Analysis of interactions between CytR and CRP at CytR-regulated promoters

Methods in Enzymology

Volumn 295, Issue , 1998, Pages 403-424

  Senear, Donald F ^a   Perini, Laura T ^a   Gavigan, Stacey A ^a  

^a NONE

Author keywords

[No Author keywords available]

Indexed keywords

ARTICLE; BINDING SITE; DNA FOOTPRINTING; DNA SEQUENCE; ESCHERICHIA COLI; GEL MOBILITY SHIFT ASSAY; MOLECULAR INTERACTION; MOLECULAR MODEL; NONHUMAN; PRIORITY JOURNAL; PROMOTER REGION; PROTEIN DNA BINDING; PROTEIN DNA INTERACTION; STOICHIOMETRY; THERMODYNAMICS; TRANSCRIPTION REGULATION;

ESCHERICHIA COLI;

EID: 0032321545     PISSN: 00766879     EISSN: None     Source Type: Book Series    
DOI: 10.1016/S0076-6879(98)95051-0     Document Type: Article

References (23)

1. P. Valentin-Hansen, L. Sogaard-Andersen, and H. Pedersen, Mol Microbiol 20, 461 (1996).
2. K. Hammer-Jespersen, in "Nucleoside Catabolism" (A. Munch-Petersen), p. 203. Academic Press, London, 1983.
3. M. J. Weickert and S. Adhya, J. Biol. Chem. 267, 15869 (1992).
4. P. Valentin-Hansen, B. Albrechtsen, and L. J. Love, Nature 325, 823 (1987).
5. J. Martinussen, N. E. Mollegaard, B. Holst, S. R. Douthwaite, and P. Valentin-Hansen, in "A New Version of Negative Control: DNA Sequences Involved in Expression and Regulation of CytR and cAMP/CRP Controlled Genes in Eschericia coli" (J. D. Gralla), p. 31. A. R. Liss, New York, 1989.
6. E. Bremer, P. Gerlach, and A. Middendorf, J. Bacteriol. 170, 108 (1988).
7. C. S. Barbier, S. A. Short, and D. F. Senear, J. Biol. Chem. 272, 16962 (1997).
8. N. Savery, V. Rhodius, and S. Busby, Philos. Trans. R. Soc. Lond. B Biol. Sci. 351, 543 (1996).
9. L. T. Perini, E. A. Doherty, E. Werner, and D. F. Senear, J. Biol. Chem. 271, 33242 (1996).
10. G. K. Ackers, M. A. Shea, and F. R. Smith, J. Mol. Biol. 170, 223 (1983).
11. J. Wyman, Adv. Prot Chem. 19, 223 (1964).
12. For example, a common feature of cooperative protein-DNA interactions in regulation appears to be a balance between favorable contributions from the protein-protein assembly reactions and unfavorable contributions from DNA topological changes [cf. E. Rusinova, J. B. A. Ross, T. M. Laue, and D. F. Senear, Biochemistry 36, 12994 (1997)].
13. M. Brenowitz, D. F. Senear, M. A. Shea, and G. K. Ackers, Methods Enzymol. 130, 132 (1986).
14. M. Brenowitz and D. F. Senear, in "DNase I Footprint Analysis of Site-Specific Protein-DNA Binding" (F. M. Ausubel, R. Brent, R. E. Kingston, et al, eds.), p. Unit 12.4. Greene Publishing Associates and Wiley-Interscience Associates, New York, 1989.
15. D. F. Senear and G. K. Ackers, Biochemistry 29, 6568 (1990).
16. E. A. Pyles and J. C. Lee, Biochemistry 35, 1162 (1996).
17. T. Heyduk and J. C. Lee, Proc. Natl Acad. Sci. U.S.A. 87, 1744 (1990).
18. J. M. Beechem, Methods Enzymol. 210, 37 (1992).
19. M. L. Johnson and L. M. Faunt, Methods Enzymol. 210, 1 (1992)
20. D. F. Senear and D. W. Bolen, Methods Enzymol. 210, 463 (1992).
21. M. Straume and M. L. Johnson, Methods Enzymol. 210, 87 (1992).
22. Specifying the concentration of each protein for experiments in which one was held constant obviates the simplification that the fixed concentration is "saturating." In principle this allows analysis of titrations with fixed but subsaturating concentration of one ligand. This promises exceptional resolution of heterologous cooperative effects because the interacting sites will titrate together even when the concentration of only one ligand is varied. However, a concern is that footprints of neighboring sites often overlap one another. When this is the case, as it is for deoP2 and udpP, then the basic assumption of footprint analysis to obtain individual-site binding curves, i.e., that the protection pattern reflect only changes in local binding of the ligand being titrated, is violated unless the fixed ligand concentration is saturating.
23. J. R. Cann, Electrophoresis 14, 669 (1993).