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Applied and Environmental Microbiology, December 2000, p. 5340-5347, Vol. 66, No. 12
Department of Plant Pathology, Cornell
University, Ithaca, New York 14853-4203
Received 15 May 2000/Accepted 25 September 2000
Interactions between plant-associated microorganisms play important
roles in suppressing plant diseases and enhancing plant growth and
development. While competition between plant-associated bacteria and
plant pathogens has long been thought to be an important means of
suppressing plant diseases microbiologically, unequivocal evidence
supporting such a mechanism has been lacking. We present evidence here
that competition for plant-derived unsaturated long-chain fatty acids
between the biological control bacterium Enterobacter cloacae and the seed-rotting oomycete, Pythium
ultimum, results in disease suppression. Since fatty acids from
seeds and roots are required to elicit germination responses of
P. ultimum, we generated mutants of E. cloacae
to evaluate the role of E. cloacae fatty acid metabolism on
the suppression of Pythium sporangium germination and
subsequent plant infection. Two mutants of E. cloacae
EcCT-501R3, Ec31 (fadB) and EcL1 (fadL), were
reduced in
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Copyright © 2000, American Society for Microbiology. All rights reserved.
Fatty Acid Competition as a Mechanism by Which
Enterobacter cloacae Suppresses Pythium
ultimum Sporangium Germination and Damping-Off
and
-oxidation and fatty acid uptake, respectively. Both
strains failed to metabolize linoleic acid, to inactivate the
germination-stimulating activity of cottonseed exudate and linoleic
acid, and to suppress Pythium seed rot in cotton seedling
bioassays. Subclones containing fadBA or fadL
complemented each of these phenotypes in Ec31 and EcL1, respectively.
These data provide strong evidence for a competitive exclusion
mechanism for the biological control of P. ultimum-incited seed infections by E. cloacae where E. cloacae
prevents the germination of P. ultimum sporangia by the
efficient metabolism of fatty acid components of seed exudate and thus
prevents seed infections.
*
Corresponding author. Mailing address: Department of
Plant Pathology, Cornell University, 334 Plant Science Bldg., Ithaca, NY 14853-4203. Phone: (607) 255-7841. Fax: (607) 255-4471. E-mail: ebn1{at}cornell.edu.
Present address: Department of Plant Pathology, University of
Nebraska, Lincoln, NE 68588-0665.
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