Resistance: antibiosis, antixenosis, tolerance

Stylet penetration of the phloem sieve element is followed by injection of watery saliva to disable the defensive phloem-sealing mechanisms present in most host plants.

If the aphid continues to feed from the phloem for longer than 10 minutes this generally indicates complete acceptance and feeding will normally continue for several hours (Powell et al. 2006).

Saliva

During feeding, aphids secrete rapidly gelling sheath saliva and watery, digestive saliva (Tjallingii 2006). Sheath is composed primarily of proteins, phospholipids, and conjugated carbohydrates. Watery digestive saliva is a more complex mixture of enzymes and other components capable of eliciting plant defence signals (Smith and Boyko 2007). Among aphids, specificity of elicitation could be mediated by differences in the composition of saliva, which may generate different profiles of plant allelochemicals (Messina et al.

2002).

Two enzymes found in the grain aphid’s saliva, are polyphenol oxidase and peroxidase.

Both enzymes are present in the gelling saliva but only polyphenol oxidase activity is found in the watery saliva. The secretion of these enzymes was associated with the probing during penetration of the epidermal and mesophyll tissues (Urbanska et al. 1998).

2.4. Resistance: antibiosis, antixenosis, tolerance

The three well-known mechanisms of plant defence against aphids are antibiosis, antixenosis and tolerance.

Antibiosis: the ability of the plant to reduce or stop the growth and or development of the insect (El Khishen et al. 2009), the insect accepts the plant as a host, but relative growth rate; body weight and the number of offspring are decreased.

Antixenosis: reduces the probability of contact between plants and the pest by influencing insect choice (El Khishen et al. 2009). The insect does not accept or recognise the plant as a host, and will avoid it because of one or more morphological or biochemical attributes of the plant.

Tolerance: is the mechanism by which plants maintain similar levels of yield under vastly different levels of insect pressure (El Khishen et al. 2009). The aphid survives and grows, but does not damage the plant during feeding (Basky 2005, Wratten et al. 1991).

Aphids are able to produce 16-18 generations a year and for these reasons have a huge reproductive potential and therefore are able to evolve novel biotypes which are adapted to the antixenotic and/or antibiotic aspects of plants and thereby break the resistance (Basky 2005).

2.4.1. Schizaphis graminum - Greenbug

Effective resistance breeding programs began in the 1970s against this aphid. Resistance to greenbug has been reported in Triticum turgidum conv. durum, Aegilops squarosa syn.

Triticum tauschii (Castro et al. 1999) and Aegilops speltoides (Castro et al. 2004). A series of resistant varieties were introduced, but each time a new aphid biotype appeared that could damage those varieties. By 1986, 5 biotypes of aphid were known to be pests on the resistant varieties, and today there are 8 aggressive biotypes (Castro et al.1999). These biotypes are distinguishable by their ability to overcome different genes for host plant resistance, which show clear differences in mtDNA (Emden and Harrington 2007).

The first greenbug resistant wheat cultivar, TAM 110 was released in 1997 (Smith et al.

2004).

Twenty-two genes have been characterized in various Gramineae, which express resistance to greenbug (Smith et al. 2004). Six genes have been introduced into wheat to control greenbug. The resistance genes Gb2 and Gb6 derived from rye are located on the wheat/rye chromosome 1RS/1AL. The gene Gb3 in Largo derived from Aegilops tauschii it is located on chromosome 7DL. The gene Gb5 derived from Ae. speltoides was located on chromosome 7S (Castro et al. 2004) and in hexaploid wheat has been introgressed on chromosome 7AL. Mapping positions of Gb1 and Gb4 are unknown (Castro et al. 2005).

2.4.2. Diuraphis noxia – Russian wheat aphid (RWA)

The first D. noxia resistant wheat cultivar was reported by Francoise Du Toit in 1987.

However the first registration of the D. noxia resistant cultivar ‘Halt’- which was a hard red winter wheat - happened in the US in 1996 (Quick et al. 1996). Since then, resistance has been identified in several wheat lines (Qureshi et al. 2005) and today about 300 varieties are known to contain resistance genes.

Previous studies on RWA – wheat interactions showed that the resistance response was associated with the hypersensitive response, including local and systemic accumulation of chitinases, β-1,3-glucanases and peroxidases. The induction of local resistance and systemic resistance is generally accompanied by elevated levels of salicylic acid in dicotyledonous plants. In the defence response of wheat to the RWA, salicylic acid plays an important role by inhibiting catalase activity leading to an accumulation of hydrogen peroxidase (Mohase and Van der Westhuizen 2002 b).

Eleven genes have been characterized and introduced to control RWA. Resistance in Halt arises from a single dominant gene called Dn4 (Randolph et al. 2005, Qureshi et al. 2005), which is located on 1DS chromosome (Arzani et al. 2004, Castro et al. 2004). In 2003 they discovered a new biotype of D.noxia, which breaks down resistance in cultivars which have Dn2 and Dn4 resistance genes (Castro et al. 2005, Qureshi et al. 2005).

Novel resistance-breaking aphid biotypes can evolve when antibiosis is the major component of resistance. Plant resistance to D. noxia is largely based on antibiotic effects, but combining different categories of resistance would be more effective than individual resistance. (Qureshi et al. 2005)

Van der Westhuizen concluded that Dn1 based resistance to D. noxia hinged on the production of pathogenic proteins produced by the plant after aphid damage (Qureshi et al.

2005). Dn1 (Mclntosh et al. 1998), Dn2 (Zheng-Qiang et al. 1995), Dn5 (Heyns et al.

2006), Dn6 (Randolph et al. 2005) and Dnx dominant genes are tightly linked to each other on 7DS near the centromere (Castro et al. 2004, Liu et al. 2005), while 7DL is the location of Dn3 and Dn8. (Castro et al. 2005). Dn9 is located on 1DL (Castro et al. 2004, Castro et al. 2005). Other resistance genes are Dn7, which was derived from Secale cereale (Castro et al. 2005) and Dnk.

2.4.3. Rhopalosiphum padi – Bird cherry-oat aphid

The bird cherry-oat aphid is the most economically significant aphid pest of European cereal crops. Factors such as crowding, temperature, photoperiod and poor host plant quality can cause an increased production of alatae in aphid populations. Alatae may lead to greater dispersal and potential spread of barley yellow dwarf virus. Low levels of antibiosis can be important in limiting infestation levels of R. padi (Hesler et al. 1999).

Several sources of resistance have been identified to Bird cherry-oat aphid in Europe. Leaf phenolic content and phenylalanine ammonia-lyase activity have been involved in the mechanism of resistance (Smith et al. 2004)