5. VL Lipka Models 3/Preformed defense

• surface topography: cuticle (biopolymer of esterified alcohols, aldehydes, ketones, fatty acids)/ wax crystal layer

• cell wall: moncots and dicots have diffrent cell wall aritecture

• secondary metabolits (Phytoanticipins)

• The upper cuticle has a crystaline wax structure, which is recognised be the powdery mildew

• On the lower epidermis, the powdery mildew can not enter the amorphous sheets of waxes,

  —>In an experiment where the epicuticular wax was removed with chloroform, the powdery mildew was able to penetrate and build appressoria.

In common: Cellulose microfibril, Pectins,

Dicots: Xyloglucans, Extensins with Arabinosides,

Monocots: Glucoronoarabinoxylan, ß Glycans, phenolic network

Pathogens targeting only Monocots or only dicots bring different sets of Enzymes to hydrolyse the different cell wall compartments. Pathogen effectors interfere with vesicle transport of the plant cells

Phytoanticipins and phytoalexins are chemical defenses.

Phyroanticipins anticipate pathogen attack and are always in cell.

Phytoalexins are chemicals where the production is induces as a Defense response.

Examples

The effect is based on the compartimentalisation of myrosinase and glucosinolate.

The inactive glucosinolate is contained in the S-cell the myrosinase is contained in the idioblast. After physical mechanism : an insect that is chewing the plant. The enzyme and the glycosionolate are free and the myrosine hydroses the S-glycoslyic bond.

-> leads to toxic molecules

“Large White” caterpillars

They have a nitrile specifier proteins (NSP) in the digestive tract. ——>deactivates the isothiocyanates to nitrils

• hydrogen peroxide (H2O2)

• superoxide anion (O2.-)

• hydroxyl radical (OH.)

signaling function (secondary messenger) & cross-linking of cell wall carbohydrates, proteins and phenolics and/or direct toxic effect

The Arabidopsis NADPH oxidase AtRBOHD

Respepiratory Burst Oxidase Homolge

—> most essential is atrbohD

In Plasmamembrane, Transfers electrons from NADPH to O2

• 6 TM domains

Cell wall thickening. Local accumulation of different cell wall material: callose, cell wall carbohydrates, proteins

Upon fungal penetration, the cell monomerizes the actin filaments and microtubuli and repolymerizes them oriented towards the attempted entry site. These are used as a transport highway to move certain organells (nucleus, vesicles etc) to the entry site and react faster (eg faster transcription of response genes like PR genes)

many PR-proteins harbor hydrolytic activity suggesting that they are directed against microbial surface structures

- Mechanosensing

- Danger-associated Molecular Patterns (DAMPs)

- Pathogen/Microbe-associated Molecular Patterns (P/MAMPs)

PAMPs: Pathogen Associated Molecular Pattern. Plant senses non-self molecules (eG chitin or flagellin) and reacts with Defense mechanism

DAMPs: Danger Associated Molecular Pattern. Plant senses own degraded molecules (self-perception) that are freed upon pathogen infection, this induces Defense mechanism

Cytoplasmic reenrangements (moving of nucleus), ROS accumulation, some PR genes are induced (not all)

But No: cell wall reinforcement, hypersensitive cell death

Pattern Recognition Receptors (PRRs) mediate perception of pathogen/microbe associated molecular patterns. (PAMPS/Mamps)

There are two types:

• Receptor like Kinase RLK

• Receptor-Like Proteins (PLP)

Ectodomain: Ligand binding

Transmembrane domain: anchor (GPI-Anchor)

Only in Receptor like kinases (RLP): Ser/Thr protein Kinase domain: downstream signaling in cell

Lysin - Carbohydrates

• Cerk1 recognise chitin

Leucin - Peptide

• Flagellin is recognised by fls2

flg22 is a peptide (22 AA) that binds to the Leucin rich repeats (LRR) of FLS2 and is thereby recognised. flg22 is encoded in the conserved region of flagellin in almost all flagellated bacteria.

The exception: Rhizobium meliloti (symbiont) and agrobacterium tumorfaciens (pathogen) bacteria, closely related species, have changed the flagellum sequence to avoid immune detection

• FLS2: BAK1

• CERK1: LYK4+LYK5 —> no active kinase domians (phosphorylation inactive)

• in addition to the co-receptors: receptors-like cytoplasmic kinases (RLCKs)

• Receptors and co-receptors bind the ligand together (molecular glue model) —> close contact of the compontents is mediated

• this enables phosphrylation of kinase domains —> cytosolic kinases dissociate and activates downstream signaling

• downstream signaling of MAPK kinases phosphorylates and activates transcription factors (TF) —> expression of defence genes

• (additional receptor triggered early responses: Ca2+ influx, apoplast alkalinisation, local production of ROS)

1. PAMP (e.g. flg22) perception by PRR (FLS2 + BAK1)

2. complex is activated by kinase domain —> phosphorylation

3. recruitment + activation (by phosphorylation) BIK1

4. BIK1 + CPK (calcium dependent protein) phosphorylate + activate RBOHD (=NADPH oxidase) —> additional Ca2+ regulation

5. ROS production by RBOHD —> defense against pathogen

   
   

• controls transcritptional activation of defence genes (through phosphorylation)

  • e.g. TF WRKY and/or bZIP TF

• applies for both CERK1 and FLS2

• later, not so rapid response

flg22

chitin