History of Breeding for Disease Resistance
Theophrastus, in the third century B.C, noted that cultivated varieties differed in their ability to avoid disease. That diseases are produced by a pathogen was conclusively shown by Benedict Prevost, he showed that wheat bunt was produced by a fungus. During the middle of nineteenth century. Various workers, E.g. Andrew, Knight, noted that crop varieties differed for disease resistance. In 1904, Blakeslee described mating type differentiation in Rhizophus. In 1905, Biffen demonstrated that resistance to yellow rust in wheat was governed by a recessive gene segregating in the ratio 3 resistant: 1 susceptible in F2. Breeding for disease resistance is believed to have started with the work of Orton in 1900, who selected lines of cotton resistant to Fusarium wilt by growing cotton on wilt stick soil. He also used hybridisation to develop wilt (Fusarium oxysporum) resistant varieties of watermelon.
In 1894, Erikson showed that pathogen, although morphologically similar, differed from each other in their ability to attack different related host species. Later, in 1911, Barrus showed that different isolates of a microorganism differed in their ability to attack different varieties of the same host species, this finding is the basis for physiological races and or Pathotypes. Barrus distinguished two races, alpha, and Bita , of the pathogen. It was subsequently established that the ability of a pathogen to infect a host strain, i.e. pathogenicity is genetically determined; this was shown by Johnson and Newton in 1940 in case of black rust of wheat. Thus both the ability of host to resist invasion by a pathogens as well as the ability of a pathogen to infect a host strain, i.e pathogenicity, is genetically determined; this was shown by Johnson and Newton in 1940 in case of black rust of wheat . Thus both the ability of host to resist invasion by a pathogen as well as the ability of a pathogen to invade its host are genetically controlled. The concept of physiological differentiation was extensively applied to wheat stem rust by Stakman in 1910. In 1952, Flor postulated the hypothesis of gene for gene relationship between host and pathogen, which holds true in most of the cases and is widely accepted.
The information available so far clearly shows that the disease resistance of host is not a function of the host genotype alone; it is determined by the genotype of the pathogen as well. The host strains differ in resistance, while those of the pathogen differ in pathogenicity; both variations have genetic basis. The pathogen has a remarkable capacity for generating new variation in pathogenicity by a variety of reproduction methods and mutation. Thus the task of breeders is not only to develop varieties resistant to the prevalent Pathotypes of the pathogens, but also to be ready to face the challenge to be posed by the new Pathotypes in future.