During evolution, different forms of natural resistance to parasites have been established. Plant innate plant defense mechanisms like morphological barriers, diverse compounds of the secondary metabolism and induced resistance mechanisms (PTI) allow only a selected number of parasitic pests to attack a specific range of plant species (Schuler 1998). Often active plant defense is induced immediately after insect attack, leading to the production of various anti-insect compounds, including anti-feedants, toxins and digestibility reducers (Korth 2003; Voelckel and Baldwin 2004a, b). Also indirect defense mechanisms are activated that recruit natural enemies from the plant's surroundings to attack feeding insects (Turlings and Tumlinson 1992; De Moraes et al. 1998; Kessler and Baldwin 2001).
Insect resistance loci have been reported in crop plants like wheat, barley, maize, potato and rice (Yencho et al. 2000). So far, little is known about the underlying molecular mechanisms as the majority of insect resistance loci are mapped as QTLs, making the characterization and the use of these resistance traits for plant breeding difficult and time-consuming. The only cloned insect resistance gene is Mi-1. Mi, originally isolated as a root knot nematode (Meloidogyne spp.) resistance gene from wild tomato (Lycopersicon peruvianum) also confers resistance against potato aphids (Macrosiphum euphorbiae) and whiteflies (Bemisia tabaci; Vos et al. 1998; Martinez de Ilarduya et al. 2001; Nombela et al. 2003).
In contrast, a set of nematode resistance genes have been identified from various crop plants. Economically the most important plant-parasitic nematodes are cyst nematodes of the genus Heterodera and Globodera and root-knot nematodes of the genus Meloidogyne. Root-knoot nematodes of Meloidogyne spp. are obligate sedentary endoparasites. Agronomically important species of cyst nematodes, mainly active in temperate regions of the world, are G. rostochiensis and G. pallida on potato and H. glycines on soybean. In addition, more than 80% of the Cheno-podiaceae and Brassicaceae species are hosts of H. schachtii (Steele 1965), including economically important crops like sugar beet (Beta vulgaris), spinach (Spinacea oleracea), radish (Raphanus sativus) and rape seed (Brassica napus). Today H. schachtii is spread over 40 sugar beet-growing countries throughout the world (McCarter et al. 2008).
Nematodes completely penetrate main and lateral roots in the elongation or root hair zones of a susceptible plant as motile infective second-stage juveniles (J2) which hatch in the soil from eggs contained within a protective cyst (cyst nema-todes) or egg sac (root-knot nematodes). They penetrate the plant cell walls using their robust stylet. However, before the stylet penetrates, cell walls are degraded by a number of enzymes released from the nematode's subventral glands. These include |b-1,4-endoglucanases (cellulases; Gao et al. 2001), apectate lyase (Doyle and Lambert 2002) and an expansin (Qin et al. 2004). J2s migrate within the root cortex towards the vascular cylinder and induce remarkable changes in a number of host cells, to establish highly metabolically active feeding cells sustaining the nematode throughout its life cycle (syncytium for cyst nematodes; giant cell for root-knot nematodes; Davis et al. 2004, 2008; Fuller et al. 2008). After three additional molts, adult males emerge from the root and are attracted to the females, where fertilization occurs. At maturity, the female of a cyst nematode dies and the body is transformed into a light brown cyst where eggs and juveniles survive and remain dormant until root exudates stimulate juveniles to hatch and emerge from the cyst. By contrast, eggs of Meloidogyne spp. are released on the root surface in a protective gelatinous matrix.
Chemical control of nematodes is restricted. Most of the nematicides have been withdrawn from the market due to high environmental risks. Crop rotations with non-host plants including wheat, barley, corn, beans and alfalfa as well as nematode-resistant radish and mustard are functional, but often not economically practical. In this context, the breeding of resistant cultivars is the most promising alternative.
The majority of cloned nematode resistance genes originate from crop wild relatives. The first nematode R gene to be cloned was Hs1pro'1 from sugar beet, which confers resistance against the sugar beet cyst nematode H. schachtii (Cai et al. 1997). Other cloned nematode R genes closely resemble known plant R genes in their domain structure. Four of these genes, Mi-1, Hero, Gpa2 and Gro1-4, all cloned from tomato or potato relatives, fall into the NBS-LRR class of R genes (Williamson and Kumar 2006). The tomato genes Mi-1 and Hero, respectively, confer broad-spectrum resistance to several root knot nematode species (Milligan et al. 1998; Vos et al. 1998) and to several pathotypes of the potato cyst nematodes G. rostochiensis and G. pallida (Ernst et al. 2002). Mi resistance was first transferred into commercial tomato cultivars in the 1950s (Gilbert et al. 1956). Mi also confers resistance to two totally unrelated parasites, the potato aphid Macrosiphum euphorbiae and the white fly Bemisia tabaci (Rossi et al. 1998; Nombela et al. 2003), whereas the potato genes Gpa2 and Gro1-4 mediate resistance to a narrow range of pathotypes of the potato cyst nematode G. pallida (van der Vossen et al. 2000;
Paal et al. 2004). So far, little is known about the action mode of the cloned nematode resistance genes. It is generally believed that these genes recognize nematode effectors triggering specific signaling pathways that lead to resistance responses. Agronomically more important nematode R genes are likely to be cloned in the near future, including the H1 gene that confers resistance to G. rostochiensis in potato (Bakker et al. 2004) and the Me gene of pepper for resistance to Meloidogyne species (Djian-Caporalino et al. 2007).
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