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van Beek et al. found that there were no significant differences in the ET50 of the recombinant AcMNPVs expressing LqhIT2 under an early (hr5/ie1 or hr5/lef3)orearly/late(hr5/39K)genepromoter. Furthermore, regardless of the larval instar or dose applied, when the early hr5/ie1 promoter was used to drive the expression of LqhIT2 or AaIT, the ET50s of the recombinant AcMNPV expressing LqhIT2 were consistently lower (by 8–32 h) in comparison to those of the recombinant AcMNPV expressing AaIT. This was putatively due to differences in the effectiveness of the two toxins. As described above, Gershburg et al. (1998) have constructed recombinant AcMNPVs expressing the excitatory toxin LqhIT1 or depressant toxin LqhIT2 under either the early p35 gene or very late p10 gene promoters. They found that the recombinant AcMNPV expressing LqhIT1 under the p35 promoter had a slightly slower ET50 (73 versus 66 h) in comparison to the recombinant AcMNPV expressing LqhIT1 under the p10 promoter. However, they detected a clear paralytic effect when the p35 promoter was used to express LqhIT1 even when they were unable to detect the LqhIT1 by immunochemical analysis. Thus, they suggested that baculovirus expression of toxin in cells that are adjacent to the target sites of the motor neural tissues overcomes the pharmacokinetic barriers that the toxin may face when, for example, purified toxin is injected to the insect. Consistent with this hypothesis, Elazar et al. (2001) have shown that the concentration of AaIT in the hemolymph of paralyzed B. mori larvae is approximately 50-fold lower when the paralyzing dose is delivered by a baculovirus (BmAaIT) rather than by the direct injection of purified AaIT. They hypothesized that baculovirus expression of AaIT provides a continuous, local supply of freshly produced toxin (via the tracheal system) to the neuronal receptors, thus providing access to critical target sites that are inaccessible to toxin that is injected. Therefore, a lower level of continuous expression under an early promoter may be sufficient to elicit a paralytic response. As discussed above, Tomalski and Miller (1992) have constructed an occlusion-negative recombinant AcMNPV (vETL-Tox34) that expresses the tox34 gene under the baculoviral early PETL promoter. In early fifth instar larvae of T. ni, this virus induced much slower paralysis (occurring after 48 h in 95% of larvae) in comparison to control larvae infected with recombinant AcMNPVs (vEV-Tox34, vCappolh-Tox34, or vSp-Tox34) expressing tox34 under a very late or chimeric promoter (all larvae were paralyzed or dead by 48 h). Additionally, the average cumulative weight gain of vETL-Tox34 10: Genetically Modified Baculoviruses for Pest Insect Control 349 infected larvae at 24 h post injection was not significantly different to that of control larvae injected with AcMNPV or cell culture medium (mock infection). Lu et al. (1996) have also constructed a recombinant AcMNPV (vDA26tox34) expressing the tox34 gene under the early Da26 gene promoter. In comparison to vp6.9tox34 (tox34 under a late promoter) or vSp-tox34 (tox34 under a very late promoter) infected Sf-21 or TN-368 cells (derived from S. frugiperda and T. ni, respectively), TxP-I expression was detected at least 24 h earlier (but at dramatically lower levels) in Sf-21 and TN-368 cells infected with vDA26tox34. In time-mortality bioassays (at an LC95 dose), the ET 50 of vDA26tox34 in neonate larvae of S. frugiperda and T. ni was reduced by approximately 39% (61.8 versus 101.3 h) and 28% (71.2 versus 99.0 h), respectively, in comparison to wild-type AcMNPV. However, this was 17.1 and 29.5 h slower, respectively, in comparison to neonate larvae of S. frugiperda and T. ni that were infected with vp6.9tox34 (ET 50s of 44.7 and 41.7 h, respectively). Even though the TxP-I is expressed significantly earlier under the early promoter, it is apparently not expressed in sufficient quantity, at least initially, to paralyze larvae of S. frugiperda or T. ni. Popham et al. (1997) have also expressed the tox34 gene under the early DA26 and late p6.9 promoters (of AcMNPV) by recombinant HzSNPVs (HzEGTDA26tox34 and HzEGTp6.9tox34, respectively). They found that the ET50s of HzEGTDA26tox34 and HzEGTp6. 9tox34 in neonate larvae of H. zea were reduced by approximately 47% (35.4 versus 67.3 h) and 44% (38.0 versus 67.3 h), respectively, in comparison to a control virus. In contrast to the results of Lu et al. (1996), the early promoter was more effective in the case of HzSNPV and neonate H. zea suggesting that the effectiveness of a promoter will be virus and insect specific. With toxins of current potency, the use of early (and weak) promoters such as ie1, lef3, p35, etl, orDA26 may or may not provide any benefit in terms of improved crop protection. However, if toxins that act at lower concentration (i.e., with much greater potency) are identified, the use of early promoters may offer a great advantage. Tomalski and Miller (1992) have used a chimeric promoter (Pcap/polh) comprised of both the late capsid and very late polyhedrin promoter elements to drive the expression of the tox34 gene in an occlusion-negative recombinant AcMNPV (vCappolh- Tox34). In Sf-21 cell cultures infected with vCappolh-Tox34, TxP-I is detected in the culture medium at 12 h p.i. at levels that are similar to those found in vEV-Tox34 (tox34 under a very late
350 10: Genetically Modified Baculoviruses for Pest Insect Control promoter) infected Sf-21 cells at 24 h p.i. (i.e., highlevel expression occurred approximately 12 h earlier). When early fifth instar larvae of T. ni were injected with vCappolh-Tox34 approximately 50% of the insects were paralyzed by 24 h post injection. In comparison, only 10% or less of control virus (e.g., vEV-Tox34) infected larvae were paralyzed. Larvae infected with vCappolh-Tox34 also showed a significantly lower cumulative weight gain in comparison to control virus infected larvae. An occlusion-positive construct (vSp-Tox34) in which the tox34 gene was placed under another hybrid late/very late promoter (P SynXIV; Wang et al., 1991) has also been constructed by Tomalski and Miller (1991, 1992). The induction of paralysis by vSp-Tox34 in fifth instar T. ni was slightly delayed, but all of the larvae were paralyzed or dead by 48 h post injection (as were vCappolh-Tox34 injected larvae; Tomalski and Miller, 1991, 1992). In timemortality bioassays (at an LC95 dose), the ET50 of vSp-Tox34 in neonate larvae of S. frugiperda and T. ni was reduced by approximately 45% (55.4 versus 101.3 h) and 41% (58.5 versus 99.0 h), respectively, in comparison to control larvae infected with AcMNPV (Tomalski and Miller, 1992; Lu et al., 1996). Furthermore, the yield (2.1 10 9 versus 3.5 10 9 polyhedra per larva) of vSP-Tox34 polyhedra from infected last instar larvae of S. frugiperda was reduced by approximately 40% in comparison to AcMNPV infected control larvae. Tomalski and Miller (1992) suggested that this reduction in yield will cripple the virus in terms of its ability to compete effectively with the wild-type virus in the environment. Sun et al. (2004) have generated a recombinant HaSNPV (HaSNPV-AaIT) that expresses the AaIT gene under a chimeric promoter (ph-p69p) consisting of the late p6.9 gene promoter inserted immediately downstream of the very late polh gene promoter in the same direction. The AaIT gene cassette was inserted at the egt gene locus of HaSNPV. Detailed dose-mortality bioassays indicated that the LD50s of HaSNPV-AaIT was unchanged compared to wild-type (HaSNPV-WT) or egt genedeleted (HaSNPV-EGTD) viruses in first to fifth instar larvae of the cotton bollworm, H. armigera. In time-mortality bioassays, first to fifth instar larvae of H. armigera infected with HaSNPV-AaIT showed reductions in the ST50s of 10% (68.5 versus 76.5 h), of 20% (60.5 versus 75.5 h), 8% (71.0 versus 77.5 h), 4% (104.6 versus 109.0 h), and 10% (108.5 versus 121.0 h), respectively, in comparison to control larvae infected with HaSNPV-EGTD. In comparison to control (first to fifth instar) larvae infected with HaSNPV-WT, the corresponding reductions were 19, 28, 25, 21, and 18%, respectively. In third to fifth instar of H. armigera infected with HaSNPV-AaIT, the median times to feeding cessation (FT50s) were reduced by 25% (51.5 versus 68.5 h), 22% (66.5 versus 85.0 h), and 12% (84.5 versus 96.5 h), respectively, in comparison to control larvae infected with HaSNPV-EGTD. In comparison to control larvae infected with HaSNPV-WT, the corresponding reductions in the FT50s were 39%, 43%, and 30%, respectively. The role of the egt deletion in improving speed of kill is discussed further below. Sun et al. (2004) did not test constructs in which only the polh or p6.9 gene promoter was used to drive expression of the AaIT gene, thus it was not possible to predict if expression under the dual promoter is more effective than expression under a single late or very late promoter. The hsp70 promoter of D. melanogaster (Snyder et al., 1982) is constitutively active in insect cells (Vlak et al., 1990; Zuidema et al., 1990). Unlike very late or late gene promoters of the baculovirus, the hsp70 promoter does not require the expression of baculovirus early gene products or the initiation of viral DNA synthesis for its activity. The hsp70 promoter shows higher activity than early gene promoters, but it is not as active as baculoviral very late or late gene promoters (Morris and Miller, 1992, 1993). McNitt et al. (1995) have constructed occlusion-positive, recombinant AcMNPVs expressing AaIT (vHSP70AaIT) and TxP-I (vHSP70tox34) under the hsp70 promoter. TxP-I was expressed at a significantly higher level under the hsp70 promoter than under the early DA26 promoter in both vHSP70tox34 infected Sf-21 and TN-368 cell cultures (McNitt et al., 1995; Lu et al., 1996). Additionally, TxP-I expression was detected as early as 6 and 12 h p.i., respectively, in the culture medium of vHSP70tox34 infected Sf-21 and TN- 368 cells. Dose-mortality bioassays using neonate larvae of S. frugiperda or T. ni indicated that the LC50s of vHSP70tox34 were unchanged from that of the AcMNPV. Time-mortality bioassays (at an LC95 dose) in neonate S. frugiperda and T. ni showed that the ET 50s of vHSP70tox34 were reduced by approximately 59% (41.8 versus 101.3 h) and 46% (53.8 versus 99.0 h), respectively, in comparison to control larvae infected with AcMNPV. In comparison to occlusion-positive, recombinant AcMNPVs expressing the tox34 gene under very late (vSp-tox34) or late (vp6.9tox34) promoters, the ET50s of vHSP70tox34 were faster than both vp6.9tox34 (44.7 h) and vSp-tox34 (55.4 h) in neonate S. frugiperda; and faster than vp6.9tox34 (41.7 h) and slower than vSp-tox34 (58.5 h) in
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INSECT CONTROL BIOLOGICAL AND SYNTH
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INSECT CONTROL BIOLOGICAL AND SYNTH
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CONTENTS Preface vii Contributors i
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PREFACE When Elsevier published the
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J T Andaloro E. I. Du Pont de Nemou
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1 Pyrethroids B P S Khambay and P J
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activity. In contrast to most other
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Figure 1 Commercial and novel pyret
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Figure 2 Pyrethroids referred to in
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4-position result in almost complet
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and their primary site of action is
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Figure 4 Folded and extended confor
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aromatic rings or methyl groups by
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pyrethroids) and consequently a sec
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1998), although the precise mechani
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polymorphisms in the protein. Of th
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observed resistance to pyrethroids,
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propoxur against Culex quinquefasci
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esistance in house fly. Insect Bioc
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Shan, G.M., Hammock, B.D., 2001. De
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A1.4. Resistance The increasing num
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B A IIS4-S5 linker, IIS5 helix and
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2 Indoxacarb and the Sodium Channel
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Figure 2 Structures of pyrazoline-l
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observed that both indoxacarb and i
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deflections resulting from stresses
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Figure 8 Dihydropyrazole block appe
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potential conduction in the CNS of
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known to affect blocker affinity, w
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Figure 13 Diagrammatic representati
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that the probable mechanism of ovil
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conventional chemistries and spinos
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Clare, J.J., Tate, S.N., Nobbs, M.,
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Tsurubuchi, Y., Karasawa, A., Nagat
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R1 N N O N H indoxacarb. Thus, whil
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3 Neonicotinoid Insecticides P Jesc
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esidues, like the pyrid-3-ylmethyl
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containing neonicotinoids, and neon
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Studies were also done using compar
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Becke, 1988; Klamt, 1995) level of
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sampling using forcefield methods (
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Figure 9 Stable conformations and p
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Figure 13 Binding to putative catio
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Figure 14 Systemicity of neonicotin
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site (Kayser et al., 2002). Clothia
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Figure 20 Important pest insects ta
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Barley yellow dwarf virus vectors s
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investigate the mode of action of n
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within the desensitized state over
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the accumulation of this acid in th
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3.8.1. Safety Profile The introduct
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Table 7 Environmental profile of co
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substance is bound irreversibly to
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imidacloprid conferring a high leve
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nAChR are comparable to the efficac
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Figure 25 Flea control achieved wit
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and the resolution of FAD was teste
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Brown, J.K., Perring, T.M., Cooper,
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In: Ishaaya, I. (Ed.), Biochemical
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Léna, C., Changeux, J.-P., 1993. A
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patterns in Colorado potato beetle
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nach Saatgutbeizung. Pflanzenschutz
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Today, photoaffinity labeling (e.g.
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for control of stinkbugs in soybean
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Biochem. Physiol., doi: 10.1016/j.p
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4 Insect Growth- and Development-Di
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The molting process is initiated by
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Table 1 Bisacylhydrazine insecticid
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4.2.2. Bisacylhydrazines as Tools o
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to the three EcRs with either muris
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of action of ecdysone agonists was
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thus inducing effects and symptomol
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and microsomes. Subsequently, Willi
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dipteran insects, like the midge, C
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eetle (Exomala orientalis) when app
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metabolic fate studies showed the i
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y specific proteins in signaling pa
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their reduced risk for the environm
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can be reversed by applying JH. JH
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door for a more rational approach t
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apparent that it was a bHLH-PAS and
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Table 9 Continued Bemisia tabaci (s
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Table 11 Insect control with some a
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Table 13 Ecotoxicological profile o
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Flucycloxuron Nonsystemic acaricide
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The discovery of diflubenzuron spaw
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Table 15 Environmental effects of s
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ecessive (R male S female) manner,
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esistance management programs due t
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IPS Paraconfusus lanier (Coleoptera
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larvae parasitized by Microplitis r
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Kostyukovsky, M., Chen, B., Atsmi,
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Three-dimensional quantitative stru
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Riddiford, L.M., 1994. Cellular and
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characterization of resistant clone
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Biological Approaches to Pest Contr
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M389 L308 M272 T304 T393 V404 L420
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5 Azadirachtin, a Natural Product i
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and Hemiptera and was related to ef
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eported, but this is rather nonspec
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important source of pest control at
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effects with physiological effects
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eing associated with an accumulatio
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et al., 1992). Salehzadeh et al. (2
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ehavior of Spodoptera littoralis (p
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indica A. Juss. IBH Publishing Comp
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Smith, S.L., Mitchell, M.J., 1988.
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which interact directly with azadir
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6 The Spinosyns: Chemistry, Biochem
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Table 1 Structures of the spinosyns
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Table 2 Biological activity of spin
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A large synthetic effort has gone i
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216 6: The Spinosyns: Chemistry, Bi
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Figure 4 Spinosad metabolism in avi
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A6 Addendum: The Spinosyns T C Spar
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246 A6: Addendum Scott, 2008) and i
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248 7: Bacillus thuringiensis: Mech
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A7 Addendum: Bacillus thuringiensis
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280 A7: Addendum toxins is magnitud
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Table 1 Comparative properties of s
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286 8: Mosquitocidal B. sphaericus:
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Table 4 Characteristics of various
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Page 325 and 326: 314 9: Insecticidal Toxins from Pho
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Page 341 and 342: 330 A9: Addendum Lee, S.C., Stoilov
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Page 395 and 396: 384 A10: Addendum cysteine protease
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Page 399 and 400: 388 11: Entomopathogenic Fungi and
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400 11: Entomopathogenic Fungi and
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Zare, R., Gams, W., Culham, A., 200
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434 A11: Addendum although a number
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436 A11: Addendum Examination of ge
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440 12: Insect Transformation for U
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448 A12: Addendum genetic transform
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452 Subject Index Aphis gossypii (c
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454 Subject Index Bisacylhydrazine
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456 Subject Index Cry toxins (conti
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458 Subject Index Entomopathogenic
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460 Subject Index Homoptera molting
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462 Subject Index Kinoprene (ENSTAR
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464 Subject Index Muscle(s) sodium
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466 Subject Index Photorhabdus (con
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468 Subject Index Sodium channel bl
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470 Subject Index Toxocara cati, im
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