effector-triggered immune signalling

[ValWood]

We found the term meaning "effector-triggered immunity /immune signalling "

GO:0009870 defense response signaling pathway, resistance gene-dependent Rename effector-triggered immune signaling (this is what the process is almost universally called) exact synonym defense response signaling pathway, resistance gene-dependent exact synonym effector-triggered immunity (this might be broad if these terms include the signalling + response) exact R-protein mediated resistance signaling ETI

current definition A series of molecular signals that depends upon R-genes and is activated during defense response. PMID:11418339

This isn't great because it doesn't define "R-genes"

Suggest A series of molecular signals generated when a microbe effector interacts with a "NTR: resistance gene receptor" (/see issues/18031), leading to the activation, perpetuation, or inhibition of an effector-triggered signalling involved in innate immunity. In plants, effector- triggered immunity is a second line of defense occuring after microbial "effector molecules" are translocated into the host in response to host PTI signaling.

Open questions: a) When people talks about an "immune response" are they referring to the signalling, or the responses/outcomes of the signalling? or both For signalling pathways we generally separate the signalling from the response, so I was wondering if we should always refer to these as "immunity" which seems to be what arises from the signaling or as"immune signalling pathway"

b) One definition we found says that pathogens are alerted to the effectors by the " associated damage caused by pathogenic toxins or effectors." We need to find if this is true?

[ValWood]

known responses to "effector-triggered immune signalling"

GO:0009626 plant-type hypersensitive response hypersensitive response (a type of programmed cell death) is main response to ETI (also transcription of ETI pathogen resistance genes (which are likely to be genes involved in HR?)

We propose to annotate this as "positive regulation of hypersensitive response"

Hypersensitive response readouts we came across so far localized cell death (hypersensitive response (HR), markers:

• DNA laddering, PMID:22241993 TAS
• heterochromatin condensation, PMID:22241993 TAS
• cell shrinkage, PMID:22241993 TAS
• Loss of plasma membrane integrity PMID:22241993 TAS
  • efflux of hydroxide and potassium outside the cells, and an influx of calcium and hydrogen ions into the cell (Q is this specific to PCD or also for PTI?)
  • lesions form (i.e cells die)

These makers also occur but are not specific to cell death (also occur in PTI)

• oxidative burst PMID:22241993 TAS
• accumulation of reactive oxygen species (ROS) PMID:22241993 TAS
  • accumulation of hydrogen peroxide PMID:22241993 TAS
  • also superoxide anions, hydroxyl radicals and nitrous oxide.

also (at PHIbase we would like to find out more about how these relate to the cell death)

• transcriptional induction of ETI related pathogenesis-resistance (PR) genes PMID:22241993 TAS (presumably PCD promoting genes)
• production of antimicrobial chemical compounds, PMID:22241993 TAS (What is the physiological relevance of this? are these death promoting compounds?)
• rapid and localized callose deposition PMID:22241993 TAS (how is this related to death, presumably stops pathogens spreading to live cells. So the dead plant cells presumably stay intact?

BUT Ros increase also occurs during PTI (These compounds affect cellular membrane function, in part by inducing lipid peroxidation and by causing lipid damage). We are assuming that either the molecules or their levels are different for PTI.

Question ~Note that the wikipedia article says that cell wall thickening is also an output of ETI. "Ros triggers deposition of lignin and callose, crosslinking of cell wall proteins. These compounds serve to reinforce the walls of cells surrounding the infection, creating a barrier and inhibiting the spread of the infection"
We think this is incorrect because we have only seen it as a readout of PTI. It doesn't really make sense that you could thicken the cell wall of a cell as you kill it... So it would be good to have examples of this if known.~

[ValWood]

I edited the above for clarity

Q Does anyone know of any other outputs of "ETI" than Hypersensitive response ? (not readouts, see above) In other words, does ETI have any other outcomes than cell death?

[ValWood]

Note that here we envisage that mainly receptors will be annotated. We aren't sure what constitutes the downstream signalling pathway. We will look for papers on this.

[ValWood]

GO:0052158 Ontology | biological_process Term name | modulation by symbiont of host resistance gene-dependent defense response

also means the same thing as GO:0009870 defense response signaling pathway, resistance gene-dependent

found with the synonym modulation by organism of host gene-for-gene resistance

(gene-for-gene resistance is ETI)

[ValWood]

Actually... The molecular basis of necrosis-induced ETS involving necrotrophic fungi is still largely unknown, but has in several cases exhibited the hallmarks of programmed cell death (PCD); DNA laddering, heterochromatin condensation, cell shrinkage, callose deposition and an oxidative burst [9,16,17].

So callose deposition is also a hallmark of necrosis effector-induced susceptibility and therefore presumably of ETI.

I will revise above accordingly later.

[ValWood]

other tickets cover the valid part of this. Mainly this term needs taxon restrictions. It isn't a great term, because its just describing a signalling pathway involved in the immune response and there are probably better terms.

I will check the annotations and address in a new ticket.

[ValWood]

replaced by GO:0009870 defense response signaling pathway, resistance gene-dependent #18312