Interaction of azadirachtin with the lipid-binding domain: Suppression of lipid transportation in the silkworm, Bombyx mori

Pratheep, Thangaraj; Neelamegam, Ramesh kumar; Kayalvizhi, Nagarajan; Krishnan, Muthukalingan

doi:10.1016/j.pestbp.2018.09.001

Cited by 8 publications

(1 citation statement)

References 39 publications

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“…The semblable effect was also reported on the midgut in the larval of Bactrocera dorsalis and Spodoptera litura with azadirachtin exposure, ,, which could cause apoptosis and shedding of tissue cells, resulting in thinning of the intestinal wall and destruction of the intestinal tissue structure and further affecting the digestion and absorption function of the intestine. Besides, azadirachtin could suppress the lipid transportation to the ovary of Bombyx mori and cause short lifespan, ovarian abnormalities, lower fecundity, and compound eye abnormalities in Drosophila melanogaster . Azadirachtin also inhibits ecdysis in insects.…”

Section: Introductionmentioning

confidence: 99%

Azadirachtin Inhibits Nuclear Receptor HR3 in the Prothoracic Gland to Block Larval Ecdysis in the Fall Armyworm, Spodoptera frugiperda

Fan,

Wu,

Liu

et al. 2023

J. Agric. Food Chem.

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Azadirachtin has been used to control agricultural pests for a long time; however, the molecular mechanism of azadirachtin on lepidopterans is still not clear. In this study, the fourth instar larvae of fall armyworm were fed with azadirachtin, and then the ecdysis was blocked in the fourth instar larval stage (L4). The prothoracic glands (PGs) of the treated larvae were dissected for RNA sequencing to determine the effect of azadirachtin on ecdysis inhibition. Interestingly, one of the PG-enriched genes, the nuclear hormone receptor 3 (HR3), was decreased after azadirachtin treatment, which plays a critical role in the 20-hydroxyecdysone action during ecdysis. To deepen the understanding of azadirachtin on ecdysis, the HR3 was knocked out by using the CRISPR/Cas9 system, while the HR3 mutants displayed embryonic lethal phenotype; thus, the stage-specific function of HR3 during larval molting was not enabled to unfold. Hence, the siRNA was injected into the 24 h L4 larvae to knock down HR3. After 96 h, the injected larvae were blocked in the old cuticle during ecdysis which is consistent with the azadirachtin-treated larvae. Taken together, we envisioned that the inhibition of ecdysis in the fall armyworm after the azadirachtin treatment is due to an interference with the expression of HR3 in PG, resulting in larval mortality. The results in this study specified the understanding of azadirachtin on insect ecdysis and the function of HR3 in lepidopteran in vivo.

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