6.VL PAMP/ETI

penetration

• pen gene products restrict pathogen entry at the cell periphery (from plant produced)

• deletion mutants show elevated penetration percentages by pathogens

• total three proteins: PEN1, PEN2, PEN3

  • PEN1: syntaxin (used for vesicle transports) —> polarised secretion

  • PEN2: glycoside hydrolase --> turns non-toxic form of glycsylic compounds into toxic compounds

  • PEN3: ABC-transporter —> ATP-dependent secretion of toxic compounds, poisons pathogen outside of cell

PEN1 controls vesicle fusions at sites of attempted fungal invasion

• PEN1 (Qa SNARE) in closed conformation (4 helices, anchored by hydrophilic domain in plasmamembrane)

• pathogen attack: protein accumulation

• active conformational changes —> interaction with another SNARE protein

• vesicle tagged with R-SNARE —> vesicle transported to PEN1 —> fusion —> cargo release at fungal penetraton site (cargo = glycosylated proteins, polysaccharides from Golgi)

• component recycling

• process causes accumulation of cell wall material (callose, cell wall carbohydrates, proteins) at invasion site

Cellulose: beta-1,4-linkeage of glucose (cell wall compound)

Callose: beta-1,3-linkeage of glucose —> results in a linear molecule (cell division, wounds)

• pmr4=powdery mildew resistance

• harbour mutations in callose synthase gene GSL5 (=glucan synthase-like 5) —> stop codon and t-DNA insertion in putative catalytic region (responsible for polymerization

• pmr4/gsl5 mutants produce less callose with the same amount of cell wall material at penetration sites

• show enhanced resistance to adapted powdery mildew attack!!

—> expectation would be that it has lower resistance because it can’t produce callose (or fewer amounts)

• higher resistance because mutation results in hyper-induction of pathogen- and SA-induced genes —> constitutive expression of resistance genes also in non-infected plants

• enhanced hypersensitive cell death (micro lesions) —> powdery mildew is biotrophic, needs living cells

• smaller plants —> higher energy need through constitutive expression

The hypersensitive response (HR) is a defensive response. Infected cells and adjacent cells are killed through programmed cell death (PCD). The number of cells undergoing an HR is usually kept to a (necessary) minimum.

• species, race, strain specific

• secreted by fungi and oomycetes targeted to apoplast or cytoplasm

• contribute to pathogen virulence by targeting plant defences

Secretion pathways:

1. conventional ER-Golgi secretory route: ER —> Golgi —> Vesicle transport —> exo- + endocytosis

2. unconventional ER-dependent and Golgi independet route: formation of BIC (=biotrophic interfacial complex)

3. unconventional MVB(=Multivesicular body)-dependent route: for larger cargos

Apoplast = space between plasma membrane and pathogen

• plants and fungus secrete enzymes that harm each other

  • fungus: pectinases

  • plants: PR proteins, glucanases, chitinases, pectinases

    
    

• biotrophic pathogens secrete less amounts of cell wall hydrolyzing enzymes (cellulases, hemicellulases, etc.) to limit cell damage (needs host alive) and to avoid triggering host immunity response; have no polysaccharide lyase enzyme!!

• hemibiotrophic/necrotrophic pathogens have more and more diverse cell wall degrading enzymes + have polysaccharide lyases (cleave different forms of pectins)

• pathogens secrete enzyme inhibitors to counteract plant hydrolases

• glucanase inhibitor protein (GIP1) from oomycete Phytophora sojae targets soybean EGaseA (endo-beta-1,3-glucanases)

• effectors target plant peroxidases which interferes with ROS generation, Peroxidase inhibitor (Pep1) of U. maydis