**6. Response of aphids to plant characters**

The decision for suitability of the plant as a host is made in the very first phase of the host selection. *Alate* aphids use both visual [44] and chemical cues [45] to decide landing on a plant. Upon landing aphids encounter trichomes as the first line of defense. Trichomes can be either glandular or nonglandular. Regardless of their structure, trichome density has significant influence on aphid feeding [46]. Many crop wild relatives (CWRs) of cultivated plants and resistant varieties are resistant to aphid attack due to the presence of trichomes that affect aphid movement and stylet insertion [47]. For example, the presence of high density of trichomes (both simple and glandular) in wild tomato, *Lycopersicon pennellii* (Corr.) D'Arcy, imparts high level of resistance (R) to aphid attack. In addition, the glandular trichomes produce toxic exudates that trap aphids and kill them.

In addition to trichomes, plants possess other constitutive defenses such as thorns and thick cell walls that provide direct resistance to plants against aphid

**163**

*Aphid-Plant Interactions: Implications for Pest Management*

plants in the family Brassicaceae and Solanaceae.

aid in faster resistance development [52].

and for development.

feeding. Though these mechanical barriers are constitutive defenses, they can also

Brassica plants possess a well-studied class of sulfur-containing secondary metabolites—glucosinolates—that defend them from insects. However, during the course of evolution, some (though only a few) insects have been specialized to feed even on these plants. The examples include the turnip aphid, *Lipaphis erysimi* (Kaltenbach); cabbage aphid, *Brevicoryne brassicae* (L.); and cabbage white butterflies, *Pieris brassicae* and *P. rapae* [51]*.* These insects have evolved to use otherwise toxic compounds to their advantage—as cues for the identification of host plants

Similarly, members of family Solanaceae, e.g., potato and tomato, possess glycosidic alkaloids (tomatine, solanine) that defend them from not only insect pests but bacteria and fungi as well. However, some of the species have evolved to overcome this defense, for example, *Macrosiphum euphorbiae* (Thomas) and *Myzus persicae* (Sulzer). The well-known insecticidal compound, nicotine, found in *Nicotiana* spp. provides protection against feeding aphids. However, continuous selection pressure exerted by these compounds leads to the development of resistance in aphid populations to these compounds. The presence of both sexual (that includes a genetic variability) and asexual modes of reproduction (that leads to faster multiplication)

The resistance gene present in resistant plant provides protection against avirulent strains of insects. To date, one R gene (*Mi-1.2*) has been characterized at molecular level. Plants that possess *Mi-1.2* gene are resistant to potato aphid, two whitefly biotypes (silverleaf whitefly and biotype Q ), syllid, and three nematode species [53–55]. Due to the high selection pressure on insect population, there are chances of resistance breakdown in plants due to the development of counter resistance to the *Mi-1.2* [56]. The other genes associated with aphid resistance include virus aphid transmission (*Vat*) resistance gene in melon that confers antixenotic resistance to melon aphid, *Aphis gossypii* Glover, and to virus transmission associated with this species [57] and recombination-activating gene (*Rag1*) in soybean

that provides resistance to soybean aphid, *Aphis glycines* Matsumura [58].

The defense-signaling mechanism in plants after aphid attack is similar to incompatible responses in plant-pathogen interactions. Aphid feeding triggers SA-dependent response similar to that triggered by biotrophic pathogens and/or *PR*

be produced in response to aphid feeding (directly induced defenses). In addition to these structural defenses, constitutive defenses can also be chemical. For example, glandular trichomes of *Solanum berthaultii* Hawkes produce (E)-farnesene—aphid alarm pheromone that triggers aphid dispersal and prevents colonization [48]. Such antixenotic defenses are of great significance and particularly effective against aphid species that act as vectors of plant pathogenic viruses. However, successful virus transmission can occur even on nonhost plants as stylet insertion is sufficient for some successful infection by quickly acquired viruses. Aphid salivation occurs on even resistant plants even if they do not feed on such resistant plants [23]. The depth of the sieve elements is an important factor determining successful feeding. The length of the aphid stylets must be compatible with the depth of sieve elements. In addition, thickness at the tip of stylets is also crucial for successful feeding [49]. The movement of stylets through plant tissue is mostly intercellular, and aphids probe all the cells that they encounter during probing. Sensorial structures located at the back of the mouth characterize the plant sap, and aphids recognize the substrate as host or nonhost. On nonhost plants, aphids retract the stylets and leaves in search of suitable host unless the plant produces toxins [50]. Many plant species possess toxic compounds that can be either constitutive or induced that have detrimental effect on insects. The well-known examples include

*DOI: http://dx.doi.org/10.5772/intechopen.84302*

### *Aphid-Plant Interactions: Implications for Pest Management DOI: http://dx.doi.org/10.5772/intechopen.84302*

*Plant Communities and Their Environment*

compatible aphid-plant interactions.

which is otherwise the nutritionally poor diet.

**6. Response of aphids to plant characters**

produce toxic exudates that trap aphids and kill them.

**5. Aphid endosymbionts**

phytohormone-dependent pathways. In response to infestation/infection, different phytohormone-dependent pathways are activated. The ethylene (ET) and jasmonate (JA) pathways are activated by different necrotrophic pathogens [27] and grazing insects [28], while salicylate (SA)-dependent responses are activated by biotrophic pathogens [27]. These responses lead to the production of various defense-related proteins and secondary metabolites with antixenotic or antibiotic properties. In the case of infestation by aphids, a SA-dependent response appears to be activated, while the expression of JA-dependent genes is repressed [29–32]. All these responses lead to the manipulation of the plant metabolism to ensure

The plant phloem sap is a highly unbalanced diet composed principally of sugars and amino acids with high C:N content. To cope with excess of sugars in their diet, aphids have evolved modification in their intestinal tract and filter out excess of sugars and water in the form of honeydew [33]. The most of amino acids are present at very low concentrations. Despite their nutritionally poor diet, aphids exhibit high growth and reproduction rates. Since aphids directly feed on the sugars and amino acids, they need not spend extra energy to digest complex nutrients such as proteins which remarkably increases their assimilation efficiency. In addition to this, the essential amino acids required by their growth and development are synthesized by symbiotic bacteria present in their body. Generally two types of symbiotic bacteria are known to be present in aphids: the primary (obligate) symbionts and secondary (facultative) symbionts. *Buchnera aphidicola* (γ3-proteobacteria: *Escherichia coli* is also a member of this group) is the most common vertically transmitted primary symbiont present in most aphid species [34]. Some species of aphids also bear other bacteria, i.e., "secondary symbionts." These include several species of γ-proteobacteria such as *Serratia symbiotica*, *Regiella insecticola*, and *Hamiltonella defensa* [35–43]. *B. aphidicola* is a coccoid hosted in the cytoplasm of specialized cells called mycetocytes/bacteriocytes in the hemocoel of insect. These endosymbionts upgrade the aphid diet by converting nonessential amino acids to essential amino acids. The evolution of symbiotic relationship with endosymbionts has enabled aphids to exploit new ecological niches, i.e., to feed on the plant phloem sap

The decision for suitability of the plant as a host is made in the very first phase of the host selection. *Alate* aphids use both visual [44] and chemical cues [45] to decide landing on a plant. Upon landing aphids encounter trichomes as the first line of defense. Trichomes can be either glandular or nonglandular. Regardless of their structure, trichome density has significant influence on aphid feeding [46]. Many crop wild relatives (CWRs) of cultivated plants and resistant varieties are resistant to aphid attack due to the presence of trichomes that affect aphid movement and stylet insertion [47]. For example, the presence of high density of trichomes (both simple and glandular) in wild tomato, *Lycopersicon pennellii* (Corr.) D'Arcy, imparts high level of resistance (R) to aphid attack. In addition, the glandular trichomes

In addition to trichomes, plants possess other constitutive defenses such as thorns and thick cell walls that provide direct resistance to plants against aphid

**162**

feeding. Though these mechanical barriers are constitutive defenses, they can also be produced in response to aphid feeding (directly induced defenses).

In addition to these structural defenses, constitutive defenses can also be chemical. For example, glandular trichomes of *Solanum berthaultii* Hawkes produce (E)-farnesene—aphid alarm pheromone that triggers aphid dispersal and prevents colonization [48]. Such antixenotic defenses are of great significance and particularly effective against aphid species that act as vectors of plant pathogenic viruses. However, successful virus transmission can occur even on nonhost plants as stylet insertion is sufficient for some successful infection by quickly acquired viruses. Aphid salivation occurs on even resistant plants even if they do not feed on such resistant plants [23].

The depth of the sieve elements is an important factor determining successful feeding. The length of the aphid stylets must be compatible with the depth of sieve elements. In addition, thickness at the tip of stylets is also crucial for successful feeding [49]. The movement of stylets through plant tissue is mostly intercellular, and aphids probe all the cells that they encounter during probing. Sensorial structures located at the back of the mouth characterize the plant sap, and aphids recognize the substrate as host or nonhost. On nonhost plants, aphids retract the stylets and leaves in search of suitable host unless the plant produces toxins [50]. Many plant species possess toxic compounds that can be either constitutive or induced that have detrimental effect on insects. The well-known examples include plants in the family Brassicaceae and Solanaceae.

Brassica plants possess a well-studied class of sulfur-containing secondary metabolites—glucosinolates—that defend them from insects. However, during the course of evolution, some (though only a few) insects have been specialized to feed even on these plants. The examples include the turnip aphid, *Lipaphis erysimi* (Kaltenbach); cabbage aphid, *Brevicoryne brassicae* (L.); and cabbage white butterflies, *Pieris brassicae* and *P. rapae* [51]*.* These insects have evolved to use otherwise toxic compounds to their advantage—as cues for the identification of host plants and for development.

Similarly, members of family Solanaceae, e.g., potato and tomato, possess glycosidic alkaloids (tomatine, solanine) that defend them from not only insect pests but bacteria and fungi as well. However, some of the species have evolved to overcome this defense, for example, *Macrosiphum euphorbiae* (Thomas) and *Myzus persicae* (Sulzer). The well-known insecticidal compound, nicotine, found in *Nicotiana* spp. provides protection against feeding aphids. However, continuous selection pressure exerted by these compounds leads to the development of resistance in aphid populations to these compounds. The presence of both sexual (that includes a genetic variability) and asexual modes of reproduction (that leads to faster multiplication) aid in faster resistance development [52].

The resistance gene present in resistant plant provides protection against avirulent strains of insects. To date, one R gene (*Mi-1.2*) has been characterized at molecular level. Plants that possess *Mi-1.2* gene are resistant to potato aphid, two whitefly biotypes (silverleaf whitefly and biotype Q ), syllid, and three nematode species [53–55]. Due to the high selection pressure on insect population, there are chances of resistance breakdown in plants due to the development of counter resistance to the *Mi-1.2* [56]. The other genes associated with aphid resistance include virus aphid transmission (*Vat*) resistance gene in melon that confers antixenotic resistance to melon aphid, *Aphis gossypii* Glover, and to virus transmission associated with this species [57] and recombination-activating gene (*Rag1*) in soybean that provides resistance to soybean aphid, *Aphis glycines* Matsumura [58].

The defense-signaling mechanism in plants after aphid attack is similar to incompatible responses in plant-pathogen interactions. Aphid feeding triggers SA-dependent response similar to that triggered by biotrophic pathogens and/or *PR* gene RNAs in resistant than in susceptible plants [59–61], while there is downregulation of jasmonic acid-dependent genes [62]. From the very first stylet insertion in epidermal tissues to sustained feeding on sieve elements, aphids continuously inject saliva in the plant tissue which continuously interacts with plant cells to determine compatible/incompatible aphid-plant interactions. However, such interactions have been partially understood. Aphid saliva plays an important role in countering plant defense response and modifying the incompatible interaction to compatible one by modifying the plant metabolism. Aphid feeding may lead to alterations in host plants, including morphological changes, alteration in resource allocation and production of local, and systemic symptoms [32].
