Thesis title: Improved pathogen resistance in plants through on command release of pectin-derived damage-associated molecular patterns (DAMPs)
Recognition of endogenous molecules acting as “Damage-Associated Molecular
Patterns” (DAMPs) is a key feature in plant defense strategy. A well-known class of
DAMPs is made by Oligogalacturonides (OGs), cell wall fragments derived from the
degradation of the homogalacturonan. The interaction of microbial
Polygalacturonases (PGs) with plant-derived inhibitors (PGIPs) promotes the
accumulation of OGs in vivo. Transgenic Arabidopsis thaliana plants expressing an
inducible PGIP-PG chimera, named "OG machine" (OGM), have been generated,
allowing the release on command of OGs in planta. If the command persists plant
development is inhibited, reflecting a role of the OGs in the so-called growth-defense
“trade-off”. To genetically dissect the molecular mechanism involved in plant defense
against pathogens and the key aspects of the trade-off between development and
defense that takes place in response to the OGM action, plants expressing the OGM in
the defective mutant background of key elements involved in immunity have been
generated. One of the OGM phenotype, i.e. inhibition of the root growth, is totally
recovered in rbohDxOGM and jar1.1xOGM and partially recovered in eds1-2xOGM
double mutants. The compromised radical growth of the OGM is connected to an
altered root meristem, consisting of a decreased number of cells. In plants expressing
the OG-machine in an eds1-2, rbohD, or jar1.1 background, this meristematic defect is
not observed. Furthermore, I observed that OGM expressed in rbohD and eds1-2
mutant backgrounds leads to a higher resistance against the necrotrophic fungus
Botrytis cinerea. This resistance seems to be not dependent on ROS generated by
RBOHD, a membrane NADPH oxidase. The study of the transcriptome of OGM
expressing plants sheds light on the signaling pathways activated by the OGs.
Moreover, preliminary results suggest that OGs derived from OGM play a negative
role in grafting and tissue regeneration, probably antagonizing the auxin vascular
formation activity in wounding healing