Virus resistance RLR 031115

Virus resistance mechanisms in plants


Three basic ways of Resistance
 Healthy planting material and cultural practices.
 Host plant resistanceVectors,
Viruses,
Cross protection

 Transgenic approach
▪

Pathogen derived genes and other sources


Stages of viral infection cycle
Co-ordinated expression of viral and plant genome essential for virus
Entry, un coating of NA,
Virus infection

Epidermal

translation of viral proteins
Replication,

cells

Asssembly of

Replication

progeny virus

Cell-to-cell
movement
Mesophyll
cells
Phloem

Systemic
movement

Other host plants
Bundle
sheath cells

Plant-to-plant
movement

Phloem
Parenchyma
Companion cells



Prevention Of Viral Uncoating



If a virus is prevented from uncoating, its DNA will not be exposed to cellular replication

machinery and the virus will not be able to reproduce shown in

tobacco mosaic virus, TMV.



Inoculation of a tobacco plant with the treated virus (Ph 8.0 for a brief period of time, which
if the virus is not treated,



removes about sixty coat protein subunits ) causes an infection, but

no infection results in transgenic coat proten mediated resistant plant.

This lack of infection is due to the viral mRNA not being translated

Two theories exist to explain why this may be so.
Theory One: TMV has a specific uncoating receptor which is blocked by coat protein
High coat protein concentrations would block the uncoating receptor
 which also controls encapsidation in a normal replication cycle
 In a transgenic plant the large coat protein concentration blocks the uncoating receptor of the
therefore preventing infection.

Theory Two :TMV uncoats when it enters a plant cell due to local physiological changes
If a transgenic plant has a high coat protein concentration, it will favour viral coating.
 This would effectively prevent uncoating of the invading virus

viral RNA,

CELL-TO-CELL MOVEMENT OF COWPEA MOSAIC

VIRUS

Movement of virus particle
through modified plasmodesmata

Viral movement protein
Disassembly of viral
movement complex
Assembly of viral
movement complex

coat protein

Virus disassembly

Virus assembly

virus particles

viral RNA

Viral RNA replication,
translation, etc

Plasmadesmata = junction between plant cells

More cell-to-cell

movement


RESPONSES OF PLANTS TO VIRUS INOCULATION

 Immune - no replication at all
 Complete resistance in a plant to virus infection is referred to as immunity.
 The immunity is usually manifested in preventing virus replication.
 If immunity occurs against all biotypes of a pathogen and in all cultivars or accessions of a particular plant species the situation is re
ferred to as

non-host resistance

 For viruses, this is a largely an unexplored Area unlike in fungi etc




Nonhost resistance



All genotypes within plant species show resistance or fail to be infected by a particular virus. Unlike in fungus it is not understoo
d against virus




One of the first innate immune responses all plant viruses encounter when
Ai) and

invading a host consists of antiviral RNA silencing (RN

post-transcriptional gene silencing (PTSG)].



RNA silencing is a host response triggered by double stranded (ds)RNA.



These molecules thus act as a MAMP/PAMP and in which RNAi can be

regarded as PTI.



The main difference with pathogens such as fungi and bacteria is that

recognition of viral MAMPs/PAMPs occur intra-cellular

ly




One of the most common strategies plant viruses use to counteract RNAi is to

encode RNA silencing suppressors (RSS), viral proteins that i

nterfere with a specific part of the RNAi pathway and thereby reduce its effectiveness



The majority of plant virus RSS proteins exert this activity through binding of small
hereby prevent their



uploading into RISC and Dicer-cleavage, respectively.

In recent years some RSS have also been discovered to inhibit the RNAi pathway in
ke AGO1, the core

interfering (si)RNAs, or sometimes (also) long dsRNA, and t

component of RISC during the antiviral RNAi response

other ways, e.g., by binding directly to key-enzyme proteins li


Second layer of defense that involves resistance genes. (HOST PLANT RESISTANCE)

Most of these are triggered by and confer resistance to a specific virus only

Some act against several (related) viruses.

The major class of these genes represent single dominant resistance genes (and of which the biggest group consists of the NB-LRR type),

Others are recessive, tolerance, or partial resistance genes.



Infectible (host) - can replicate in at least a single cell

Resistant -extreme hypersensitivity

 Resistance genes have been described as conveying extreme
resistance (ER).



Virus can replicate only in initially infected cell (due to ineffectual virus-encoded

Movement Protein)

 In the case of Potato virus X (PVX), replication occurred to a
limited extent and then an induced resistance occurred, leading to

prevention of further replication

 In these instances where replication of viruses occurred at
normal levels, but the virus was prevented from moving outside of the inoculated cells


Resistant -hypersensitivity

▪

Virus replicates only in a few of the cells surrounding the initially infected cell (host response limits the spread)

In some plant genotypes the virus can move cell-to-cell to a limited extent, before a

multicellular hypersensitive response (HR) occurs, which first

activates defense response preventing the infection from spreading further and then kills the cells within the infected zone .

The ER and HR are referred to as types of inbuilt resistance.

Both are associated with dominant resistance genes

Plants undergoing an HR also induce a state of pathogen-nonspecific resistance called

systemic acquired resistance (SAR)




In some cases the virus cannot spread to upper leaves of the plant.



It is likely that there is a barrier to infection preventing the virus from ingressing into the sieve elements of the phloem.




This barrier may prevent movement into one or more of the cell types within the vasculature: bundle sheath cells,
vascular or phloem parenchyma cells, and/or companion cells

Host Plant Resistance



Resistance Mechanisms to Plant Viruses




Dominant resistance to plant viruses
Recessive resistance to plant viruses


Resistance Mechanisms
Virulence factor

Viral Proteins

Susceptive

Host factor

Switching host system
for viral infection

Interaction with Host factors

Avirulence

factor

Dominant
resistant
Host R protein

Recognized by R protein

Recessive
resistant
Host factor
(mutated)

Active defense signaling

No interaction with host factors

Blocking virus infection


Resistance Mechanisms


Dominant resistance




(Incompatible interactions between the host R-gene and pathogen avirulence gene).
Hypersensitive response (HR): Specific recognition of the virus → rapidly induced programmed cell death → necrotic local l

esion



Tobacco mosaic virus/N gene interaction: a classic hypersensitive response (HR) model system.

Most of the resistance genes isolated are dominant genetically and are involved in resistances manifested by an HR



Recessive resistance



Mutation or loss of host components required for a step of the virus life cycle


Dominant resistance

Most of these proteins are similar to those associated with resistance to bacteria, fungi, insects and nematodes. They are all considered to be involved
in activating defense

signaling responses

Dominant R genes basically can be grouped into two classes, namely those that encode NB-LRRs



The largest class of R genes





Nucleotide binding site + leucine-rich repeat (NBS-LRR)

NBS-LRR sub-division can be made on basis of N-terminal domain.





Coiled-coil (CC) domain (CC-NBS-LRR)
Leucine zipper domain (LZ-NBS-LRR)
Drosophila Toll and the mammalian interleukin (IL)-1 receptors (TIR-NBS-LRR)

and all others.


Single dominant resistance(R) gene products (in)directly sense the presence of a
actors(Avr), as a counter

defense

specific pathogen by their effector, termed avirulenc ef

against ETS, leading to a stage called Effector-Triggered Immunity (ETI)

Triggering of R genes is generally associated with a (concomitant) induction of HR

Recognition of the viral elicitor results in the induction of a cascade of host defense
of hydrolytic enzymes,

responses that include oxidative H2O2 bursts and up-regulation

PR proteins, and callose and lignin biosynthesis. An induced HR is quite characteristic and involves the activation and expression

of SA, jasmonic acid (JA), nitride oxide (NO), ethylene, reactive oxygen species etc

As a consequence, viral movement may be limited to a small number of cells, illustrated by classic examples as the tobacco N gene (160) and the
tomato Tm-2 and Tm-22 alleles


Dominant virus resistance genes
Dominant resistance against plant viruses

Dryas de Ronde, Patrick Butterbach and Richard Kormelink* 2014 Fronteirs in plant sciences volume5.




Antiviral R genes in plants


Interestingly all R genes lack a transmembrane domain





consistent with Intracellular life style of viruses

Avr could be Replicases/Helicases, Movement protein, Coat protein etc
Direct interaction between TMV replicase (TMV-p50 helicase domain) and

N protein is observed

Interaction leads to Oligomerization of N protein and resistance triggering.



For elicitation of Ry-mediated resistance, the protease domain of PVY NIaPro,

specifically the integrity of the protease active site, is required

Avr and R interaction need not be associated with HR or cell death
For example Rx against Potato virus x provide qualitative Resistance that inhibits viral replication without HR
Similar for SW5 in tomato and RSv1 in soybean