**1. Introduction**

Globally the area under vegetable cultivation is growing annually at the rate of 4.12% and production by 6.48%. The mean productivity is 15.49mt/ha which is quite low. In vegetables infestation of biotic stresses reflect highly on production productivity and quality. Application of chemicals leaves chemical residues in vegetables above threshold levels. Resistance is a relative attribute and refers to the ability of the plant to withstand the pest or pathogen. The susceptible plant shows severe symptoms due to which yield loss occur. A completely resistant plant shows nil reaction and a moderately resistant or field tolerant plant develops less disease development. Plants have selective resistance to some pests or pathogens and susceptible to others. They are species-specific or strain-specific. The rate of spread depends on the pest load or population, spore count and multiplication rate of pest/pathogen.

Improvement of cultivated plants through tapping germplasm resources depends on introducing variability through traditional and molecular breeding techniques. Wild species provides a vast gene pool for resistance development.

They have been used for decades to transfer genes of resistance or tolerance to the cultivated species. The use of wild species in breeding varieties particularly for increased vigor and resistance has been well recognized [1]. Introgression is the movement of genes or gene flow from one species into the gene pool. Inter specific hybridisation breaks the species barrier for gene transfer and makes it possible to transfer the resistant genes.

Complete exploitation of genetic variation enables the breeder to produce not only heterotic F1 hybrids but also recombinants with desirable attributes. Further, selection based on genetic nature will be highly useful to a great extent to screen out the parents and hybrids. Identification of resistance is also possible through quantifying the biochemical components present in the genotype. Further, in view of less marked host specificity, a plant breeding programme for insect resistance has to be handled separately from that of disease resistance.

In 3rd century B.C, Theophrastus observed that degree of resistance differ among varieties. It was later established in 1894, by Erikson that though pathogens are morphologically similar, they differ among each other in their ability to attack host plant. In 1911 Barrus narrated that various isolates of a pathogen differ in its ability to attack different varieties of the same plant species. This made the basis for the identification of physiological races and pathotypes. It was then called as pathogenecity *i.e* the infection of a host strain by a pathogen is genetically determined. In 1955, Flor formulated the of gene-for-gene hypothesis which denotes the relationship between host and pathogen. According to that disease resistance is determined by host and the genotype of the pathogen. The hosts differ in type of resistance while the pathogen differ in pathogenicity, but both are genetically controlled. The pathogen has the capacity to generate new variations in pathogenicity by reproduction methods and mutation. Therefore, the task of the breeder is to develop varieties resistant to the prevalent pathotypes of the pathogen and also for the new pathogen genotypes which will arise in future.

### **2. Genetic basis of resistance**

According to the experimental results so far reported in vegetable crops, the genetic basis of insect resistance is monogenic. The resistance of muskmelon to melon aphid. The tolerance of muskmelon to western biotypes of *Aphis gossypii* in breeding line LJ 90234 was governed by a single dominant gene [2]. Inheritance studies of fruit fly resistance in pumpkin cultivar Arka Suryamukhi showed that the resistance was controlled by a dominant gene. Similar studies in water-melon also indicated that the resistance to fruit fly was governed by a single dominant gene. The work on *Cucurbita pepo* revealed that the resistance to squash bug, was controlled by at least 3 genes and gene action appeared to be additive in nature. In an interspecific cross between resistant *Cucumis callosus* and susceptible *Cucumis melo* it was revealed that the susceptibility to fruit fly was governed by two pairs of complimentary genes. While working with tomato for resistance to fruitworm Fery and Cuthbert [3] reported that the antibiotics factor present in *Lycopersicon hirsutum* appeared to be inherited recessively.

Since interest in resistant vegetable varieties started more than half a century ago work has been done on major insect pests. However, studies have shown that the Mendelian segregation has led to the identification of major genes and that the alleles for resistance were dominant over those for susceptibility in number of instances except in some where it was found to be additive or complementary gene action or recessive.

The genetics of disease resistance was first studied by Britten in 1905. Then Person and Sidhu [4] reviewed 1000 Published papers and concluded that regardless of species, resistance generally segregated in the mendelian ratios. Resistance was dominant over susceptibility. Resistance in vegetable crops have been reported to be governed by mono or oligo or polygenes and effect of genes may be additive or dominant or epistatic. The information on inheritance of various diseases of vegetables is very meager. However, some workers reported different kinds of nature of inheritance. Resistance to buck eye rot of tomato appeared to be dominant over susceptibility. Resistance to fusarium wilt of tomato was conditioned by a single dominant gene. Tomato leaf curl virus is transmitted by white fly and is most serious problem. According to Som and Chaudhary [5], resistance to TLCV was incompletely dominant and governed by polygenes.

Resistance to most of the diseases in watermelon is controlled by a single dominant gene. Walker [6] reported resistance to fusarium wilt in watermelon as recessive. Powdery mildew is a major limiting factor in the production of muskmelon in most of the parts of the world. Resistance to *Erysiphae cichoracearum* race- 1 and race-2 is monogenic dominant. A study on resistance to powdery mildew caused by *Sphaerotheca fuligina*, in two resistant varieties campo and PMR-6 indicated that they have the same locus/loci conferring resistance. Genetic studies of resistance to *E. cichoracearum* race-2 had indicated that resistance is partly dominant and controlled by Pm-2 [7]. Resistance to downy mildew *(Pseudoperonospora* cubensis) of muskmelon in PI 124111 is controlled by two independently dominant gene [8]. Whereas resistance in PI 124112 was controlled by two partially dominant genes [9].

Antonio *et al*. [10] studied the inheritance of resistance by antixenosis for tomato leaf miner and reported that the inheritance of antixenosis resistance of genotype BGH-1497 is ruled by a polygenes in epistatic interactions, with a phenotypic proportion of 13:3 between susceptible and resistant genotypes respectively. In another experiment Gabriele Vitelli et al. [11] reported three transgenic eggplant lines bearing a mutagenized *Bacillus thuringiensis* Berl. gene coding for the Cry3B toxin. The fruit production was almost twice in the highly resistant lines (3–2 and 9–8). The 6–1 transgenic line showed an intermediate level of resistance. Analysis by double antibody sandwich–enzyme linked immune sorbent assay (DAS–ELISA), performed on different tissues, revealed a lower amount of Cry3B protein in the 6–1 transgenic line.

The root knot nematode, *Meloidogyne* is one of the most economically damaging plant parasitic nematode and is widely distributed throughout world [12]. The genus *Meloidogyne* is composed of 100 species, with *M. arenaria, M. incognita, M. hapla and M. javanica* being considered as "major" species [13]. Natural resistance genes "R-genes" are responsible for inducing resistance against nematodes in tomato. The genes Mi-1, Mi-2, Mi-3, Mi-4, Mi-5, Mi-6, Mi-7, Mi-8, Mi-9, and Mi-HT confer resistance to the root Knot nematode [14].
