Plant Breeding for Disease Resistance:
Plant breeders concentrate on an important part of their effort on selection and growth of disease-resistant plant lines. Plant diseases can as well be partially controlled by the use of pesticides, and by cultivation practices like tillage, crop rotation, planting density, buy disease-free seeds and cleaning of equipment, however plant varieties with inherent (or genetically determined) disease resistance are usually the first choice for the disease control. Breeding for disease resistance has been in progress since plants were first domesticated, however it needs continual effort. This is due to the reason pathogen populations are frequently under natural selection for increased virulence, new pathogens can be introduced to a region, and cultivation processes can favor increased disease incidence over time, modifications in the cultivation practice can favor new diseases, and plant breeding for other traits can disrupt the disease resistance which was present in older plant varieties. A plant line having acceptable disease resistance against one pathogen might still lack resistance against the other pathogens.
1) Plant breeding for disease resistance usually comprises:
a) Recognition of resistant breeding sources (plants which might be less desirable in other manners, however which carry a helpful disease resistance trait). Ancient plant varieties and wild relatives are much significant to preserve as they are the most common sources of improved plant disease resistance.
b) Crossing of a desirable however disease-susceptible plant variety to the other variety which is a source of resistance, to produce plant populations which mix and segregate for the features of the parents.
c) Growth of the breeding populations in a disease-conducive setting. This might need artificial inoculation of pathogen onto the plant population. Cautious attention should be paid to the kinds of pathogen isolates which are present, as there can be important variation the efficiency of resistance against various isolates of the similar pathogen species.
d) Selection of the disease-resistant individuals. It is necessary to note that breeders are trying to sustain or enhance many other plant traits associated to plant yield and quality, comprising other disease resistance characteristics or traits, while they are breeding for enhanced resistance to any specific pathogen.
2) Host Range:
The plant pathogenic microorganisms comprise thousands of species. Just a small minority of such pathogens encompass the capacity to infect a wide range of plant species. Most of the pathogens rather show a high degree of host-specificity. Non-host plant species are frequently said to deduce non-host resistance. The word host resistance is employed if a pathogen species can be pathogenic on the host species however certain strains of that plant species resist some strains of the pathogen species.
There can be overlap in the causes of host resistance and non-host resistance. Pathogen host range can modify quite all of a sudden if, for illustration, the capacity to synthesize a host-specific toxin or effectors is gained through gene shuffling or mutation or through horizontal gene transfer from an associated or relatively unrelated organism.
3) Epidemics and Population Biology:
Plants in the native populations are frequently characterized trough substantial genotype diversity and dispersed populations. They as well have undergone millions of years of plant-pathogen Co-evolution. Thus as long as novel pathogens are not introduced from the other portions of the globe, natural plant populations usually show merely a low incidence of severe disease epidemics. In the agricultural systems, humans frequently cultivate single plant species at high density, having many fields of that species in an area, and with considerably reduced genetic diversity both in fields and among fields. Moreover, quick travel of people and cargo across the large distances raises the risk of introducing pathogens against which the plant has not been chosen for resistance. Such factors make modern agriculture specifically prone to disease epidemics. Common solutions to this problem comprise constant breeding for disease resistance, utilization of pesticides to suppress recurrent potential epidemics, utilization of border inspections and plant import limitations, maintenance of important genetic diversity in the crop gene pool.
In epidemiology, the term epidemic (epi- means 'upon or above' and demic- means 'people'), takes place whenever new cases of a certain disease, in a given human population and throughout a given period, substantially surpass what is 'expected', based on the recent experience (that is, the number of recent cases in the population throughout a specified time period is termed as the 'incidence rate'). Examples comprise cancer or heart disease. The other illustration comprises the infamous Black Plague of the middle Ages.
Defining the epidemic can be subjective, based in part on what is 'expected'. An epidemic might be limited to one locale (an outbreak), more general (an epidemic) or even global (or pandemic). As it is mainly based on what is 'expected' or thought normal, a few cases of a much rare disease might be categorized as an 'epidemic', while numerous cases of a common disease (like the common cold) would not.
The word Syndemics signifies to interacting epidemics which raise the health burden of influenced populations. Social conditions which heighten the health risk of populations (example: poverty, discrimination-stigmatization and marginalization) by rising stress, interpersonal violence, malnutrition and the experience of deprivation, raise the clustering of epidemic diseases and the probability of their interaction.
7) Non-infectious disease usage:
The word 'epidemic' is frequently employed in a sense to signify to prevalent and growing societal problems, for illustration, in discussions of obesity or drug addiction. It can as well be employed metaphorically to relate a kind of problem similar to those illustrated above.
8) Factors stimulating the new epidemics:
Factors which have been illustrated to stimulate the increase of new epidemics comprise:
a) Modifications in agricultural practices and land usage.
b) Variations in the society and human demographics.
c) Poor population health (example: malnutrition, high prevalence of HIV)
d) Hospitals and medical methods.
e) Evolution of the pathogen (example: increased virulence and drug resistance)
f) Contamination of the water supplies and food sources.
g) International travel.
h) Breakdown of public health programs.
i) International trade
j) Reduced levels of biodiversity (example: via environmental destruction)
Breeding for pest resistance:
1) Resistance Breeding before Mendel:
Wild relatives of crop plants like wheat, beans and maize are not consistently resistant to insect and disease pests. This can be explained in an easy fashion - when selections of such wild populations are set out in plant-rows, a few of them are highly susceptible, others are resistant, and a few are intermediate in resistance to the common pests of the area. The first plant breeders, those men and women who domesticated crops like maize, beans and wheat, could save just those genotypes which had some level of resistance, that is, those individual plants that didn't succumb to pest depredation. In consequence, thus, they chosen for pest resistance and therefore modified the population structure of their crop species in the favor of resistance genes. This change made it likely to grow the crops in monoculture that was convenient for food production and harvest. It was as well convenient for the multiplication of disease and insect pests which might not be influenced by the limited sample of resistance genes.
2) Resistance Breeding after Mendel:
Genetics-based plant breeding, begin in the early years of the 20th century, generated new crop varieties having enhanced resistance to main disease and insect pests. Generally such resistance was build up as a second stage - a rescue operation - after new varieties, chosen primarily for high yield, were discovered to be susceptible to a specific insect or disease. Breeders found early on that they could recognize single genes (generally dominant) which conferred in essence complete resistance to the pest in question. Varieties having such exceptional resistance were developed and discharged for large-scale farmer use. However breeders then discovered, all too frequently, that the 'perfect' resistance lost its efficiency after a few seasons. They soon learnt, by the help of entomologists and plant pathologists that insect and disease pests are highly diverse genetically and that almost devoid of fail a rare pest genotype will turn up (or perhaps be made de novo through natural mutation) which is not influenced by the newly-deployed resistance gene. The latest pest genotype multiplies and the crop variety's resistance 'breaks down'.
As years go by, breeders discovered that some types of resistance didn't fail, and that such resistance frequently was less than complete; the plants suffered some damage however gave performance overall. This longer lasting resistance was dubbed 'durable' resistance. Moreover, the breeders found out that durable resistance generally (however not always) were governed by some genes instead of by one main gene. The multifactorial type of resistance has been termed as 'horizontal resistance'. The major-gene resistance has been termed 'vertical resistance'.
The excellent news, then, was that breeders could recognize and breed for durable resistance. The horrific news was that the breeding was harder as some genes had to be transferred at one time, thus needing bigger populations for selection, and also multiplying the common problems with 'linkage drag' (or undesirable genes which are tightly associated to the desired ones). To this day, breeders utilize both types of resistance in differing proportions, according to the crop and where it is grown.
At on this time, breeders acknowledged that it would be significant to conserve remnant seed of landraces from all around the world, however particularly from the centers of diversity of their crop. As farming global grew more commercial, farmers turned more and more to professionally bred varieties which were better suited to the commercial production, and in so doing they discarded their landraces. When remnant seed of such landraces was not collected and saved in special storage facilities, the genetic base for crop breeding in the future would be severely narrowed. Seed banks were required. Via the efforts (particularly in the year 1960 and 1970) of a few far-sighted plant breeders, seed banks were established in some countries and in international research centers.
Therefore at the end of the 20th century, plant breeding for pest resistance had laid out the genetic frame-work of horizontal and vertical resistance and recognized significant sources of new resistance genes, that is, plant germplasm from anywhere in the world. Sources were limited, though, to the crop species itself or its relatives, either wild or cultivated. All of the introduced genes thus came from plants.
Plant breeders elected not just for tolerance or resistance to disease and insect pests, they as well elected for tolerance to abiotic stresses like heat and drought, cool temperatures and nutrient imbalance.
3) Four questions regarding pest resistance traits:
The discussion above represents that plant breeders have modified the genetic composition of crop species to a high degree as they chose for pest resistance and as well for resistance to ecological stresses. These changes are in addition to the main phenotypic changes (example: non-shattering, uniform and fast germination) which were a result of domestication. What have been the effects of these modifications, either on the crop species and it's near relatives or on the ecosystems in which such species are grown? Experienced plant breeders have addressed this question as they reacted to four queries sent to them. The questions were as follows:
A) Have the resistance characteristics or traits been stable over time?
B) Have they led to unwanted effects with respect to weediness of the crop or its relatives?
C) What have been the main sources of pest resistance genes which employed in the classical breeding (example: same species, related species and mutation)?
D) Are there appropriate differences among the resistance genes presently being engineered into plants and those which have been transferred through conventional breeding?
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