INSECTICIDAL AND INHIBITORY POTENTIAL OF TWO CHITIN SYNTHESIS INHIBITORS, BUPROFEZIN AND LUFENURON ON OKRA SHOOT AND FRUIT BORER, EARIAS VITTELLA

In this laboratory study, insecticidal and inhibitory potential of two chitin synthesis inhibitors (CSIs) viz. Buprofezin and Lufenuron were evaluated against okra shoot and fruit borer (OSFB). CSIs were applied on three days old larvae through different bioassay methods like topical or direct, okra-dip or indirect and combined (topical + leaf-dip). Data were collected on larval mortality, weight reduction and deformations of larvae and adults. Results showed that larval mortality and weight reduction were clearly dose, application methods and time dependent. In case of both CSIs, the highest mortality was found @ 1.0 ml/L that was followed by 0.75 ml and 0.50 ml/L respectively. Likewise, the highest body weight reduction was also found from 1.0 ml/L. In both cases, the concentration 0.5 ml/L was found less effective. In case of application methods, combined bioassay method was found superior than that of rest of the two methods. Moreover, a significant percentage of deformed larvae and adults were developed when 3 days old larvae were treated with either Buprofezin or Lufenuron @ 1.0 ml/L through combined bioassay method. The concentration 0.5 ml/L had very less efficacy on the development of deformed larvae or adults. Therefore, based on the laboratory findings Buprofezin and Lufenuron may be the potential component in IPM programmed, rather than their individual application, for controlling okra shoot and fruit borer as well as production of safe okra.

EFFICACY OF CHITIN SYNTHESIS INHIBITORS IN ARRESTING GROWTH AND DEVELOPMENT OF OKRA JASSID, AMRASCA BIGUTTULA BIGUTTULA (ISHIDA)

Chitin synthesis inhibitors (CSIs) are potential inhibitory chemical compound that disrupt molting process by interfering chitin synthesis and kill insects before attaining maturity. In this study, some chitin synthesis inhibitors (CSIs) viz. Tacoma 40SC (Buprofezin), Heron 5EC (Lufenuron), Pyrifen 10.8EC (Pyriproxifen) and Chitosan 75WP were tested against okra jassid, Amrasca biguttula biguttula (Ishida) to elucidate their potential effects in arresting body growth and development. The nymphs of jassids were exposed to selected CSIs through different application methods like topical, leaf-dip and the combination of both topical and leaf-dip. Weight data was collected at 7 days after treatment (DAT) application. Results showed that all of the CSIs except Chitosan had significant effect on the body weight reduction of okra jassid. Growth reduction was clearly concentrations and application method dependent. It has shown that higher concentrations were found to be more effective than lower concentrations. Bioassay study has showed that all the selected CSIs became able to enter in the insect body through contact as well as stomach action to disrupt molting process by inhibiting chitin synthesis that confirmed the contact and systemic actions of the selected CSIs. This study recommends that Tacoma 40SC @ 1.0 ml/L, Heron 5EC @ 1.5 ml/L and Pyrifen 10.8 EC @ 1.5 ml/L may be the potential alternatives of conventional neurotoxic insecticides in controlling jassids as they reduced 50-60% weight compared to untreated control. Moreover, protocols developed in this study for jassids collection and their safe transferring inside the petri dishes would be a useful and convenient approach for the researchers.

GFAT and PFK genes show contrasting regulation of chitin metabolism in Nilaparvata lugens

Glutamine:fructose-6-phosphate aminotransferase (GFAT) and phosphofructokinase (PFK) are enzymes related to chitin metabolism. RNA interference (RNAi) technology was used to explore the role of these two enzyme genes in chitin metabolism. In this study, we found that GFAT and PFK were highly expressed in the wing bud of Nilaparvata lugens and were increased significantly during molting. RNAi of GFAT and PFK both caused severe malformation rates and mortality rates in N. lugens. GFAT inhibition also downregulated GFAT, GNPNA, PGM1, PGM2, UAP, CHS1, CHS1a, CHS1b, Cht1-10, and ENGase. PFK inhibition significantly downregulated GFAT; upregulated GNPNA, PGM2, UAP, Cht2-4, Cht6-7 at 48 h and then downregulated them at 72 h; upregulated Cht5, Cht8, Cht10, and ENGase; downregulated Cht9 at 48 h and then upregulated it at 72 h; and upregulated CHS1, CHS1a, and CHS1b. In conclusion, GFAT and PFK regulated chitin degradation and remodeling by regulating the expression of genes related to the chitin metabolism and exert opposite effects on these genes. These results may be beneficial to develop new chitin synthesis inhibitors for pest control.

There is more than chitin synthase in insect resistance to benzoylureas: Molecular markers associated with teflubenzuron resistance in Spodoptera frugiperda

Chitin synthesis inhibitors are successfully used in pest control and are an excellent option for use in integrated pest management programs due to their low non-target effects. Reports on field-evolved resistance of lepidopteran pests to chitin synthesis inhibitors and the selection of laboratory resistant strains to these products require a detailed investigation on the resistance mechanisms and on the identification of molecular markers to support the implementation of efficient monitoring and resistance management programs. Teflubenzuron is a chitin synthesis inhibitor highly effective in controlling lepidopteran pests, including nowadays the world widely distributed fall armyworm (FAW), Spodoptera frugiperda (J.E. Smith, 1797) (Lepidoptera: Noctuidae). We report the selection of a laboratory strain of S. frugiperda resistant to teflubenzuron, and its use for the characterization of the inheritance of resistance, evaluation of cross-resistance to other chitin-synthesis inhibitors and the identification of a set of single nucleotide polymorphisms (SNPs) for use as candidate molecular markers for monitoring the evolution of resistance of S. frugiperda to teflubenzuron. The resistance of the selected strain of S. frugiperda to teflubenzuron was characterized as polygenic, autosomal, and incompletely recessive. The resistance ratio observed was nearly 1,365-fold. Teflubenzuron-resistant strain showed some cross-resistance to lufenuron and novaluron but not to chlorfluazuron. We also detected a set of 72 SNPs that could support monitoring of the resistance frequency to teflubenzuron in field populations. Our data contribute to the understanding of the resistance mechanisms and the inheritance of polygenic resistance of S. frugiperda to benzoylureas. We also contribute with candidate markers as tools for monitoring the emergence and spread of teflubenzuron resistance in S. frugiperda.