host of origin haplotype resistance gene couch et al. 2005

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Page 1: Host of origin haplotype resistance gene Couch et al. 2005

host of originhaplotype resistance gene

Couch et al. 2005

Page 2: Host of origin haplotype resistance gene Couch et al. 2005

Magnaporthe oryzae

Page 3: Host of origin haplotype resistance gene Couch et al. 2005

positive regulation negative regulation

heterotrimeric G protein dissociation

Xreceptor

+adenyl cyclase

MAPK

factortranscription

MAPK

stage ofdevelopment signal

protein kinase

Signaling on the leaf surface

Page 4: Host of origin haplotype resistance gene Couch et al. 2005

spore tip mucilage

Howard and Valent 1996

Page 5: Host of origin haplotype resistance gene Couch et al. 2005

Reintroduction of MPG1 restores pathogenicity, appressorium development and cell surface hydrophobicity

Cosegregation of the appressorium deficiency phenotype with the mpg1::Hph deletion allele.

WTmpg1-

hygR

hygR

hygS

hygS

mpg1-;hygR MPG1-;hygS

WTMPG1+ MPG1+

mpg1-

MPG1 directs formation of the hydrophobic rodlet layer of conidia.

WT mpg1-

Page 6: Host of origin haplotype resistance gene Couch et al. 2005

Importance of melanized appressoria

Howard, R

Page 7: Host of origin haplotype resistance gene Couch et al. 2005

albino

melanin

WTchitin

appressorium pore

Howard and Valent 1996

Page 8: Host of origin haplotype resistance gene Couch et al. 2005

Dean et al, 2005

Penetration and invasion

penetration site

Page 9: Host of origin haplotype resistance gene Couch et al. 2005

melanin biosynthesis

Howard and Valent 1996

Page 10: Host of origin haplotype resistance gene Couch et al. 2005

appressorium

conidium

germ tube

Collapse

high concentration of non-permeable solute

sonicated cells

Howard and Valent 1996

Page 11: Host of origin haplotype resistance gene Couch et al. 2005

Appressoria build turgor during incubation

Howard et al., 1991

Page 12: Host of origin haplotype resistance gene Couch et al. 2005

WT mutants

homeodomain Zn finger

Park et al. 2004

The transcription factor MST1 is important for penetration peg formation

Page 13: Host of origin haplotype resistance gene Couch et al. 2005

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

Page 14: Host of origin haplotype resistance gene Couch et al. 2005

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

Page 15: Host of origin haplotype resistance gene Couch et al. 2005

Fig. 3. AVR-Pita176 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-Pita176 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-Pita176 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-Pita176 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

Jia et al. 2000

YM YT14 Ni YT16

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

Page 16: Host of origin haplotype resistance gene Couch et al. 2005

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

Page 17: Host of origin haplotype resistance gene Couch et al. 2005

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-

Page 18: Host of origin haplotype resistance gene Couch et al. 2005

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

Page 19: Host of origin haplotype resistance gene Couch et al. 2005

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