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Environmental Control of Microbial Gene Expression and Evolution

  • A. M. Chakrabarty

Summary

The survival of microorganisms is dependent on their ability to respond to a changing environment. In the very stressed environment of the CF lung, with salty and dehydrated mucus, the microorganisms need to protect themselves from losing their intracellular water and one way to accomplishing this is to produce an exopolysaccharide capsule with strong gelling properties as a barrier to dehydration. It is interesting that the algD promoter is activated by those environmental factors that are characteristic of the CF disease, which explains why CF patients are particularly vulnerable to infections by mucoid P. aeruginosa. It is also interesting to note that the alginate capsule, which is presumably produced to protect P. aeruginosa from intracellular dehydration, also affords protection The activation of the algD promoter has been measured by measuring catechol 2,3-dioxygenase (C230) activity, since a construct containing the xylE gene placed under the algD promoter was used in these experiments (see ref. 18 and 19). One unit of catechol 2,3-dioxygenase activity is defined as the amount of enzyme oxidizing one mmol of catechol to 2-hydroxymuconic semialdehyde, a product with a molar extinction coefficient of 4.4 × 104 at 375 nm. against antibiotics and antibodies to the detriment of the human patients. When the environment is beset with chlorinated compounds, the immediate response of natural microorganisms is to evolve degradative genes in the form of a plasmid. As a first step, they tend to recruit genes that allow degradation of a structurally analogous non-chlorinated compound, which undergo mutational or recombinational divergence to the appropriate genes whose products have broad substrate specificities to include chlorinated compounds. Such evolutionary processes apparently are not very effective for highly chlorinated compounds for which appropriate enzyme systems have not yet fully developed. In a single incidence of directed evolution, the chromosomal DNA shows the presence of multiple copies of a transposable element near the evolved genes, suggesting that an accelerated process of evolution may bypass the requirement of genetic relatedness of the evolved genes to the genome of the recruiting cells.

Keywords

Cystic Fibrosis Directed Evolution Chlorinate Compound Public Health Service Grant Natural Microorganism 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Ronson, C.W., Nixon, B.T. and Ausubel, F.M. (1987). Cell 49:579–581.PubMedCrossRefGoogle Scholar
  2. 2.
    Stock, J.B., Ninfa, A.J. and Stock, A.M. (1989). Microbiol. Rev. 53:450–490.PubMedGoogle Scholar
  3. 3.
    Matin, A., Auger, E.A., Blum, P.H. and Schultz, J.E. (1989). Ann. Rev. Microbiol. 43:293–316.CrossRefGoogle Scholar
  4. 4.
    Lee, C.A. and Falkow, S. (1990). Proc. Natl. Acad. Sci. USA 87:4304–4308.PubMedCrossRefGoogle Scholar
  5. 5.
    Roy, C.R., Miller, J.F. and Flakow, S. (1990). Proc. Natl. Acad. Sci. USA 87:3763–3767.PubMedCrossRefGoogle Scholar
  6. 6.
    McPherson, M.A. and Goodchild, M.C. (1988). Clin. Sci. 74:337–345.PubMedGoogle Scholar
  7. 7.
    Darzins, A., Wang, S.K., Vanags, R.I. and Chakrabarty, A.M. (1985). J. Bacteriol. 164:516–524.PubMedGoogle Scholar
  8. 8.
    Wang, S.K., Sa-Correia, I., Darzins, A. and Chakrabarty, A.M. (1987). J. Gen. Microbiol. 133:2303–2317.PubMedGoogle Scholar
  9. 9.
    Darzins, A., Nixon, L.L, Vanags, R.I. and Chakrabarty, A.M. (1985). J. Bacteriol. 161:249–257.PubMedGoogle Scholar
  10. 10.
    Deretic, V., Gill, J.F. and Chakrabarty, A.M. (1987). J. Bacteriol. 169:351–358.PubMedGoogle Scholar
  11. 11.
    Deretic, V., Dikshit, R., Konyecsni, W.M., Chakrabarty, A.M. and Misra, T.K. (1989). J. Bacteriol. 171:1278–1283.PubMedGoogle Scholar
  12. 12.
    Kato, J., Chu, L, Kitano, K., DeVault, J.D., Kimbara, K., Chakrabarty, A.M. and Misra, T.K. (1989). Gene 84:31–38.PubMedCrossRefGoogle Scholar
  13. 13.
    Kato, J., Misra, T.K. and Chakrabarty, A.M. (1990). Proc.Natl.Acad. Sci. USA 87:2887–2891.PubMedCrossRefGoogle Scholar
  14. 13a.
    Zielinski, N.A., Chakrabarty, A.M. and Berry, A. (1991). J. Biol. Chem. 266:9754–9763.PubMedGoogle Scholar
  15. 14.
    Darzins, A., Frantz, B., Vanags, R.I. and Chakrabarty, A.M. (1986). Gene 42:293–302.PubMedCrossRefGoogle Scholar
  16. 15.
    Deretic, V., Gill, J.F. and Chakrabarty, A.M. (1987). Nucleic Acid Res. 15:4567–4581.PubMedCrossRefGoogle Scholar
  17. 15a.
    Shinabarger, D., Berry, A., May, T.B., Rothmel, R., Fialho, A. and Charkrabarty, A.M. (1991). J. Biol. Chem. 266:2080–2088.PubMedGoogle Scholar
  18. 16.
    Roychoudhury, S., May, T.B., Gill J.F., Singh, S.K., Feingold, D.S. and Chakrabarty, A.M. (1989). J. Biol. Chem. 264:9380–9385.PubMedGoogle Scholar
  19. 17.
    DeVault, J.D., Berry, A., Misra, T.K., Darzins, A. and Chakrabarty, A.M. (1989). Bio/Technology 7:352–357.CrossRefGoogle Scholar
  20. 17a.
    Kato, J. and Chakrabarty, A.M. (1991). Proc. Natl. Acad. Sci. USA 88:1760–1764.PubMedCrossRefGoogle Scholar
  21. 18.
    Berry, A., DeVault, J.D. and Chakrabarty, A.M. (1989). J. Bacteriol. 171:2312–2317.PubMedGoogle Scholar
  22. 19.
    DeVault, J.D., Kimbara, K. and Chakrabarty, A.M. (1990). Molec. Microbiol. 4:737–745.CrossRefGoogle Scholar
  23. 20.
    Kimbara, K. and Chakrabarty, A.M. (1989). Biochem. Biophys. Res. Commun. 164:601–608.PubMedCrossRefGoogle Scholar
  24. 21.
    Sangodkar, U.M.X., Aldrich, T.L, Haugland, R.A., Johnson, J., Rothmel, R.K., Chapman, P.J. and Chakrabarty, A.M. (1989). Acta Biotechnol. 9:301–316.CrossRefGoogle Scholar
  25. 22.
    Ghosal, D., You, -I.S., Chatterjee, D.K. and Chakrabarty, A.M. (1985). Science 228:135–142.CrossRefGoogle Scholar
  26. 23.
    Frantz, B. and Chakrabarty, A.M. (1987). Proc. Natl. Acad. Sci. USA 84:4460–4464.PubMedCrossRefGoogle Scholar
  27. 24.
    Aldrich, T.L and Chakrabarty, A.M. (1988). J. Bacteriol. 170:1297–1304.PubMedGoogle Scholar
  28. 25.
    Rothmel, R.K., Aldrich, T.L, Houghton, J.E., Coco, W.M., Ornston, L.N. and Chakrabarty, A.M. (1990). J. Bacteriol. 172:922–931.PubMedGoogle Scholar
  29. 26.
    Rothmel, R.K., Haugland, R.A., Coco, W.M., Sangodkar, U.M.X. and Chakrabarty, A.M. (1989). In Recent Advances in Microbial Ecology (T. Hattori, Y. Ishida, Y. Maruyama, R.Y. Morita and A. Uchida, Eds.), Japan Scientific Societies Press, Tokyo, p. 605–610.Google Scholar
  30. 27.
    Schlomann, M., Pieper, D.H. and Knackmuss, H.-J. (1990).In: Pseudomonas: Biotransformations, Pathogenesis, and Evolving Biotechnology (S. Silver, A.M. Chakrabarty, B. Iglewski and S. Kaplan, Eds.), American Society for Microbiology, Washington, D.C., p.185–196.Google Scholar
  31. 28.
    Ghosal, D., You, -I.S., Chatterjee, D.K. and Chakrabarty, A.M. (1985). Proc. Natl. Acad. Sci. USA 82:1638–1642.PubMedCrossRefGoogle Scholar
  32. 29.
    Ghosal, D. and You, -I.S. (1989). Gene 83:225–232.PubMedCrossRefGoogle Scholar
  33. 30.
    Sangodkar, U.M.X., Chapman, P.J. and Chakrabarty, A.M. (1988). Gene 7l:267–277.CrossRefGoogle Scholar
  34. 31.
    Tomasek, P.H., Frantz, B, Sangodkar, U.M.X., Haugland, R.A. and Chakrabarty, A.M. (1989). Gene 76:227–238.PubMedCrossRefGoogle Scholar
  35. 32.
    Haugland, R.A., Sangodkar, U.M.X. and Chakrabarty, A.M. (1990). Mol. Gen. Genet. 220:222–228.PubMedCrossRefGoogle Scholar
  36. 33.
    Haugland, R.A., Sangodkar, U.M.X., Sferra, P.R. and Chakrabarty, A.M. (1991). Gene 100:65–73.PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1992

Authors and Affiliations

  • A. M. Chakrabarty
    • 1
  1. 1.Dept. of Microbiology & ImmunologyUniversity of Illinois College of MedicineChicagoUSA

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