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The recA gene of Mycobacterium tuberculosis is unusual in that it is expressed from two promoters, one of which, P1, is DNA damage inducible independently of LexA and RecA, while the other, P2, is regulated by LexA in the classical way (E. O. Davis, B. Springer, K. K. Gopaul, K. G. Papavinasasundaram, P. Sander, and E. C. Bottger, Mol. Microbiol. 46:791-800, 2002). In this study we characterized these two promoters in more detail. Firstly, we localized the promoter elements for each of the promoters, and in so doing we identified a mutation in each promoter which eliminates promoter activity. Interestingly, a motif with similarity to Escherichia coli [[sigma].sup.70] -35 elements but located much closer to the -10 element is important for optimal expression of P1, whereas the sequence at the -35 location is not. Secondly, we found that the sequences flanking the promoters can have a profound effect on the expression level directed by each of the promoters. Finally, we examined the contribution of each of the promoters to recA expression and compared their kinetics of induction following DNA damage.

Research was conducted to examine the role of protein Cra in transcription of the icd gene. In vitro transcription method revealed that in addition to its main promoter a second promoter was contained in the icd control region. Tests conducted on specific point mutations in the alpha subunit of RNA polymerase demonstrated that various RNAP-DNA contacts have an important role to play in the transcription of the icd gene.

Protein PknH possesses an autokinase activity and belongs to large STPK family found in macobacterium tuberculosis. EmbR possesses an FHA domain, a newly described phosphoprotein recognition domain, which plays an essential role in PknH-EmbR interaction and phosphorylation of EmbR by PknH.

The systemic and renal hemodynamic effects of tertatolol, a new noncardioselective beta blocker without partial agonist activity, given alone or in combination with cyclooxygenase inhibition by acetylsalicylic acid (aspirin), were investigated in eight healthy volunteers. Tertatolol 5 mg, aspirin 1 g, tertatolol 5 mg together with aspirin 1 g and placebo were administered at 1-week intervals in a random order and in a double-blind fashion. Cardiac output was measured by Doppler echography and renal blood flow and glomerular filtration rate (GFR) by constant infusion techniques using (123I) iodohippurate and (51Cr) EDTA, respectively. Measurements were performed before and then successively 2 and 4 hours after oral intake of drugs or placebo. Tertatolol decreased cardiac output by 22% (P < .05) and heart rate by 17% (P < .05) without change in blood pressure, renal blood flow, and GFR. The same effects occurred when tertatolol was given together with aspirin. Either placebo or aspirin alone had no effect on systemic and renal hemodynamics. These results suggest that cardiac output is redistributed to the kidneys after tertatolol intake in normal humans. This favorable effect on renal hemodynamics is probably not mediated by a local release of vasodilating prostaglandins. [ABSTRACT FROM AUTHOR]