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Published on: December 21, 2011
Lipo-chitooligosaccharide signalling blocks a rapid pathogen-induced ROS burst without impeding immunity
Thomas Rey1, Olivier André1, Amaury Nars1
1Laboratoire de Recherche en Sciences Végétales, Université de Toulouse, CNRS, UPS, 24 chemin de Borde Rouge, Auzeville, BP42617, 31326, Castanet Tolosan, France.
Plant symbiosis signals, lipo-chitooligosaccharides (LCOs), inhibit pathogen-induced reactive oxygen species (ROS) bursts. This allows symbiosis while maintaining plant defense mechanisms against pathogens.
Area of Science:
- Plant-microbe interactions
- Molecular plant pathology
- Plant symbiosis
Background:
- Microbial signals at plant surfaces dictate host immunity or symbiosis.
- Lipo-chitooligosaccharides (LCOs) from symbionts initiate symbiotic programs.
- Pathogen perception typically triggers reactive oxygen species (ROS) bursts and defense gene expression.
Purpose of the Study:
- Investigate the cross-talk between symbiotic and pathogenic signals in Medicago truncatula.
- Determine how LCO perception affects the plant's response to pathogen-associated molecular patterns.
- Elucidate the role of ROS in mediating plant responses to coincident microbial signals.
Main Methods:
- Incubation of Medicago truncatula seedlings with Aphanomyces euteiches culture filtrate (CF) and Sinorhizobium meliloti LCOs.
- Measurement of ROS release in response to microbial signals.
- Analysis of immunity-associated gene expression and disease resistance.
Main Results:
- Simultaneous or sequential application of CF and LCOs resulted in a strong ROS release.
- Pre-incubation with LCOs completely inhibited CF-induced ROS release.
- LCO treatment did not affect the expression of immunity-associated genes or disease resistance to A. euteiches.
Conclusions:
- Medicago truncatula evolved a ROS inhibition response to LCOs, facilitating symbiosis.
- This ROS inhibition allows for the establishment of symbiosis without compromising existing defense mechanisms.
- Plants can concurrently manage symbiotic and defense pathways through differential regulation of ROS.
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