Vol.12_No.2 - Pesticide Alternatives Lab - Michigan State University

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Spring 2003 Resistant Pest Management Newsletter Vol. 12, <strong>No.2</strong>after 17 generations of selection in the laboratory(Zhao et al.1998). Liang et al. (2000) found that theresistance ratio of H. armigera to Bt transgenic cotton,after selection for 16 generations was 43.3, andinheritance of resistance was controlled by a singleautosomal incomplete recessive allele.European corn borer, Ostrinia nubilalisThere has been a significant decrease insusceptibility across generations for selected strains ofO. nubilalis after chronic exposure to formulatedCry1Ab (Huang et al. 1997, Josette et al. 2001).Similarly, a 162-fold increase in resistance totransgenic Cry1Ac has been observed in European cornborer after 8 generations of laboratory selection (Bolinet al. 1999). Event 176 Bt corn hybrids express highlevels of Cry1Ab toxin in green plant tissue and pollen,but extremely low levels in the silk and kernels (Kozielet al. 1993), on which second generation O. nubilalislarvae have been shown to survive (Siegfried et al.2001). Zoerb et al (2003) stated that successfullydeveloped O. nubilalis larvae have either survivedexposure to sublethal doses of Cry1Ab Bt toxin orexploited plant tissues that do not express the toxin,and they further implicated that Event 176 hybrids donot satisfy requirements for high dose that arerecommended for resistance management purposes.Pink bollworm, Pectinophora gossypiellaField collected pink bollworm quickly evolvedresistance to Cry1Ac under laboratory selection (Patinet al. 1999, Simmons et al. 1998, Tabashnik et al.2000). Pectinophora gossypiella selected with Cry1Acprotoxin developed 300-fold resistance to Cry1Acprotoxin, and high levels of cross-resistance to Cry1Aaand Cry1Ab protoxin, and low levels of resistance forCry1Bb protoxin (Tabashnik et al. 2000a). Threeselections with Cry1Ac in artificial diet increasedresistance of pink bollworm to >100-fold relative to asusceptible strain (Liu et al. 2001).Tobacco caterpillar, Spodoptera spp.In general, Spodoptera spp. larvae are not verysusceptible to the Cry toxins (Strizhov et al. 1996).However, Cry1C toxin had been reported to be toxicagainst S. exigua (Visser et al .1988) and Spodopteralittoralis (Van Rie et al. 1990a). Selection to Cry1Cacaused 850-fold resistance to Cry1Ca and crossresistanceto Cry1Ab, Cry9C, and Cry2A, as well as toa recombinant Cry1E-Cry1C fusion protein in S.exigua (Moar et al. 1995), while in S. littoralis, 500-fold resistance to Cry1Ca and partial cross-resistance toCry1D, Cry1E, and Cry1Ab has been recorded(Muller-Cohn et al. 1996).BASIS for DEVELOPMENT of RESISTANCE Mutations ininsects that cause disruption of any of the stepsinvolved in the mode of action could confer resistanceto Bt (Heckel 1994). Decreased solubilization of the Btcrystal, decreased cleavage of the full-length Bt proteininto an active fragment, increased proteolytic digestionof the active fragment, decreased binding of the activefragment to the midgut epithelium, and decreasedfunctional pore formation are the major changes in theBt toxicity pathway responsible for evolution ofresistance (Gill et al. 1992). Previous genetic andbiochemical analyses of insect strains with resistance toBt toxins has indicated that: (i) resistance is restrictedto single group of related Bt toxins, (ii) decreased toxinsensitivity is associated with changes in Bt-toxinbinding to sites in brush-border membrane vesicles ofthe larval midgut, and (iii) resistance is inherited as apartially or fully recessive trait. If these threecharacteristics are common to all resistant insects,specific crop-variety deployment strategies couldsignificantly diminish problems associated withresistance in field populations of the target pests(Gould et al. 1992). Recent studies have shown that thegenetic basis of resistance to Bt toxins in insects issimilar to resistance to chemical insecticides, which isconferred by multiple physiological mechanisms underindependent genetic control. In Heliothis, the existenceof separate, independently assorting resistance geneshas already been confirmed by linkage analysis withmarker loci (Heckel 1994). Heckel et al. (1997)identified a major Bt- resistant locus in a strain of H.virescens exhibiting up to 10000-fold resistance toCry1Ac toxin. Despite many potential mechanisms ofresistance, the best-characterized and most widelyobserved mechanism of resistance to B. thuringiensis isreduced binding of toxin to midgut membranes (VanRie et al. 1990b). Changes in the binding affinities oftoxin receptors on the brush border membranes of theinsect midgut have been identified in Bt resistant P.interpunctella (Van Rie et al. 1990b), P. xylostella(Ferre et al. 1991), H. virescens (MacIntosh et al.1991), and Trichoplusia ni (Ballester et al. 1994).Cry1Ab and Cry1Ac have the same receptor in themidgut of O. nubilalis, with the receptor having ahigher affinity for Cry1Ab than for Cry1Ac (Denolf etal. 1993).Studies on a field population of P. xylostella havealso suggested that, apart from reduced binding, otherbiochemical mechanisms are involved in resistance toBt (Martinez-Ramirez et al. 1995). Some evidence forreduced conversion of protoxin to toxin and increaseddegradation of toxin also has been reported (Forcada etal. 1996, Oppert et al. 1994, 1997). In H. armigera, theexcessive degradation of protoxin in midgut juicetriggered by receptor binding of activated toxin waspresumed to be responsible for low sensitivity of theinsect to Bt (Shao et al. 1998). Toxin binding inresistant T. ni selected with Cry1Ab did not correlatewith resistance, since there was no cross-resistance to18
Spring 2003 Resistant Pest Management Newsletter Vol. 12, <strong>No.2</strong>Cry1Ac (Estada & Ferre 1994), which shares the samebinding site of Cry1Ab as demonstrated in O. nubilalismidgut membrane (Denolf et al. 1993).When the midgut proteinases from resistant strainof European corn borer were characterized, there was a35% decreased hydrolyzing efficiency in activation ofBt protoxin compared with the susceptible strain(Huang et al. 1999). However, in studies by Liu et al.(2000), Cry1C toxin was found to be significantly moretoxic than was Cry1C protoxin to resistant strain ofdiamond back moth, but not to susceptible strain. Ifreduced conversion of Cry1C protoxin to toxin is thesole mechanism of resistance, both susceptible andresistant larvae should be equally susceptible to Cry1Ctoxin. Further, they observed similar binding of 125I-Cry1C to brush border membrane vesicles from theCry1C resistant and susceptible strains and concludedthat reduced binding of Cry1C to midgut target siteswas not a mechanism of resistance in diamondbackmoth. Mohan & Gujar (2003) also found no differencesin proteolytic patterns of Cry1A protoxins in bothsusceptible and resistant populations of diamondbackmoth. They also stated that the differences insusceptibility of two populations to B. thuringiensisCry1Ab were not due to midgut proteolytic activity.McGaughey et al (1998b) indicated that apart fromtoxin solubility and/or proteinase activation in theinsect midgut, postbinding events such as receptoraggregation, pore formation, ionic fluxes, and insectrecovery may also be involved in resistancedevelopment. Following Cry1Ac ingestion by H.virescens, similar histopathological changes wereobserved in midgut epithelium in both susceptible andresistant colony (Forcada et al. 1999, Martinez-Ramirez et al. 1999), suggesting that resistance is dueto a more efficient repair (or replacement) of damagedmidgut cells (Ferre & VanRie 2002).Research conducted over the past 10 years hasindicated that it is likely that the increased use of Bttoxins from transgenics will result in a rapid evolutionof resistance in insects (Gelernter 1997). However,selection of plants for horizontal resistance is moredurable rather than vertical resistance, and the currentresearch on transgenic plants, particularlyincorporation of the Bt delta endotoxins into crops forcontrol of insects appears to be proceeding on a verticalresistance model, based on complete resistanceconferred by one or a few genes. These varieties, likethose produced through conventional resistancebreeding, may become susceptible to the target pests.This may undervalue the benefits of Bt in IPMapproaches (Waage 1996), as it runs the risk ofbreakdown of resistance in the long-term.It may be uneconomic to develop Bt-transformedcrops unless we develop strategies to extend theirusefulness. Wigley et al. (1994) proposed a plan inwhich the major elements to be considered fordeploying Bt genes among crops are: (i) assess the riskof Bt resistant insects evolving and dispersing out ofthe crop to infest others; (ii) characterize the diversityof Bt protein binding sites in the guts of keypolyphagous pests; and (iii) use the above informationto deploy Bt genes among different transgenic crops.RESISTANCE MANAGEMENT Resistant managementstrategies require detailed knowledge of the toxins'mode of action and genetic response of resistantinsects. Unfortunately, insects show great variability intheir genetic responses to Bt toxins. Schnepf et al.(1998) emphasized that laboratory selectionexperiments may give rise to very different outcomesfrom field situations. However, several resistancemanagement strategies have been proposed to delayadaptation to Bt-transgenic crops by pest populations(McGaughey & Whalon 1992, Raymond et al. 1991,Tabashnik 1994). The most promising with currentlyavailable technology is the use of refuges of nontransgeniccrops, augmented wherever possible, withhigh toxin expression in the plants and avoidingmosaics of different toxins and pesticides (Roush1997a).THE REFUGE STRATEGY The primary strategy fordelaying insect resistance to transgenic crops underlarge monocultures is to provide refuges of non-Bt cropplants that serve to maintain Bt-susceptible insects inthe population. This potentially delays the developmentof insect resistance to Bt crops by providingsusceptible insects for mating with resistant insects (Liu et al. 1999).The refuge strategy is expected to work ifresistance to Bt is inherited as a recessive trait. Thebasic goals of the mixture strategy are two fold: (i)reduce the difference in fitness between susceptible andresistant insects, and (ii) reduce the degree to which aresistant insect can pass on its phenotypic trait to itsoffspring. Refuges can consist of fields planted withnon-Bt plants or of non-Bt plants within the Bt plants.The large numbers of susceptible insects that surviveon the refuge plants are then available to mate with thesmall number of resistant insects that survive on the Btplants. The offspring of susceptible (SS) x resistant(RR) matings will be RS, and therefore, will notsurvive when they feed on high dose Bt plants.The US Environmental Protection Agency (EPA),which regulates transgenic pesticidal crops, believesthat scientifically sound long-term insect resistancemanagement (IRM) strategies are essential to theprotection of Bt microbial pesticides, transgenics, andreduction in the risks from the use of pesticides. TheEPA has imposed mandatory IRM requirements for Btcotton. Two structured refuge requirements have beenimposed: 4% unsprayed or 20% sprayed crops (Matten2000), and the refuge fields must be within 0.8 km oftheir Bt fields (EPA/ USDA 1999). Obviously,19
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