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Heat Shock Protein-Mediated Resistance to High Hydrostatic Pressure in Escherichia coli. Abram Aertsen, 2004.A random library of Escherichia coli MG1655 genomic fragments fused to a promoterless green fluorescent protein (GFP) gene was constructed and screened by differential fluorescence induction for promoters that are induced after exposure to a sublethal high hydrostatic pressure stress . This screening yielded three promoters of genes belonging to the heat shock regulon (dnaK, lon, clpPX), suggesting a role for heat shock proteins in protection against, and/or repair of, damage caused by high pressure . Several further observations provide additional support for this hypothesis: (i) the expression of rpoH, encoding the heat shock-specific sigma factor  32, was also induced by high pressure; (ii) heat shock rendered E . coli significantly more resistant to subsequent high-pressure inactivation, and this heat shock-induced pressure resistance followed the same time course as the induction of heat shock genes; (iii) basal expression levels of GFP from heat shock promoters, and expression of several heat shock proteins as determined by two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis of proteins extracted from pulse-labeled cells, was increased in three previously isolated pressure-resistant mutants of E . coli compared to wild-type levels .
A Dual Binding Site for Integration Host Factor and the Response Regulator CtrA inside the Caulobacter crescentus Replication Origin. Rania Siam, 2003.The response regulator CtrA controls chromosome replication by binding to five sites, a, b, c, d, and e, inside the Caulobacter crescentus replication origin (Cori) . In this study, we demonstrate that integration host factor (IHF) binds Cori over the central CtrA binding site c . Surprisingly, IHF and CtrA share DNA recognition sequences . Rather than promoting cooperative binding, IHF binding hinders CtrA binding to site c and nearby site d . Unlike other CtrA binding sites, DNA mutations in the CtrA c/IHF site uniquely impair autonomous Cori plasmid replication . These mutations also alter transcription from distant promoters more than 100 bp away . When the CtrA c/IHF site was deleted from the chromosome, these cells grew slowly and became selectively intolerant to a CtrA phosphor-mimic allele (D51E) . Since CtrA protein concentration decreases during the cell cycle as IHF protein concentration increases, we propose a model in which IHF displaces CtrA in order to bend Cori and promote efficient chromosome replication .
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