24 - Phytophora Flashcards
Describe P. infestans
The pathogen that causes late blight and potato blight. Hemibiotrophic. Oomycete. Has a biotrophic phase, involving whit spores on the underside of the leaf, and a necrotrophic phase, involving macroscopic death
Describe the history of P. infestans
Has been the single most important disease facing the potato industry, and has been responsible for the loss of $6 billion in control and damage. The HERB-1 strain caused the Great Famine in 1847 in Ireland, which led to the death of ~1M, and the emigration of ~1-2M. The extent of the famine was accelerated as a product of humanitarian and political failings
What is the importance of the A2 mating type?
Until 1984, ony he A1 strain of disease spread. In 1984, the sexual mating type, A2 spread internationally, and has led to increased reproductie ability of P. infestans, making it far harder to stop
Describe the asexual life cycle of P. infestans
Undergoes between low and moderate temperatures. Involves the production of a zoospore, which is mobile and can undergo chemotaxis as it spread through the leaf in a germ tube, and releases a sporangiosphore releases more zoospores on the other side. An intimate relationship with the host, during the 5-day course of its infection period.
Describe the sexual life cycle of P. infestans
Requires the A1 and A2 mating types, which are responsible for two separate sexual structures - the oogonium (egg), and the antheridium (sperm). Forms sexual oospores together, which then undergo a period of survival in the soil. Sexual stage is very important, since it allows for resilient survival in the soil, and faster adaptation due increased genetic diversity
How can we control late blight?
(1) R-genes, (2) Hygiene/Rotation, involving using different types of crops, use of sanitised tools, removal of infected tubers etc., (3) Agrochemicals, which is the main curent strategy that we have, but is not ideal in terms of environmental impact or the potential for future resistance
What are the R genes for P. infestans?
NLRs. These are Nucleotide Binding Leucine Rich Receptors. These also form NILs, like in C. fulvum.Were first found in 1949, in Black’s differential case. The recognition of P. infestans via R genes still triggers the hypersensitive response, and therefore prevents the formation of the germ tube through the leaf, and the appressorium.
What are the infection genes for pathogens?
Still Avrs! These match with the NLRs.
Give the examples of the NLR genes that we currently know about for P. infestans
R1 from 2002. R2 from 2009. R3a from 2005. R3b from 2011. R8 from 2016. R9a from 2013.
What are the two main classes of NLRs?
Sensor (contains ADR1s and NRG1s) and Helper (contains TNLs and CNLs)
Describe sensor NLRs
Often contain integrated decoys, which have a role in the specialised signal perception of the pathogen effectors. They do not require the MADA motif, since they do not make resistance, or produce HR.Instead, the evolve the Integrated Decoys (IDs), which the pathogens accidentally trigger, which then activates the helper NLRs, which then activate the CNLs/TNLs to make resistosomes. However, they often have increased flexibility.
What are the two main classes of Sensor NLRs?
ADR1s and NRG1s
Describe helper NLRs
Act redundantly. A separate NLR that is involved in downstream signalling. Includes the CC-type NLRs, which are conserved across plant species, and required for cell death.
What are the two main classes of helper NLRs?
CNLs and TNLs. These have evolved as helper NLRs
Describe CNLs
Carry the N-terminal Coiled-Coil (CC) domain. This CC domain has 5 alpha helcies. All R genes so far have been CC-type NLRs. In the inactive state, the Nucleotide Binding Domain is bound to ADP. In the active state, the ADP is replaced with ATP, leading to the stabilisation of NLRs. THe MADA motif in the CC-domain is moved to a new position in the active state, allowing the NLR to polymerise into higher order structures, and create resistosomes. The resistosomes then lodge themselves into the plasma membrane of P. infestans.
Describe TNLs
Carries the N-terminal TIR domain (Liu et al., 2021). TIR is the Toll/Interleukin-1 Receptor. Absent in mnocots, and entirely restricted to the eudicots, unlike the CNLs, which are seen across both classes.
Why is it important that the helper NLRs act redundantly?
The presence of redundancy means that it is harder for the pathogen to manipulate this system.
What is an NCR?
A CC-type NLR - AKA a CNL
What are VIGs?
Virus Induced Silencing Genes. A gene that the virus induces. But, we can use this as a genomic tool to model the plant. We can take the gene of interest from the host, make a fragment of the gene, then re-integrate this into the host genome by using a viral vector. The plant will then silence its own gene
How did the NLR network evolve?
Adachi et al., 2019 showed that the current dicot NLR system evolved from singleton NLRs that can perceive the effectors, and triggers HR (through the presence of MADA). The sensor and helper NLRs both evolved from singletons to complex networks of sensors and helpers. A logical conclusion of the plant-pathogen arms race.
What is the importance of the RxLR motif for defences against the Avr3a protein?
RxLR is present in many P. infestans effectors. It is what allows for the presence of Avr3a to be detected
Discuss the Avr3a plant-pathogen arms race.
The pathogen secretes the protein INF1 to extract phospholipids from the host. However, many hosts will have RLPs which are good membrane bound receptors, which can trigger HR. The NLRs recognise the IFN1, ready for a HR response. However, the Avr3a protein is supposed to suppress the HR signalling from inside te host cell, allowing the pathogen to explot the host.
Describe the Avr3a plant-pathogen arms race.
Certain peptides have acquired the NLR R3 mutation, which allows them to recognise the silencing activity of Avr3a activity via the RxLR-EER signal peptide, and trigger a HR response. However, even more recently, P. infestans has acquired a variant of the Avr3a effector that is not recognised by the RxLR-EER receptor.
What is the relevance of gene-sparse regions in P. infestans?
Haas et al., 2009 used genomic techniques to show that most effectors of P. infestans are located in gene sparse regions, with a large intergenic distance to each other. This has allowed for the evolution of a two-speed genome, which contributes to faster adaptation during arms races and host jumpers. These gene-sparse regions contain the genes that are (1) Induced during infection, and (2) Have faster rates of evolution. Dong et al., 2014 used the recent divergence from P. mirabilis to show that these gene sparse regions are important for the rapid evolution of P. infestans.
How can we use effectoromics to limit the impact of P. infestans?
(1) Sequence pathogen, (2) Select core effector candidate, (3) Clone into a binary PVX vector, (4) Agroinfect wild relatives with the PVX containing the wild vector, (5) Identify the NLRs that are responsible for transmission, (6) Transform the NLRs into potatoes to induce resistance
