1. host of origin haplotype resistance gene Couch et al. 2005

2. Magnaporthe oryzae

3. positive regulation negative regulation heterotrimeric G protein dissociation X receptor + adenyl cyclase MAPK factor transcription MAPK stage of development signal protein kinase Signaling on the leaf surface

4. spore tip mucilage Howard and Valent 1996

5. Reintroduction of MPG1 restores pathogenicity, appressorium development and cell surface hydrophobicity Cosegregation of the appressorium deficiency phenotype with the mpg1::Hph deletion allele. WT mpg1- hygR hygS mpg1-;hygR MPG1-;hygS WT MPG1+ mpg1- MPG1 directs formation of the hydrophobic rodlet layer of conidia. WT mpg1-

6. Importance of melanized appressoria Howard, R

7. albino melanin WT chitin appressorium pore Howard and Valent 1996

8. Dean et al, 2005 Penetration and invasion penetration site

9. melanin biosynthesis Howard and Valent 1996

10. appressorium conidium germ tube Collapse high concentration of non-permeable solute sonicated cells Howard and Valent 1996

11. Appressoria build turgor during incubation Howard et al., 1991

12. WTmutants homeodomain Zn finger Park et al. 2004 The transcription factor MST1 is important for penetration peg formation

13. From Park et al 2004 appressoria can form WT mst1- can’t penetrate no peg The transcription factor MST1 is important for penetration peg formation

14. Lauge and de Wit 1998 and others AVR-Pi-ta four Avr genes; Avr2, Avr4, Avr4E and Avr9 four extracellular protein (Ecp) genes; Ecp1, Ecp2, Ecp4 and Ecp5). Fungal avirulence genes

15. Fig. 3. AVR-Pita 176 is an elicitor. (A) AVR-Pita polypeptides tested in the transient assay. The white region indicates the putative secretory signal sequence, the gray region indicates the putative pro-protein domain and the hatched region indicates the putative protease motif. The black region indicates the putative mature protein. The number of amino acids missing from the N-terminus is indicated. GUS activity is indicated by ‘+’, whereas decreased GUS activity is indicated by ‘–’. (B) Representative rice seedlings showing GUS activity. Two-leaf Pi-ta (Yashiro-mochi and YT14) and pi-ta (Nipponbare and YT16) seedlings were co-bombarded with 35S/Adh1-6::AVR-Pita 176 and 35S::uidA. Leaves were assayed histochemically for GUS activity and cleared in 70% ethanol to visualize GUS staining. (C) RNA gel blot analysis of AVR-Pita expression in the transient assay. YT14 (Pi-ta) and YT16 (pi-ta) were co-bombarded with the 35S/Adh1-6::AVR-Pita 176 and 35S::uidA plasmids. Leaf tissue was harvested 2 days after bombardment. Poly(A) + mRNA was then extracted, blotted to Hybond-N and hybridized with a radiolabeled AVR-Pita 176 probe. The AVR-Pita transcript is indicated. Similar loading was verified before blotting by visualizing mRNA in the gel stained with ethidium bromide. Fig. 2. Genotype-specific HR in rice seedlings induced by M.grisea carrying AVR-Pita. Sparse HR flecking is seen in Pi-ta- containing rice seedlings (A) Yashiro-mochi and (B) YT14, as expected. In contrast, typical symptoms of rice blast disease are seen in susceptible rice seedlings (C) Nipponbare and (D) YT16. Representative leaves are shown from rice seedlings germinated in plant nutrient medium and infected with avirulent M.grisea strain 4360-R-62 (see Materials and methods for details). Shown at 4 days after inoculation Jia et al. 2000 YMYT14NiYT16 pi-taPi-ta Intracellular (metalloprotease) direct interaction with Pi-ta Pi-ta dependent resistance response M. oryzae Pi-ta / AVR-Pi-ta Genotype specific response resistant susceptible

16. a−c, GFP-tagged M. grisea (Guy11) forms classical appressoria (AP) on a hydrophobic surface (a) and simple hyphopodia (HY) and infection pegs (IP) on rice roots (cultivar CO39) (b, c). d−k, Guy11- infected barley (d, e, j, k) and rice (f−i) roots stained with chlorazole black E showing: dark runner hyphae (RH) and simple hyphopodia (d, e); bulbous infection hyphae invading epidermal cells (f); microsclerotia (previously reported in culture). Scale bar, 25 µm. Magnaporthe oryzae is also a root pathogen Sesma and Osbourn roots Sesma and Osbourn hydrophobic surface

17. Sesma and Osbourn Pigment and cAMP are not required a, Roots of barley seedlings (cultivar Golden Promise) that have been mock-inoculated or infected with the M. grisea wild type (WT) or mutant (mel, cpkA) strains. b, Formation of hyphopodia-like structures (HY) and invasive growth within epidermal cells during the early stages of infection. Scale bars, 25 µm (b), 40 µm (c). albino cAMP- albino cAMP-

18. Roots of barley seedlings (cultivar Golden Promise) that have been mock-inoculated or infected with the M. grisea wild type (WT) strain.. c, M. grisea penetrates the stele. Confocal imaging of radial and longitudinal sections of a three-week-old rice seedling (cultivar Nipponbare) infected with GFP-tagged M. grisea (strain Guy11). Scale bars, 25 µm (b), 40 µm (c). M. oryzae can move systemically from roots to leaves Sesma and Osbourn

19. a−c, Four-week-old root-infected rice seedlings (cultivar Nipponbare) showing disease symptoms on the leaf (upper box) and collar (lower box) (a). Disease symptoms on the collar (b) and stem (c) with confocal images showing GFP- expressing M. grisea Guy11 in the diseased areas and also in the vascular tissue of the leaf and stem. d−f, Pi-CO39(t)-mediated specific disease resistance operates in rice roots. Confocal microscopy of compatible (d, e) and incompatible (f) interactions. Cultivar, cv. Scale bar, 40 µm. Sesma and Osbourn M. oryzae can move systemically from roots to leaves Pi-CO39(t)- mediated specific disease resistance operates in rice roots