User:Raoulrob

Plant Pathosystems A pathosystem (3) is a subsystem of an ecosystem, and it is defined by parasitism. In a plant pathosystem, the host population is usually a single species of plant, and the parasite population is usually a single species of insect, mite, nematode, parasitic Angiosperm, fungus, bacterium, phytoplasma, virus, or viroid. Exceptions include the pathosystems of heteroecious aphids and rusts, which each have two species of host, and those of insect vectors of plant viruses, which each involve two species of parasite. Polyphagous species of parasite may have quite a wide host range. Pathosystem studies are conducted at the higher systems levels, and normally involve the interaction of a population of the parasite with a population of the host. In a wild plant pathosystem, both the host and the parasite populations exhibit genetic diversity and genetic flexibility; conversely, in a crop pathosystem, the host population normally exhibits genetic uniformity and genetic inflexibility (i.e., clones, pure lines, hybrid varieties), and the parasite population assumes a comparable uniformity. This distinction means that a wild pathosystem can respond to selection pressures, but that a crop pathosystem cannot. It also means that a system of locking (see below) can function in a wild pathosystem but not in a crop pathosystem. Pathosystem balance means that the parasite does not endanger the survival of the host; and that the resistance in the host does not endanger the survival of the parasite. This is self-evident from the evolutionary survival of wild pathosystems, as systems, during periods of geological time (7). The gene-for-gene relationship (1) is an approximate botanical equivalent of antigens and antibodies in mammals. For each resistance gene in the host, there is a corresponding, or matching, gene in the parasite. When the genes of the parasite match those of the host, the resistance does not operate. There are two kinds of resistance to parasites in plants: Vertical resistance (8) involves a gene-for-gene relationship. This kind of resistance is genetically controlled by single genes, although several such genes may be present in a single host or parasite individual. Vertical resistance is ephemeral resistance because it operates against some strains of the parasite but not others, depending on whether or not a match occurs. Vertical resistance requires pedigree breeding and back-crossing. It has been the resistance of choice during the twentieth century. Horizontal resistance. (8) does not involve a gene-for-gene relationship. It is the resistance that invariably remains after vertical resistance has been matched. It is genetically controlled by polygenes and it is durable resistance as many ancient clones testify. It requires population breeding and recurrent mass selection. Infection is the contact made by one parasite individual with one host individual for the purposes of parasitism. There are two kinds of infection: Allo-infection (3) means that the parasite originates away from its host and has to travel to that host. The first infection of any individual host must be an allo-infection. Vertical resistance can control allo-infection only. It normally does this with a system of locking (see below) which reduces the proportion of allo-infections that are matching infections. Auto-infection (3) means that the parasite originates on, or in, the host that it is infecting. Auto-infection and all the consequences of a matching allo-infection, can be controlled only by horizontal resistance. This is because the parasite individual reproduces asexually to produce a clone (or else reproduces sexually and quickly reaches homogeneity of matching individuals) and all auto-infection is thus matching infection. An epidemic is the growth of a parasite population which is made at the expense of the host population. There are two kinds of epidemic: Continuous epidemics (4) have no break in the parasitism; they have no gene-for-gene relationships; they involve evergreen trees, and many herbs in the wet tropics. Discontinuous epidemics (4) have regular breaks in the parasitism, due to an absence of host tissue during an adverse season, such as a winter or tropical dry season; they often have a gene-for-gene relationship against some of their parasites; they involve annual plants, and the leaves and fruits of deciduous trees and shrubs. The n/2 model (pronounced ‘en over two’) indicates the mode of operation of the gene-for-gene relationship in a wild plant pathosystem (5). It apparently functions as a system of locking in which every host and parasite individual has half of the genes in the gene-for-gene relationship (i.e., n/2 genes, where n is the total number of pairs of genes in that relationship). Each gene in the host is the equivalent of a tumbler in a mechanical lock, and each gene in the parasite is the equivalent of a knob on a mechanical key. Provided that each n/2 combination of genes occurs with an equal frequency, and with a random distribution, in both the host and parasite populations, the frequency of matching allo-infections will be reduced to the minimum. For example, with six pairs of genes, each host and parasite individual would have three genes, and there would be twenty different locks and keys; with a twelve-gene system, there would be 924 6-gene locks and keys. Given an equal frequency and a random distribution of every lock and key, the frequency of matching allo-infection would be 1/20 and 1/924, respectively. These figures are obtained from Pascal’s triangle. (2, 5).	This system of locking cannot function in a crop pathosystem in which the host population has complete uniformity. A crop pathosystem is the equivalent of every door in the town having the same lock, and every householder having the same key which fits every lock. A system of locking is ruined by uniformity, and this is exactly what we have achieved when protecting our genetically uniform crops with vertical resistance. A gene-for-gene relationship can evolve only in a discontinuous pathosystem (4). This is because it functions as a system of locking. A matching allo-infection is the equivalent of a lock being unlocked. With the end of the season, all matched (i.e., unlocked) host tissues disappear. With the onset of a new growing season, all host tissue (e.g., new leaves of a deciduous tree, newly germinated annual seedlings) is unmatched and each host individual has a vertical resistance that is functioning. This is the equivalent of re-locking. This alternation of matching and non-matching (or unlocking and re-locking) is an essential feature of any system of locking, and it is possible only in a discontinuous pathosystem. Conversely, in a continuous pathosystem just one matching allo-infection on each host individual is required for that individual to be parasitised for the rest of its life which, in the case of some evergreen trees, may endure for centuries. A gene-for-gene relationship is useless in such a pathosystem and, consequently, it will not evolve. Crops that are derived from a continuous wild pathosystem (e.g., aroids, banana, cassava, citrus, cocoa, coconut, date palm, ginger, mango, oil palm, olive, papaya, pineapple, pyrethrum, sisal, sugarcane, sweet potato, tea, turmeric, vanilla, yams) have no gene-for-gene relationships, not withstanding a few erroneous reports to the contrary. Horizontal resistance is the resistance that invariably remains after a matching allo-infection has occurred (3). To postulate that horizontal resistance does not occur would be to postulate an absolute susceptibility. Such a level of susceptibility is experimentally unproved, and is theoretically impossible. Horizontal resistance is polygenically inherited and it can be exhibited at any level between its minimum and its maximum. Its maximum level should provide a virtually complete control of a parasite under conditions of maximum epidemiological competence. Comprehensive horizontal resistance will control all the parasites that have epidemiological competence in a particular agro-ecosystem. The greater the area of a uniform host population with a single vertical resistance, the more dangerous that resistance becomes. This is because of an increased selection pressure for the matching parasite, and an increased loss when the matching does occur. The greater the are of uniformity of vertical resistance, therefore, the greater the danger (7). The greater the area of a uniform host population with horizontal resistance, the more effective the horizontal resistance becomes. This is because parasite interference declines as the area of a horizontally resistant host population increases, and it is least when the entire crop of a region has a high level of horizontal resistance in all of its cultivars. The greater the area of uniformity of horizontal resistance, therefore, the greater the security (7). There are two kinds of plant breeding. Pedigree breeders work with single-gene characters, they use back-crossing, they emphasise one characteristic at a time, and they look to the parents and to the past. Population breeders work with many-gene characters, they use recurrent mass selection, they screen for all desirable characteristics simultaneously, and they look to the progeny and to the future. The latter process is more representative of natural evolution (6). In breeding crop plants for horizontal resistance to their parasites, the disciplines of plant breeding, plant pathology, and crop entomology should be regarded as being amalgamated into a single discipline.

References:

Flor, H.H. (1942); “Inheritance of pathogenicity in Melampsora lini.” Phytopath., 32; 			653-669. Person, C.O. (1959); “Gene-for-gene relationships in host-parasite systems.” Can. J. Bot. 37; 1101-1130. Robinson, R.A. (1976); “Plant Pathosystems.” Springer-Verlag, Berlin, Heidelberg, New 		York, 184pp. Robinson, R.A. (1987) Host Management in Crop Pathosystems. Macmillan, New York, 		Collier-Macmillan, London, 263pp Robinson, R.A. (1996) Return to Resistance; Breeding Plants to Reduce Pesticide 			Dependence”. agAccess, Davis, California, 480pp. Robinson, R.A. (2009) Plant Breeding and Farmer Participation, Food & Agric. Org, 			Rome; Chpt 15; pp 367-390 Robinson, R.A.(2010) Self-Organising Agro-Ecosystems; Sharebooks Publishing 				 Vanderplank, J.E. (1963); “Plant Diseases; Epidemics and Control.” Academic Press, 			New York & London, 349pp.