Targeting conserved effectors and effector motifs for broad spectrum resistance against oomycetes and fungi

• Published in: Phytopathology 2010-06, Vol.100 (6), p.S158-S158
• Main Authors: Tyler, B M, Kale, S D, Gu, B, Capelluto, D G, Dou, D, Arredondo, F, Deb, D, Anderson, R, Antigliani, V, Fudal, I, Rouxel, T, McDowell, J, Lawrence, C, Shan, W
• Format: Article
• Language: English
• Subjects: Oomycetes
• ISSN: 0031-949X

Fungal and oomycete pathogens of both plants and animals produce effectors and/or toxins that act within the cytoplasm of host cells to suppress host efenses and cause disease. Effector proteins of oomycete plant pathogens utilize an N-terminal motif, RXLR, to enter host cells. Genome sequences of oomycete pathogens have revealed hundreds of RXLR effectors. Most of these are rapidly evolving, but a small number are highly conserved, suggesting they may be good targets for broad-spectrum R genes. By detailed mutagenesis of oomycete RXLR motifs, we defined a new bioinformatic model for these motifs and used it to identify candidate RXLR-like motifs in fungal effectors. Several of these motifs were then confirmed experimentally to be responsible for cell entry by these effectors. We have found that both oomycete and fungal RXLR(-like) motifs are responsible for binding of the effectors to phosphatidyl-inositol-3-phosphate (PI-3-P). Using this information, we have succeeded in blocking entry of oomycete and fungal effectors into host cells by using the head-group mimic inositol-1,3-diphosphate or by using PI-3-P-binding proteins. These findings suggests that agrochemicals that mimic inositol-1,3-diphosphate, or transgenes that encode secreted PI-3-P binding proteins, may confer broad-spectrum protection against oomycete and fungal infection.