من انا

صورتي
الرياض, Saudi Arabia
مسلم، وأناأحوج ما أكون إلى معرفة نفسي

الثلاثاء، 31 يناير، 2012

Resistance


INTRODUCTION

        In general, hosts defend themselves against pathogens by a combination of weapons from two arsenals: 

(1)structural characteristics that act as physical barriers and inhibit the pathogen from gaining entrance and spreading through the plant.

(2) biochemical reactions that take place in the cells and tissues of the plant and produce substances that are either toxic to the pathogen or create conditions that inhibit growth of the pathogen in the plant.

Follow of Introduction

The combinations of structural characteristics and biochemical reactions employed in the defense of host are different in different host–pathogen systems and even within the same host and pathogen according to many factors:

1.The age of the host.

2.The kind of host organ and tissue attacked.

3.The nutritional condition of the host.

4.The weather conditions.

Whatever the host defense or resistance, it is controlled by its genes

One concept that must be made clear at the outset is that whatever the kind of defense or resistance a host plant employs against a pathogen or against an abiotic agent, it is ultimately controlled, directly or indirectly, by the genetic material (genes) of the host plant and of the pathogen (Fig.1).

FIGURE 1
Types of reaction of plants to attacks by various pathogens in relation to the kind of resistance of the plant.

Quantitative (polygenic) resistance. Some infections and symptoms possible. Plants generally survive and produce.

Monogenic (R gene) resistance. Plants either are resistant and remain healthy or are susceptible and Karnme severely diseased.

Non-host Resistance

Non-host resistance means the plant can stay resistant (immune) when it is brought in contact with a pathogenic biotic agent to which the plant is not a host. Non-host resistance is the most common form of resistance (or defense from attack) in nature. For example, apple trees are not affected by pathogens of tomato, of wheat, or of citrus trees because the genetic makeup of apple is in some way(s) different from that of any other kinds of host plants, which, of course, are attacked by their own pathogens. However, apple can be attacked by its own pathogens, which, in turn, do not attack tomato, wheat, citrus, or anything else. Similarly, the fungus that causes powdery mildew on wheat (Blumeria graminis f. sp. tritici) does not infect barley and vice versa, the fungus that causes powdery mildew on barley (B. graminis f. sp. hordei) does not infect wheat, and so on.

Partial, Polygenic, Quantitative, or Horizontal
Resistance (H.R.)

Introduction for H.R.

Each plant, of course, is attacked by its own pathogens, but there is often a big difference in how effectively the plant can defend itself against each pathogen.

Many genes are responsible for protection of plant against pathogens. Some of these plant genes code for chemical substances that are toxic to pathogens or neutralize the toxins of the pathogens, and these substances may be present in plants regardless of whether the plant is under attack or not.


Plants also have genes that produce and regulate the  formation of structures that can slow down or stop the advance of a pathogen into the host and cause disease. These structures can also be present in a plant throughout its life or they may be produced in response to attack by one of several pathogens or following injury by an abiotic agent.




When a pathogen attacks a host plant, the genes of the pathogen are activated, produce, and release all their weapons of attack (enzymes, toxins, etc.) against the plants that they try to infect.

plants manage to defend themselves partially With the help of different combinations of preexisting or induced toxic chemical substances or defense structures. This type of defense or resistance is known as horizontal, field, durable, partial, polygenic, general,  quantitative, or minor gene resistance because it depends on many genes for the presence or formation of the various defense structures and for preexisting or induced production of many substances toxic to the pathogen.

Preexisting Defense Structures

The first line of defense of a plant against pathogens is its surface, which the pathogen must adhere to and penetrate if it is to cause infection. Some structural defenses are present in the plant even before the pathogen comes in contact with the plant as the following:

1.Amount and quality of wax and cuticle that cover the epidermal cells.

2.The structure of the epidermal cell walls.

3.The size, location, and shapes of stomata.

4.The presence of tissues made of thick-walled cells that hinder the advance of the pathogen on the plant.


Preexisting Chemical Defenses

The resistance of a plant against pathogen attacks depends not so much on its structural barriers as on the substances produced in its cells before or after infection. This is apparent from the fact that a particular pathogen will not infect certain plant varieties even though no structural barriers of any kind seem to be present or to form in these varieties.

Moreover, many pathogens that enter non-host plants naturally or that are introduced into non-host plants artificially, fail to cause infection, although no apparent visible host structures inhibit them from doing so. These examples suggest that defense mechanisms of a chemical rather than a structural nature are responsible for the resistance to infection exhibited by plants against certain pathogens.

Inhibitors Released by the Plant in Its Environment

Plants exude a variety of substances through the surface of their aboveground parts as well as through the surface of their roots. Some of the compounds released by certain kinds of plants, however, seem to have an inhibitory action against certain pathogens.

Fungitoxic exudates on the leaves of some plants, e.g., tomato and sugar beet, seem to be present in sufficient concentrations to inhibit the germination of spores of fungi Botry-tis and Cercospora, respectively, that may be present in dew or rain droplets on these leaves.


Similarly, in the case of onion smudge, caused by the fungus Col-letotrichum circinans, resistant varieties generally have red pigments, the  phenolic compound protocatechuic acid and cate-chol. In the presence of water drops or soil moisture containing conidia of the onion smudge fungus on the surface of red onions, these two fungitoxic substances diffuse into the liquid, inhibit the germination of the conidia, and cause them to burst, thus protecting the plant from infection.

Both fungitoxic are missing in white-scaled, susceptible onion varieties (Fig. 2). It was noticed that applications of acibenzolar-S-methyl (ASM) on sunflower reduced infection by the rust fungus Puccinia helianthi through the reduction of spore germination and appressorium formation. It was subsequently shown that ASM accomplished this by increasing the production and secretion by the plant on the leaf surface and other toxic phenolics that inhibit spore germination.

FIGURE 2
Onion smudge, caused by the fungus
Colletotrichum

circinans, develops on white onions but not on colored ones.

Induced Biochemical Defenses in Horizontal
Resistance (H.R.)

In horizontal resistance, plants depend on the action of numerous genes, expressed upon attack by a pathogen (induced resistance). These genes provide the plants with defensive structures or toxic substances that slow down or stop the advance of the pathogen into the host tissues and reduce the damage caused by the pathogen. Quantitative resistance is particularly common in diseases caused by non-biotrophic pathogens. 

Function of Gene Products in Quantitative
Resistance

Genes involved in quantitative resistance are present in the same areas of plant chromosomes that contain the genes involved in defense responses, such as the production of phenylalanine ammonia lyase, hydroxyproline-rich gly-coproteins, and pathogenesis–related proteins. The defenses in quantitative resistance, however, develop slower and perhaps reach a lower level than those in the race-specific (R gene) resistance. Quantitative resistance is also affected much more by changes in the environment, mostly of changes in temperature during the various stages of development of resistance.

Mechanisms of Horizontal (Quantitative) Resistance

Studies of defense mechanisms in diseases with quantitative resistance are few and far between. For example, in the early blight of tomato caused by the fungus Alternaria solani, all resistant tomato lines had higher constitutive levels of the pathogenesis-related proteins chitinase and b-1,3-glucanase than the susceptible lines. In the quantitatively controlled resistance of the soybean–Phytophthora interaction, soybean tissues actually caused the release of phytoalexin elicitors from the cell walls of the fungus, again showing that the plant can play an important role in forcing the release of defense triggering signals from the pathogen.

Effect of Temperature on Quantitative Resistance

Quantitative resistance is often affected greatly by the temperature in the environment. This effect, however, is not unique to plants with quantitative resistance, as even in plants with monogenic (R) gene resistance, the resistance of the host may be changed drastically by changes in temperature. For example, in R resistance-carrying wheat, a change in temperature from 18 to 30°C changes the reaction of wheat plants carrying the Sr6 R gene from rust resistant to rust susceptible.


Race-Specific, Monogenic, R Gene, or Vertical
Resistance (V.R.)

In many plant–pathogen combinations, defense (resistance) of a host plant against many of its pathogens is through the presence of matching pairs of genes for disease in the host plant and the pathogen. The host plant carries one or few resistance genes (R) per pathogen capable of attacking it, while each pathogen carries matching genes for a virulence (A) for each of the R genes of the host plant.


The a virulence gene of the pathogen (A) serves to trigger the host gene (R) into action. This then sets in motion a series of defense reactions that neutralize and eliminate the specific pathogen that carries the matching gene for a virulence (A), while the attacked and a few surrounding cells die.

This type of defense or resistance is known as vertical, hypersensitive response, race-specific, major gene, or  R gene resistance.

Induced biochemical defenses in the
hypersensitive response (vertical
resistance)

The hypersensitive response is a localized induced cell defense in the host plant at the site of infection by a pathogen (Fig. 3). The hypersensitive response is the result of quick mobilization of a cascade of defense responses by the affected and surrounding cells and the subsequent release of toxic compounds that often kill both the invaded and surrounding cells and, also, the pathogen. The hypersensitive response is often thought to be responsible for limiting the growth of the pathogen and, in that way, is capable of providing resistance to the host plant against the pathogen.

FIGURE 3
Hypersensitive response expressed on leaves of a resistant cowpea variety following sap inoculation with a strain of a virus that causes local lesions. The virus remains localized in the lesions.

Compatible & Incompatible

Earlier studies, for example, of a compatible interaction of Phytophthora infestans and potato, 43 genes appeared to be induced, 10 of which showed increased activity as a result of the infection. Some of them were homologous to genes already known to be activated during infection, e.g., for b-1,3-glucanase, some have homology to enzymes involved in detoxification, and some code for proteins that had not been reported earlier to be induced by infection.


In more recent studies, almost 2,400 genes were examined for transcriptional changes that may occur after inoculation with the incompatible fungal pathogen Alternaria brassicicola or after treatment with defense signaling compounds such as salicylic acid (SA), methyl jasmonate (MJ), or ethylene. More than 700 of the genes exhibited transcriptional changes in response to one or more of the treatments. Based on similarity of the sequences of these genes to known gene sequences, the majority of the activated genes were already known, but an additional 106 genes were also activated. Treatments with salicylic acid and methyl jasmonate activated 192 and 221 genes, respectively, but they also repressed the transcription of 131 and 96 genes, respectively.

Phytoalexins

Phytoalexins are toxic antimicrobial substances produced in appreciable amounts in plants only after stimulation by various types of phytopathogenic microorganisms or by chemical and mechanical injury. Phytoalexins are produced by healthy cells adjacent to localized damaged and necrotic cells in response to materials diffusing from the damaged cells.

Phytoalexins accumulate around both resistant and susceptible necrotic tissues. Resistance occurs when one or more phytoalexins reach a concentration sufficient to restrict pathogen development. Most known phytoalexins are toxic to and inhibit the growth of fungi pathogenic to plants, but some are also toxic to bacteria, nematodes, and other organisms.


Phytoalexin production and accumulation occur in healthy plant cells surrounding wounded or infected cells and are stimulated by alarm substances produced and released by the damaged cells and diffusing into the adjacent healthy cells. Most phytoalexin elicitors are generally high molecular weight substances that are constituents of the fungal cell wall, such as glucans, chitosan, glycoproteins, and polysaccharides. The elicitor molecules are released from the fungal cell wall by host plant enzymes. Most such elicitors are nonspecific, i.e., they are present in both compatible and incompatible races of the pathogen and induce phytoalexin accumulation irrespective of the plant cultivar.


The chemical structures of phytoalexins produced by plants of a family are usually quite similar; e.g., in most legumes, phytoalexins are isoflavonoids, and in the Solanaceae they are terpenoids (figure 7).

FIGURE 7
Chemical structure of phytoalexins

Capsidiol is a phytoalexin produced by certain plants in response to pathogenic attack.

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