Fenoxycarb and methoxyfenozide (RH-2485) affected development and chitin synthesis through disturbing glycometabolism in Lymantria dispar larvae

BACKGROUND In holometabolous insects, the major developmental transitions – larval molting and pupation – are triggered by a pulse of 20‐hydroxyecdysone (20E) and coordinated by juvenile hormone. Methoxyfenozide (MF), an ecdysteroid agonist, represents a new class of insect growth regulators and is effective against lepidopteran pests. Fushi‐tarazu factor 1 (FTZ‐F1) is an ecdysone‐inducible transcription factor. To date, the effect of MF on 20E‐response genes remains unclear, and we speculate the involvement of FTZ‐F1 in MF's growth regulating effect. RESULTS MF at LC25 and LC10 caused severe ecdysis failure in Helicoverpa armigera, extended their larval duration, lowered their pupal weight, and reduced the respiratory, pupation and emergence rates. Furthermore, sublethal doses of MF inhibited ecdysteroidogenesis and lowered the intrinsic 20E titer, but showed an inductive effect on 20E‐response genes including HaFTZ‐F1. HaFTZ‐F1, predominantly expressed in larval epidermis, was markedly upregulated before or right after larval ecdysis, and maintained a high level in prepupal stage. Knockdown of HaFTZ‐F1 in 4th‐instar larvae severely impaired larval ecdysis, whereas its knockdown in final‐instar larvae caused abnormal pupation. Moreover, knocking down HaFTZ‐F1 downregulated three critical ecdysteroidogenesis genes, lowered 20E titer, and suppressed the expression of 20E receptors and 20E‐response genes. The introduction of 20E into HaFTZ‐F1‐RNAi larvae partly relieved the negative effects on the 20E‐induced signaling cascade. CONCLUSION Our findings reveal the adverse effects of sublethal doses of MF on the development of H. armigera and elucidate the resulting perturbations on the 20E‐induced signaling cascade; we propose that HaFTZ‐F1 regulates ecdysis and pupation by mediating 20E titer and its signaling pathway. © 2020 Society of Chemical Industry

Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Likewise in Lymantria dispar, MF treatment led to premature with incomplete molting phenotype and development obstruction. 38 To date, the toxic effects of MF,…”

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

Dissecting the roles of FTZ‐F1 in larval molting and pupation, and the sublethal effects of methoxyfenozide on Helicoverpa armigera

Zhang

Liu

et al. 2020

Transcriptome analysis of emamectin benzoate caused midgut damage by inducing oxidative stress, energy metabolism disorder and apoptosis in gypsy moth (Lymantria dispar)

Bai

et al. 2022

BACKGROUND Emamectin benzoate (EMB) is a semisynthetic bioinsecticide, which has been widely used in the control of forestry and agricultural pests. However, the mechanism of its toxic effects on the non‐neural tissues has been rarely reported. Here, we explored the mechanism of the midgut damage induced by EMB in gypsy moth (Lymantria dispar) in order to better understand the toxicological mechanism of EMB. RESULTS Our results confirmed that EMB caused damage to the midgut of gypsy moth by inducing apoptosis. Transcriptome showed that 1469, 650 and 950 genes were significantly differentially expressed in the midgut of gypsy moth after 24, 48 and 72 h of EMB exposure, and oxidative stress, energy metabolism disorder and apoptosis may be related to the toxic effects of EMB. The indicators related to oxidative stress, energy metabolism and apoptosis were further examined. The results showed that EMB could cause oxidative stress by increasing ROS level and inhibiting antioxidant enzymes (P < 0.05), such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), which in turn causes mitochondria injury. Subsequently, energy metabolism was inhibited by downregulating the activities and mRNA level of energy metabolism enzymes. Furthermore, the mitochondrial apoptosis pathway was activated, triggering apoptosis, and eventually causing midgut injury in gypsy moth. CONCLUSION Our results indicated that EMB caused damage to midgut by inducing oxidative stress, energy metabolism disorder and apoptosis in gypsy moth. Our findings shed new light on the toxicological mechanism of EMB on non‐neural tissues from oxidative stress, energy metabolism and apoptosis perspectives. © 2022 Society of Chemical Industry.

Chlorbenzuron downregulated HcLCP‐17 expression by depressing two 20E‐responsive transcription factors Br‐C and βFTZ‐F1 in Hyphantria cunea (Lepidoptera: Erebidae) larvae

Zhao,

Zhang,

Zou

et al. 2024

BACKGROUNDCuticular proteins (CPs) play essential roles in forming cuticular structures in insects. However, the specific functions and regulatory mechanisms of CPs remain largely unexplored. In this study, the Larval cuticular protein 17 (HcLCP‐17) gene was identified from Hyphantria cunea, a highly destructive and polyphagous forest pest. To investigate the role of HcLCP‐17 in cuticular function and transcriptional regulation mediated by 20E‐responsive transcription factors (ERTFs), we employed RNA interference (RNAi) and yeast one‐hybrid assay techniques. Additionally, we examined the molecular mechanism by which chlorbenzuron, a type of benzoylphenylurea (BPU) that functions as a chitin synthesis inhibitor (CSI), affects the 20E signaling pathway and ultimately regulates HcLCP‐17 expression.RESULTSHcLCP‐17 encodes a polypeptide consisting of 393 amino acids, which includes a chitin‐binding domain. Silencing HcLCP‐17 resulted in a disturbance in the structural organization of the larval cuticle and a notable reduction in chitin levels. HcLCP‐17 expression was controlled by the interaction between Broad‐Complex (Br‐C) and beta Fushi Tarazu Factor‐1 (βFTZ‐F1) with its promoter fragment. Furthermore, the inhibitory effect of chlorbenzuron on HcLCP‐17 expression was found to be potentially mediated by Br‐C and βFTZ‐F1.CONCLUSIONThe study presents a novel mode of action for the 20E signaling pathway in regulating the expression of CPs and reveals the potential mode‐of‐action of BPUs in insect cuticles. These findings provide a theoretical basis for future utilization of LCP‐17 as a pesticide target making a significant contribution to the development of effective pest management strategies. © 2024 Society of Chemical Industry.