MLO: a signal transduction component involved in fungal disease resistance and cell death protection

Pietro Piffanelli*, Ralph Panstruga §, Fasong Zhou, Catarina Casais¤, Alessandra Devoto¤, James Orme¤, Ulrich Schaffrath #, and Paul Schulze-Lefert §
* CIRAD-AMIS - Biotrop - Avenue Agropolis - Montpellier - France
¤ The Sainsbury Laboratory, John Innes Centre, Colney Lane, NR4 7UH Norwich, United Kingdom
# Rheinisch-Westfälische Technische Hochschule Aachen, Institut für Biologie III, Worringer
Weg 1, D-52074 Aachen, Germany
§ Max-Planck-Institut für Züchtungsforschung, Abteilung Biochemie, Carl-von-Linné-Weg 10, D-50829 Köln, Germany

Barley lines homozygous for mutant alleles (mlo) of the wild type Mlo gene confer broad-spectrum disease resistance to the biotrophic powdery mildew fungus, Bgh.
The resistance is manifested in the failure of the fungus to penetrate the epidermal cell wall, and at these sites cell wall remodelling and oxidative crosslinking processes lead to a fortification of the cell wall. Because mlo plants exhibit enhanced disease susceptibility to the hemibiotrophic fungal pathogen Magnaporthe grisea, the wild type gene must modulate defense responses to more than one species of pathogens in opposite directions.
Lack of the barley seven transmembrane MLO protein leads to potentiated defence upon attack of the fungal pathogen, Blumeria graminis f. sp. hordei (Bgh). Following Bgh attack, MLO dampens an early cell wall-restricted H2O2 burst in epidermal cells attacked first, blocks a late oxidative burst at subtending mesophyll cells, and protects the latter from executing cell death. Mlo expression is rapidly induced and coordinately regulated with the cellular protectant glutathione-S transferase in response to biotic or abiotic stress cues, thereby supporting a direct role of the wild type gene in stress protection. A paraquat-triggered endogenous oxidative burst was sufficient to stimulate MLO transcript upregulation. Mlo induction occurred also in pre-senescent leaves and lack of the wild type protein accelerated the senescence program by several days. Our data indicate a cell death protection function for MLO and imply shared cell death rescue mechanisms in leaf senescence and upon biotic stress.

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