2 R-gene mediated host resistance

Transcript

Hello! I welcome you to the second talk of this week that is R-Gene mediated host resistance. In the previous talk we have seen how planted microbes basically interact and how plant respond to pathogenic attack through mediation of resistant genes or R genes. So here in this talk particularly we will be focusing on the R genes that are present in plants and how do they behave in response to pathogen attack. Let us see the Genetic basis of plant disease resistance. So plant basal resistance and R-gene mediated Pathogen response.

These are the two general mechanisms of plant defense against particular pathogens. The R-gene mediated pathogen resistance can be either qualitative and quantitative. If it is qualitative then we can see that there are certain major genes that are involved in this particular process which confers complete resistance to a specific pathogen or a pathogenic race. Our genes can be rapidly overcome by new virulent pathogens, this is the demerit of this particular strategy. When there are only one of you major genes are conferring resistance to the host then there is every possibility that the genes will be overcome by a new pathogenic race. So that is why Quantitative loci for disease resistance has become more significant because it provides durable resistance as it is effective against a large number of pathogenic races and this is governed by a number of minor genes. Quantitative Disease Resistance is controlled by multiple genes and each contribute to partial resistance of QDR that means here unlike the qualitative gene resistance which is complete resistance here the pathogen is allowed to cause a little amount of disease thereby the pressure on the pathogen was less in comparison to qualitative disease resistance. The mechanisms that underlie plant resistance to pathogens involved that are so diverse including fungi, bacteria and viruses can plant confer resistance against all these pathogens in the same way or in a different way, let us see that. If we just see some of the bacterial pathogens like gentlemen as Xanthomonas campestris, Xanthomonas oryzae, Pseudomonas syringae pv. tomato or Pseudomonas syringae, they cause disease in variety of hosts and there are genes that are identified against these pathogens are very very different. So that means there are different R- genes that are present or plant harbors a variety of R-genes to combat different types of Bacterial pathogens. At the same time if the plant is encountered by certain fungal pathogens then like Blumeria graminis, Cochliobolus carbonum, Erysiphe orontii and so on. We can see that there is a range of different R-genes or Resistant genes involved in suppressing the progress of these diseases caused by a different fungi. So plant again it harbors a flurry of diverse R-genes that are responsible for suppression of fungal and bacterial pathogens in a host specific manner.

Let us see the interaction between R and Avr genes. If a plant carry in R-gene then once the gene is expressed it will produce a or synthesize in R-protein and these are the products of the R-protein and the same time if the pathogen has an a Avr gene it will also synthesize some a virulent proteins and if the plant R-gene product are able to recognize the Avirulent gene product then there will be a incompatible interaction that leads to HR development and finally the incompatibility is manifested in terms of resistance. But if the plant does not contain a R[1]gene so it will not produce any R-protein. So there won’t be any protein that we’ll be targeting to bind this AVR protein products so this protein product will be free and there won’t be any response like HR and the plants will be susceptible and they will be subjected to disease. Then there is a model known as guard model for disease resistance because many a times the Pathogen protein does not directly interact with the R-protein rather they interact with the effect at the target side or the Guardee protein and if the Guardee protein is not attached with the R-protein then the ultimate outcome is susceptibility or disease. So it is very important that the R- protein is attached to the target protein that binds with the Pathogen effectors protein.

So plant disease resistance can be looked into the eyes of R-genes that are present in the plant system. There are different types of R-genes, many of them carries a conserved domain that is LRR that is leucine-rich repeat. Then there is a domain Kinase. In some cases along with LRR we have NBS domain that is nucleotide binding site, then using cheaper so, these are domains that are present in some R- genes and in some R-genes we have a toll/interleukin-1 receptor like domain along with NBS domain and LRR domain. so these different types of R[1]genes are present on different host and they are able to suppress infection by different pathogens. So modern classification shows that there are 8 types of different classes of R-genes and the major classes of R-genes based on the arrangement of functional domains are LRR- Leucine-rich repeats; NBS that is Nucleotide binding site; TIR- Toll/ interleukin 1 receptor; C-C- is coiled-coil domaine; TRD that is Transmembrane domain; PEST – domain that is Protein degradation domain; ECS domain Endocytosis cell signaling domain; NLS domain that is – Nuclear localization signal; WRKY domain that is – Amino acid domain; HM1 domain that is – Helminthosporium carbonum toxin reductase enzyme. So these are the different classes of R-genes that has been identified so far and these R-genes are responsible for development of resistance in the host against certain AVR producing pathogens. So if you just see Elicitor suppressor model and elicitor receptor modal. We can understand this model for understanding the plant and microbe interaction for developing of a resistance response need that the Elicitor molecules of the pathogen to be identified by a receptor. But at the same time pathogen can also produce some suppression molecules and if they bind with a receptor it leads to susceptibility. Then again Elicitors must be compatible with the R-gene product to develop resistance but if the Elicitors are not compatible with R-gene product of the host then it leads to susceptibility. There are two basic concepts of interaction of Effectors and the Guardee proteins, one is known as Guard model and the other one is known as Decoy model. One particular effectors that is produced by a pathogen may have multiple site or targets.

So these Guardee proteins when they are associated with a plant R-gene product then they will Effect a triggered immunity that leads to disease resistance. At the same if the same Guardee proteins are not associated with a say plant R-protein. Then the ultimate outcome will be susceptibility. There won’t be any resistance development in the host. The decoy model proposes in a slightly different manner where they gain when the effectors are identified by the receptor molecules or you can say that the regarding molecules but these Guardee molecules once they are attached with the R-gene product of the plant they trigger defense responses. But since we look into the evolutionary pattern of these proteins then sometimes find that these proteins get modified under a particular environmental situation and these modified proteins they are not compatible with the R-gene product of the plants. So they are not associated with the R-gene product of the plant and that is why this Effector triggered immunity response is not present in this case. So the ultimate result is there is increased susceptibility of the plant towards these effector molecules or that the pathogen that is releasing these effector molecules.

To summarize the interaction between Biotrophic and Necrotrophic pathogens this model expresses the summary of the interaction. Suppose the pathogen is necrotrophs then the PAMP is responded by recognizing the host receptors those are known as receptor like Kinases and there is a signature gene that is PDF 1.2 which is expressed that leads to either development of Jasmonic Acid signaling and the ultimate result is enhanced defense response. But if the pathogen is Biotrophs then it can be sensed by PRRS the pattern recognition receptors by the host plant and this P/DAMPS when it is recognized by PRR it leads to a signal that leads to true MAP Kinases and WRKY activities and that leads to defense responses against the multiple pathogens. But if the pathogen is able to secret Effectors molecules then the effectors molecules then interrupt with this signal mechanism and the resistance response may be lost. So when the Effectors are synthesized the plant respond to those effectors by synthesizing R-proteins and when they interact then the ultimate R-gene mediated response is seen which is manifested through the response of hypersensitive response and there is induction of systemic acquired resistance in the form of SAR and both leads to enhancement in defense responses and that is resistance. So we have seen that in this particular talk what are those different types of R- genes that are present in plants? How do they interact with the plant pathogens which releases effectors to suppress their mechanism and what is the guard and decoy model which again help us to understand the interaction of AVR gene product that is the Elicitors along with, R-gene products, along with Guardee proteins and the ultimate outcome it may lead after their interaction.

Thank you.