PAMGO Hypersensitive Response

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See this SF item for response from TAIR:

https://sourceforge.net/tracker/?func=detail&atid=440764&aid=1524725&group_id=36855

Marcus

I think Donghui Li’s thoughts (from the link above) on PCD and HR make it clear that [in plants] PCD comprises both developmentally-related forms of cell death and cell death in response to a pathogen. In this light, even if mechanisms underlying HR are not distinct from those of PCD (and the distinction is therefore artificial), I see HR as a useful narrower child term to capture the context of PCD as response to a pathogen. Therefore, I agree with Donghui that the terms should not be merged, and I offer further justification for not merging the terms.

What would happen if host cells were induced to die in response to a non-pathogenic symbiont, e.g. a case of non-HR PCD in response to an organism? It would be interesting to capture this information as distinct from HR type PCD. I found an interesting paper abstract (PMID: 16946237) that documents symbiont-induced apoptosis during light organ formation in the squid Euprymna scolopes by the marine luminous bacterium Vibrio fischeri. I think it would be interesting to capture this case of non-HR PCD induced by another organism as distinct from HR PCD.

Currently there is no term for apoptosis induced by another organism (that I could find), with the exception of virus-infected cell apoptosis (GO:0006926). Although “induction of apoptosis by extracellular signals” (GO:0008624) is a possibility, all its children appear to be endogenous factors such as hormones, and I want to capture that another organism is causing the phenomenon. Perhaps killing of host cells (GO:0001907) would be the best term to use since it is under the IBO node (GO:0051704), but its definition is “any process mediated by an organism that results in the death of cells in the host organism…” In the case of the Euprymna-Vibrio interaction, although host PCD is triggered by a symbiont-induced signal, the killing is done via pathways endogenous to the host. That term is inappropriate for the same reason that it would be to characterize HR.

I believe we should create a new term “symbiont-induced programmed cell death” as a child of programmed cell death. We could move hypersensitive response from its current position as a child of programmed cell death to a child of the new term. We could create a new sibling for HR called “programmed cell death induced by non-pathogen symbiont.” This would allow us clearly to draw the distinction between PCD as a response to a pathogen and PCD as part of a beneficial symbiotic interaction. If HR had been merged upward into PCD, this distinction between symbiont-induced PCD and pathogen-specific PCD would not be possible. Furthermore, if a case arises where it is unclear whether PCD in a host that is induced by a symbiont is “harmful” or “beneficial” (as I imagine would happen sometimes), that case could be annotated to the new parent term “symbiont-induced programmed cell death.”

  • programmed cell death (PCD) GO:0012501, Definition: Cell death resulting from activation of endogenous cellular processes.
    • symbiont-induced programmed cell death GO:XXXXXXX, Definition: Cell death in a host resulting from activation of endogenous cellular processes after direct or indirect interaction with a symbiont. Comment: An example of direct interaction is penetration by hyphae, and examples of indirect interaction include encounter with secreted enzyme and interaction with MAMP such as cell wall fragment.
      • hypersensitive response (HR) GO:0009626, Definition: The rapid death of plant cells in response to invasion by a pathogen.
      • programmed cell death induced by non-pathogen symbiont GO:XXXXXXX, Definition: Cell death in a host resulting from activation of endogenous cellular processes after direct or indirect interaction with a non-pathogenic symbiont. Comment: This includes interactions typically viewed as beneficial from the perspective of the host, such as luminous bacteria in the light organs of marine squid.

==

Trudy

I agree with Donghui Li and Marcus that HR should not be merged with PCD. In addition to the reasons that both Donghui Li and Marcus present, it has not been conclusively shown that these two phenomena are the same. Infact most papers refer to HR as a type of PCD.

I am still thinking through Marcus’s response on creating the term "programmed cell death induced by non-pathogen symbiont GO:XXXXXXX" as I am not sure the use of the term non-pathogen is appropriate in light of the way PAMGO defines symbiosis.... All the same, I thought of throwing in this bit about apoptosis so we can consider it whilst working on the PCD/HR node. Apoptosis is referred to as a type of PCD (can be found in GO defn of apoptosis GO:0006915) and HR is also sometimes said to be a type of apoptosis (see below)


Eur. J. Biochem. 267, 5078-5084 (2000) Apoptosis (programmed cell death) is a ubiquitous active process that occurs during development and in response to environmental stimuli. Apoptosis has been dAescribed in animal cells in great detail at the morphological, biochemical and genetic levels [1-3]. In plants, apoptosis has been associated with various phases of development and senescence [4,5], germination [6], response to salt stress [7] or cold [8]. A particularly interesting type of apoptosis has been observed during the plant response to pathogen attack, and was termed ‘hypersensitive response’ (HR) [5,9]. Signal transduction pathways are activated during HR, leading to biosynthesis or release of potential anti-microbial effector molecules, which are thought to contribute to both host and pathogen cell death [5,9]. The molecular mechanism of plant apoptosis and HR are being disclosed, and involve small GTP-binding proteins [10], arabinogalactan proteins [11], subcellular reorganization of mitochondria [12], Rubisco proteases [13], mannose-inducible endonucleases [14] and Bax [15]. Among other signals, rapid generation of reactive oxygen species has been implicated in HR of plants against pathogens [16-18]. In particular, hydrogen peroxide (H2O2) has been shown to be a crucial component of the HR control circuit, to such an extent that a short pulse of exogenous H2O2 is sufficient to activate the hypersensitive cell death programme [19,20]. Reactive oxygen species, H2O2 and lipid peroxides have been long considered crucial elements of apoptosis in animals [21,22]. More recently, the peroxides produced by lipoxygenase activity have received attention as mediators of apoptosis in animal cells [23-27]. Remarkably, lipoxygenase-dependent pathways are implicated also in plant response to abiotic stress [28] and development of HR [29]. Lentil (Lens culinaris), a member of the Fabaceae, is an annual legume crop of nutritional quality higher than that of cereals, meat and fish, and is severely affected by pathogens [30]. Lentil seedlings contain different lipoxygenase (LOX) isozymes and we have characterized [31], cloned [32] and expressed in Escherichia coli [33] the isozyme most abundant in shoots. Lentil roots contain a different LOX, which shares several properties (e.g. molecular weight, pH optimum, substrate specificity) with the shoot enzyme and is recognized by the same monoclonal antibodies [34,35]. Therefore, lentil root cells were chosen to investigate the possible role of the lipoxygenase pathway in plant response to oxidative stress by exogenous H2O2.

Do we need to incorporate apoptosis in the PCD hierarchy as well?


Candace

I’m sending more comments in response to the SourceForge item #1524725: merge hypersenstive response with programmed cell death.

I have read the comments of Donghui (TAIR), and Marcus and Trudy (PAMGO -- http://wiki.geneontology.org/index.php/Talk:PAMGO_work_in_progress#Hypersensitive_response), and also looked at some more papers. First, I want to say that I am trying to comment from the perspective of what I understand to be the guiding principles of PAMGO from the beginning---that we try to create terms that will be useful to annotate both prokaryotes and eukaryotes, pathogens as well as mutualists, and animals as well as plants. One of our ideas was that we hoped, through the use of GO, to be able to learn things we did not know before (in addition to creating knowledge through annotating the genes in our organisms). You all know the history of the desire for a term that we could use to annotate genes in our pathogens whose gene products were shown to play a role in inducing the endogenous process of PCD in plant cells during pathogen attack. I understand that there are two (at least) quite different types of PCD in both plants and animals---a PCD that is developmental (turned on by the plant or animal itself) and one caused by another organism (like a pathogen or a non-pathogenic symbiont, as described by Marcus). The important concept here seems to be that we need a term that differentiates those, but one that also captures an important process that occurs in both plant and animal cells under attack. I like Marcus’s proposal of a term “symbiont-induced programmed cell death” – this seems perfect for our needs, and it can be used by both animal and plant people. I personally would prefer that we make the term “hypersensitive response” a synonym to that term, so plant people can easily find the appropriate GO term, and also so that we have a broad term that will work for both plant and animal people. I think the Pseudomonas people would like to have a home where the secreted effectors of both the plant pathogenic pseudomonads and Yersinia, the animal pathogen, reside. It seems to me that most papers I have looked (e.g. PMID: 11755421) that talk about PCD induced by animal pathogens, like Salmonella, call it PCD because that is what it appears to be – a process that at the moment can be distinguished from development PCD only by what was the stimulus that started it (i.e. a pathogen in this case). If it becomes clear that the HR in plants is conceptually and biologically different from the PCD that is a normal part of development, like the formation of phloem cells, then at that time it seems that a distinguishing term, HR, is appropriate. For right now, it appears to me that that term would be confusing to the greater biological world as a whole, because the term “hypersensitive” means something quite different in the animal pathogen world. I would like to see GO terms developed that whenever possible speak to the unity across plants and animals (if possible, of course), rather than using terms that might artificially create a difference when there might be none, and which have very different meanings in the 2 worlds. So---and sorry that is such a long-winded comment---that’s my concern about having a separate term – HR – for what seems to be symbiont-induced PCD, specifically in plants. Is that term necessary? Again, if the HR in plants is biologically different in important ways from the process of symbiont-induced PCD in animal cells, then it’s fine – so long as both terms – separate ones for plants and animals – have a common parent in the GO trees so we can use GO to find genes products we did not know existed, but that do similar things in 2 quite different hosts – plants and animals.

Also in line with the early guiding principles of PAMGO, and I think also of GO in general (re: Alex Diehl), I do not think the proposed term “programmed cell death induced by non-pathogen symbiont” is a good one, for the reason Marcus himself mentioned – that one cannot always tell when a microbe involved in an interaction with a host will turn out to be pathogenic or not – that was the main reason we went with the broad view of symbiosis from the beginning of the proposed PAMGO terms.


Candace

added 10/16/06

Dear Donghui and others: Sorry it’s been so long since your last comment. You are absolutely correct in raising the question about whether we could annotate effectors to the proposed term “symbiont-induced PCD.” I’m sorry to have implied that in my last comment, as I forgot for a minute that these terms in this tree (under PCD) are meant to be for annotating genes in the host – the plant or the animal. So, GO terms appropriate for annotating bacterial effectors would have to be found under the “symbiosis” trees, where we have proposed a term that would be appropriate for annotating the effectors – those proteins produced by the microbe that travel into the plant or animal cell and then interact with the genes of the host – the plant or animal — involved in inducing PCD. I’m sorry to have confused the issue again, after we all worked so hard to fix it. --Candace

Trudy_Michelle_Candace

programmed cell death (PCD) GO:0012501, Definition: Cell death resulting from activation of endogenous cellular processes.

We've suggested a slightly modified version of the term suggested by Marcus to try to make it more clear that the term should be used to annotate gene products in the host (we also added this to the Comment field).

host programmed cell death induced by symbiont GO:XXXXXXX Definition: Cell death in a host resulting from activation of host endogenous cellular processes after direct or indirect interaction with a symbiont.


Comment: This GO term is to be used to annotate gene products in the host, not the symbiont. For the corresponding term to use for annotating gene products in the symbiont that induce PCD in the host see GO:XXXXXXXXX. An example of direct interaction is penetration by hyphae, and examples of indirect interaction include encounter with secreted enzyme and interaction with MAMP such as cell wall fragment.

So, where we are now is with the tree below:

programmed cell death (PCD) GO:0012501, Definition: Cell death resulting from activation of endogenous cellular processes.

  * host programmed cell death induced by symbiont GO:XXXXXXX, Definition: Cell death in a host resulting from activation of endogenous cellular processes after direct or indirect interaction with a symbiont. 
         o hypersensitive response (HR) GO:0009626, Definition: The rapid death of plant cells in rsponse to invasion by a pathogen.

So, what to do with the current term: HR (above)? We can either make it a more narrow synonym of the new term (host PCD induced by symbiont) or add to the term name somewhere the word "plant", to make it clear it is different from the way the term "hypersensitive" is used in the animal world. One possibility is "Hypersensitive response in plant." What would the GO editors suggest here?

Jane

How about calling it 'programmed cell death via hypersenstive response'?