10. VL Corinna Jamonic acid

A new oat cultivar was bred that was resistant against the biotrophic fungus Puccinia coronata, by inducing HR upon detection.

By chance, this variety was very succeptible against the necrotrophic fungus Cochliobolus victoriae, as necrotrophs live off dead tissue. Cochliobolus victoriae hijacks this oat cultivars Programmed cell death mechanism.

The same locus that causes resistance against biotroph (PC-2) causes succeptibility against nectrotroph (VB).

Necrotrophic fungi benefit of the recognition of the pathogen by the plant.

Here: Victorin C mimics a biotrophic effector, to be recognized and induce cell death in plant. (normaly effective against biotrophs, but feeds necrotroph)

LOV1 senses if TRXh5 is reduced

example for guard model recognition

• LOV encondes an CC-NBS-LRR protein (CNL!)

• LOV recognizes Victorin (via TRXh5) —> leads to programmed cell death

• Vb locus encodes LOV? (not sure, assumption from jessi)

JA is a plant hormone derived from linolenic acid

Production is induces locally and systemically upon tissue wounding

It is a defense hormone and activates the plant immune system

hemibitrophs: effectors suppress PTI and manipulate host metabolism

necrotrophs: effectors suppress PTI but want to be recognized to induce HR

SA: biotrophic defense —> local cell damage

JA/ET: necrotrophic —> avoid cell damage, activate cellular repair mechanisms, inactivate/export fungal toxins

JA is derived from linolenic acid, which has 18 carbons (18:3)

The pathway starts in the chloroplast, and three rounds of beta-oxidation take place

In each oxidation, the fatty acid is reduced by two carbons

If there are C16 fatty acids, only two ß-oxidation are needed

• lipoxygenase

• reaction: linolenic acid —> 13(S)-hydroxyperoxy-octadecatrienoic acid (13-HPOT)

Eselsbrücke: Lachs —> Hotpot—>Ausmachen—>Autsch (zu heiß) —> OPDA (Ob das heiß ist?) —-> Put in JAR

Short answer:

Chloroplast: LOX, AOS, AOC

Peroxisome: OPR3

Cytoplasm: JAR1

Long answer:

LOX (lipoxygenase): Chloroplast. Linolelic acid (FFA) is transported from the membrane to the chloroplast, where LOX adds molecular oxygen at C13, resulting in 13-HPOT

AOS (Allene oxide synthase): Chloroplast. dehydrates 13-HPOT to form an unstable allene epoxide

AOC (Allene oxide cyclase): Chloroplast. The unstable epoxide is converted to OPDA (12-oxophytodienoic acid) by AOC

OPR3(OPDA reductase): Peroxisome. Reduced OPDA. Then 3 cycles of ß-oxidation to receive C12 from C18

JAR1: Cytoplasm. Facilitates the formation of Hormone-amino acid formation (JA-Ile is the active form of the hormone)

Perception of JA leads to growth inhibition.

coi1: COI1 receptor for JA. KO of receptor —> no sensing, long roots with JA in media

jar1: “JA resistant” mutant, JAR1 is responsible for forming JA-Ile. jar1 is a biosythesis, not a signaling mutant—> short root with JA in media

Coronatine insensitive 1. Coronatine is a bacterial compound (Psm) mimicking JA in plants. Biotrophic Pseudomonas strains produce coronatine to trigger the inhibition of SA responses.

Coi1 is insensitive to coronatine and MeJA

Coi1 is more susceptible to necrotrophic pathogens (no defense cascade because no reaction to JA, no JA signaling, no PDF1.2 activation)

JAZ3 (Jasmonate ZIM Domain) is the substrate of COI1 and a repressor of JA signaling

JAZ proteins are redundant (13 proteins are encoded in the genome) ––> Knock-out mutation of one of the JAZs does not affect JA response

coi1: cannot degrade JAZ proteins, and JA signaling is suppressed

jar1: cannot conjugate JA with isoleucine to the active form

jai3/jaz3: JAZ3 is a repressor of JA signaling and is usually degraded by COI1. in the jaz3 mutant, JAZ3 is truncated (shortened) and can no longer be degraded by COI1, leading to permanent JA signal repression

jin1: has a mutation affecting the myc2 transcription factor (no JA-responsive gene expression)

• E3 ubiquitin ligase complex ubiquitinates specific substrates. COI1 is the F-box (domain of E3-ligase) and targets a substrate (JAZ3)

• ubiquitination by the E3 ligase leads to degradation of the substrate via the 26S proteasome

Keep in mind that the Jas domain is required for interaction with COI1 and for interaction with MYC2. The ZIM domain mediates the dimerization of the protein.

Dominant negative mutations => Have an altered gene product that acts antagonistically to the wildtype allele

––> In this case, WT: no gene expression; dominant negative effect: gene expression

(The Jas domain facilitates interactions with COI1; the protein cannot be degraded without it)

The Jas domain is also required for interaction with MYC2; gene expression cannot be inhibited without it ––> If JAZ lacks the Jas domain, it can no longer inhibit the gene expression leading to a dominant negative effect

MYC2 is a transcription factor activating the transcripiton of JA pathways

It can be inhibited by binding of JAZ, which is usually degraded by COI1

PDF1.2 transcription requires the TF ORA. ORA transcription is activated by TF EIN. EIN is stabilised by Ethylene.

JAZ blocks the transcription factor EIN, unless it is degraded by COI1, which requires JA.

• MYC2 TF for defense genes against insects (only JA required)

• EIN3 TF for genes for defense against necrotrophic fungi (both JA + ehtylene required)

• JA releases suppression of MYC2 and EIN3 —> activation

• ethylene activates only EIN3

EIN3 is a transcription factor for Ethylene response

It activates the transcription of the secondary TF ORA, which in turn activates PDF1.2 transcription.

It can be inhibited by JAZ, which is usually degraded by COI1