Lecture 6, Genetics of Plant Disease
The genetic information is encoded in DNA or in RNA.
Genomic DNA
Chromosome DNA
Nuclear DNA
Cytoplasmic DNA
Plasmid DNA
Mitochondrial DNA
Chloroplast DNA
Genes and Disease
Host range: the various kinds of host plants that may be attacked by a parasite.
Specificity: a pathogen can only attack certain types of plant species and cultivars; a host plant suffers diseases only from certain pathogens and pathotypes.
Pathogen adaptation
Selection
Genetic modification
Large population and rapid amplification facilitate the adaptation.
Genetic variability and mechanisms
Genetic modifications can occur on both sexual and asexual stages
General mechanisms
Both mutation and recombination are general mechanisms of variability occurring in plants and pathogens
Mutation: a change in the nucleotide sequence of DNA; the ultimate source of genetic diversity.
Substitution, addition and deletion of single or multiple base pairs.
Insertion or deletion of DNA fragments.
Insertion of transposable (mobile) elements: transposon or retro-transposon.
Mutations can be dominant and the most are recessive.
It occurs spontaneously in both nuclear DNA or cytoplasmic DNA.
Recombination: it occurs during the sexual reproduction of plants, fungi and nematodes. Recombination of genetic materials occurs during the meiotic division of the zygote as a result of genetc crossovers in which parts of chromatids (and the gene they carry) of one chromosome of a pair are exchanged with parts of chromatids of the other chromosome of the pair.
Specialized mechanisms
Sexuallike processes in fungi
Heterokaryosis: the condition of being a heterokaryon (Gr. heteros=different from, karyon=nucleus, -- a cell that contains genetically different nuclei or a thallus made up of such cell. Cf. dikaryon, homokaryon)
Parasexualism (parasexual cycle, Gr. para=besides; L.sexus=sex, -- a sequence involving heterokaryon formation, diploidization, and haploidization, often resulting in the formation of recombinant nuclei. Unlike the sexual cycle, the parasexual cycle may occur at any point or continuously throughout the life cycle).
Heteropoidy: a condition in which a cell, tissue, or organism that contains more or few chromosomes per nucleus than the normal 1N or 2N for that organism.
Sexuallike processes in bacteria and horizontal gene transfer
Conjugation: it occurs when two compatible bacteria come in contact with one another and a small portion of the chromosome or plasmid from one bacterium is transferred to the other through a conjugation bridge or pilus.
Transformation: bacterial cells are transformed genetically by absorbing and incorporating in their own cells genetic material secreted by, or released during rupture of, other bacteria.
Transduction: a bacterial virus (phage) transfers genetic material from the bacterium in which the phage was produced to the bacterium it infects next.
Genetic recombination in viruses
Genetic materials can be transferred between viruses, viruses and plants, and viruses and vectors through some unknown mechanisms - recombination?
(loss of pathogen virulence in culture - due to selection pressure?)
Stages of variation in pathogens
Species (L. spcies= a kind): Of sexually reproducing organisms, one or more natural populations in which individuals are interbreeding and are reproductively isolated from other such groups.
However, for a fungal or bacterial pathogens, certain morphological and other phenotypic characteristics in common make up the species such as Puccinia graminis.
Varieties or Special forms (L. formae specialis)
Some individuals of the species attack only certain species of host plants, which make up formae specielis such as P. graminis f.sp. tritici.
Race
Within a special form, some individuals attack a set of the host varieties but not the others, which make up a race such as P. graminis f.sp. tritici race 1, 2 and 3.
Variant
Occasionally, one of the offspring of a race can suddenly attack a new variety that it could barely infected before. This individual is called a variant.
Biotypes
The identical individuals produced asexually by a variant make up a biotype (clone). Each race consists of one or several biotypes.
(spp. -- Mixture of several species or unidentified species, such as Fuarium spp.)
Plant resistance phenotypes
I). Non-Host Resistance: inability of a pathogen to infect a plant because the plant is not a host f the pathogen due to lack of something in the plant that the pathogen needs or to the presence of substances incompatible with the pathogen (plants are outside the host range of pathogens).
Non-host resistance is completely resistant to pathogens of other plants, usually even under the most favorable conditions for disease development.
Non-host resistance often occurs at early stage of the infection associated with a penetration deficiency and a rapid cell death. However, the detail mechanisms are unknown.
II). R-Gene Resistance (cultivar-specific, true resistance or gene-for-gene resistance): Plant possess genes for resistance directed against the avirulence genes of the pathogen.
Horizontal Resistance (non-specific, general, or multigene resistance): partial resistance equally effective against all races of a pathogen.
Resistance is controlled by many genes and quantitatively inherited.
Resistance mechanisms involve in many physiological steps, providing nonspecific, general quantitative, adult plant, field, or durable resistance.
Resistance phenotypes may not provide the distinguishing among different races.
Resistance can be affected by environmental factors
Resistance can be maintained for a long period.
Vertical Resistance (specific, strong, or monogenic/ oligogenic resistance): complete resistance to some races of a pathogen but not to others.
Resistance is always controlled by one or a few genes called R-gene.
The resistance mechanism is determined at the major step of the physiological responses providing strong, major, specific, qualitative, or differential resistance.
Resistance can be distinguished among varieties, which provide the host range to determine the pathogen races.
Resistance can be easily broken down by variation of the pathogen virulence.
Cytoplasmic resistance:
Corn cytoplasmic resistance against the southern corn leaf blight.
III). Apparent Resistance: for various reasons, the plants escape or tolerate infection by some pathogens.
Disease Escape: the failure of a host to become diseased because of separation, in space or time, of susceptible host tissues and the infective units of the pathogen.
Such as unfavorable environmental conditions (anthracnose are more dominant on tropic crops), plant developmental stages(adult resistance) and absence of pathogens, these are important factors for the practical management of plant diseases.
Tolerance: the ability of a plant to sustain the effects of a disease without dying or suffering serious injury or crop loss. Also, the amount of toxic residue allowable in or on edible plant parts under the law.
Plants are susceptible to the pathogen, but show little damage resulting from heritable characteristics of the host plant.
The phenomena are often observed with some mild virus strains.
The mechanisms are unknown and in some cases it may associate with horizontal resistance.
Genetics of the plant-pathogen interaction
The Gene-for-Gene Concept: A single plant-resistance gene reacts with the matching single avirulence gene of a pathogen.
Susceptibility and resistance in each host-pathogen combination is predetermined by the genetic material of the host and the pathogen.
Plant resistance and pathogen virulence follow the stepwise evolution, which can be explained by the gene-for-gene concept, according to which for each gene that confers virulence to the pathogen there is a corresponding gene in the host that confers resistance to the host, and vice versa.
1940s, Flor discovered avirulence (avr) genes in fungal pathogens (rust) when crosses between different physiological races were tested on plant cultivars (flax) carrying defined resistance genes.
Failure to induce susceptibility is the key to avirulence.
Generally, but not always, in the host the genes for resistance are dominant (R) while genes for susceptibility, that is, lack of resistance (r), are recessive. In the pathogen, on the other hand, it is the genes for avirulence, that is, inability to infect, that are usually dominant (A) while genes for virulence are recessive (a).
The specificity is determined by matching the resistance gene and the avirulence gene.
The gene-for-gene interrelationship has been shown to operate in many other diseases caused by fungi, bacteria, viruses, nematodes, parasitic plants and even insects.
Avirulence genes: avirulence genes are believed to govern the production of elicitors (ligands) which can be recognized by receptors encoded by host resistance genes and cause a plant pathogen or pest to elicit a resistance response in a host plant.
(elicitors are compounds of the pathogen that the plant senses to initiate defense reactions; elicitors can be divided into enzymes and compounds without catalytic activity. Well-known enzymatic elicitors are hydrolytic enzymes that break down the plant cell walls, e.g. pectinases and xylanases, and it is believed that the plant cell all fragments released in this procedure initiate the defense responses. On the other hand, the elicitors without any known catalytic activity may be peptides, oligosaccarides, small metabolites as well as proteins and glycoproteins).
The avr genes of plant pathogenic bacteria were discovered first in P. s. pv. glycinea, a pathogen of soybean (Staskawicz et al., 1994).
The first fungal avirulence gene that fit the gene-for-gene concept was identified as avr9 from Cladosporium fulvum by de Wit's group in 1991.
A relatively large number of avr genes have been cloned from pathogenic bacteria, fungi and viruses. All known avr genes encode proteins and the structure of these proteins are quite different even though some of these have common structural characteristics. The function of only a few avr genes have been determined including avrD from P.s. pv. tomato which was proposed to be a glycosyl transferase catalyzing the fusion of -keto fatty acids and xylilose, AVR-pita from Magnaporthe grisea which encodes a metalloprotease with an N-terminal secretory signal and pro-protein sequences.
Bacterial avr genes are located within so called hrp gene clusters (because both the HR(hr) and pathogenicity(p) are controlled by it). AVR proteins are generally hydrophilic and show a cytoplasmic localization. These proteins are delivered into plant cells by a typeIII secretory pathway.
Fungal avr genes often encode secreted proteins including Avr4 and Avr9 from Cladosporium fulvum, NIP1 from Rhynchosporium secalis and AVR-Pita from Magnaporthe grisea.
Avr gene products from viruses are often coat proteins.
Why do pathogens then possess avr genes producing elicitors which negatively acting factors, because they delimitate the pathogens access to substrate?
The lack of a clear biological function attributable to many avirulence genes has been puzzling for some years.
Recently, this puzzlement has steadily given way to the view that many avirulence genes have dual functions, having a role in virulence as well as avirulence, and thus function as important mediators of the interaction between pathogen and plant, e.g. mutations in avrBs2 resulted in impaired ability of X. campestris pv. vesicatoria to grow on pepper cultivars that lacked the Bs2 gene for resistance. The deduced polypeptide from avrBs2 sequence relates to those of agrocinopine synthase and glycerol phosphodiesterase, suggesting an enzymatic role in the pathogenicity.
Resistance genes
-- Molecular cloning of resistance genes
In 1992, the first resistance gene Hm1 was cloned from maize by a tranposon-tagging. The gene encodes a HC-toxin reductase, which reduces and thereby detoxifies the HC-toxin in resistant varieties against the infection caused by race1 of Cochliobolus carbonum. However, this resistance gene is not the typical R-gene involved in gene-for-gene system.
The first R-gene, tomato Pto, involved in gene-for-gene system against the avrPto from P.s. pv. tomato was cloned in 1993 by Martin's group using a position cloning approach.
-- Evaluation and diversity of resistance genes
To date, more than 30 resistance genes from Arabidopsis, tomato, tobacco, rice, lettuce, potato, flax pepper, sugar beet and maize have been cloned and functionally characterized. Although these genes confer resistance to diverse bacterial, fungal, viral, and nematode pathogens, their products share striking structural similarities.
Structurally, R-genes involved in the gene-for-gene system are divided into four major classes.
NBS-LRR
LRR-TM-Kinase
LRR-TM
Protein Kinase
The direct physical interaction (elicitor-receptor interaction) between R-gene and avr-gene products has been demonstrated in two systems including Pto-AvrPto and Pita-AVR-Pita by the yeast two-hybrid system and the immuno-precipitation. Therefore, it is finally confirmed that the resistance gene product functions as the receptor and the avrulence gene product functions as the elicitor.
~200 NBS-encoding genes are present in Arabidopsis genome (~150 encoding NBS of the TIR-type and ~50 of the non-TIR type), representing 1% of the total Arabidopsis genes.
-- Specificity of resistance
Several R-gene locus sequences provide evolution or polymrphism information, which provides useful genetic background for predicting and evaluating the resistance specificity.
Recent studies showed that the LRR and N-terminal sequence in certain resistance genes might determine the resistance specificity.
-- Cloning of plant resistance genes has brought a historical event in plant pathology
Understanding the nature of resistance.
Practical application in agriculture.
Molecular breeding for plant disease resistance
A). Interspecies transfer
B). Broad spectrum resistance
C). Additional resistant resources
References:
Genetics of Host-Parasite Interaction. P.R. Day, 1974
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