, the cells become restrictive and early viral gene expression requires the E1A gene product. Coordinately, upon differentiation there is also a loss of heat shock protein expression.

scholarly journals Sequence of the lon gene in Escherichia coli. A heat-shock gene which encodes the ATP-dependent protease La.

1988 ◽  
Vol 263 (24) ◽  
pp. 11718-11728 ◽  
Author(s):  
D T Chin ◽  
S A Goff ◽  
T Webster ◽  
T Smith ◽  
A L Goldberg
Keyword(s):  
Escherichia Coli ◽  
Heat Shock ◽  
Heat Shock Gene ◽  
Shock Gene
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