Invisible signals from the underground: bacterial volatiles elicit plant growth promotion and induce systemic resistance

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Title
Invisible signals from the underground: bacterial volatiles elicit plant growth promotion and induce systemic resistance
Author(s)
Choong-Min Ryu; M A Farag; P W Pare; J W Kloepper
Bibliographic Citation
Plant Pathology, vol. 21, no. 1, pp. 7-12
Publication Year
2005
Abstract
Plant growth-promoting rhizobacteria (PGPR) are a wide range of root-colonizing bacteria with the capacity to enhance plant growth and control plant pathogens. Here we review recent progress that indicate some PGPR strains release a blend of volatile organic compounds (VOCs) that promote growth in Arabidopsis seedlings and induce resistance against Erwinia carotovora subsp. carotovora. In particular, the volatile components 2,3-butanediol and acetoin released exclusively from the PGPR strains triggered the greatest level of growth promotion and induced systemic resistance. Pharmacological applications of 2,3-butanediol promoted the plant growth and induced resistance, while bacterial mutants blocked in 2,3-butanediol and acetoin synthesis was devoid of growth-promotion and induced resistance capacities. The results suggested that the bacterial VOCs play a critical role in the plant growth promotion and induced resistance by PGPR. Using transgenic and mutant lines of Arabidopsis, we provide evidences that the signal pathway activated by volatiles from one PGPR strain is dependent on cytokinin activation for growth promotion and dependent on an ethylene-signaling pathway for induced pathogen resistance. This discovery provides new insight into the role of bacterial VOCs as initiators of both plant growth promotion and defense responses in plants.
Keyword
PGPRvolatile organic compoundsinduced systemic resistancebacterial volatiles
ISSN
0032-0862
Publisher
Wiley
DOI
http://dx.doi.org/10.5423/PPJ.2005.21.1.007
Type
Article
Appears in Collections:
Division of Research on National Challenges > Infectious Disease Research Center > 1. Journal Articles
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