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Fenoxycarb, a carbamate insect growth regulator, inhibits brassinosteroid action.

ABSTRACT: Brassinosteroids (BRs) are steroid hormones that regulate plant growth, development, and stress resistance. In this study, we evaluated the effect of agrochemicals on dark-induced hypocotyl elongation, which is regulated by BRs, to identify novel chemicals that regulate BR action. We found that the juvenile hormone agonist fenoxycarb inhibited dark-induced hypocotyl elongation in Arabidopsis. Treatment with the same class of juvenile hormone agonist, pyriproxyfen, did not affect hypocotyl elongation. Co-treatment with fenoxycarb and BR partly canceled the fenoxycarb-induced hypocotyl suppression. In addition, gene expression analysis revealed that fenoxycarb altered the BR-responsive gene expression. These results indicate that fenoxycarb is a BR action inhibitor.

SUBMITTER: Ito S

PROVIDER: S-EPMC10513946 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature

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Fenoxycarb, a carbamate insect growth regulator, inhibits brassinosteroid action.

Ito Shinsaku S Kawada Kojiro K Saeki Yasumasa Y Nakano Takeshi T Sasaki Yasuyuki Y Yajima Shunsuke S

Journal of pesticide science 20230801 3

Brassinosteroids (BRs) are steroid hormones that regulate plant growth, development, and stress resistance. In this study, we evaluated the effect of agrochemicals on dark-induced hypocotyl elongation, which is regulated by BRs, to identify novel chemicals that regulate BR action. We found that the juvenile hormone agonist fenoxycarb inhibited dark-induced hypocotyl elongation in <i>Arabidopsis</i>. Treatment with the same class of juvenile hormone agonist, pyriproxyfen, did not affect hypocotyl ...[more]

PMID: 37745175

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Project description:Insect vector-borne diseases remain one of the principal causes of human mortality. In addition to conventional measures of insect control, repellents continue to be the mainstay for personal protection. Because of the increasing pyrethroid-resistant mosquito populations, alternative strategies to reconstitute pyrethroid repellency and knock-down effects have been proposed by mixing the repellent DEET (N,N-Diethyl-3-methylbenzamide) with non-pyrethroid insecticide to better control resistant insect vector-borne diseases. By using electrophysiological, biochemichal, in vivo toxicological techniques together with calcium imaging, binding studies and in silico docking, we have shown that DEET, at low concentrations, interacts with high affinity with insect M1/M3 mAChR allosteric site potentiating agonist effects on mAChRs coupled to phospholipase C second messenger pathway. This increases the anticholinesterase activity of the carbamate propoxur through calcium-dependent regulation of acetylcholinesterase. At high concentrations, DEET interacts with low affinity on distinct M1/M3 mAChR site, counteracting the potentiation. Similar dose-dependent dual effects of DEET have also been observed at synaptic mAChR level. Additionally, binding and in silico docking studies performed on human M1 and M3 mAChR subtypes indicate that DEET only displays a low affinity antagonist profile on these M1/M3 mAChRs. These results reveal a selective high affinity positive allosteric site for DEET in insect mAChRs. Finally, bioassays conducted on Aedes aegypti confirm the synergistic interaction between DEET and propoxur observed in vitro, resulting in a higher mortality of mosquitoes. Our findings reveal an unusual allosterically potentiating action of the repellent DEET, which involves a selective site in insect. These results open exciting research areas in public health particularly in the control of the pyrethroid-resistant insect-vector borne diseases. Mixing low doses of DEET and a non-pyrethroid insecticide will lead to improvement in the efficiency treatments thus reducing both the concentration of active ingredients and side effects for non-target organisms. The discovery of this insect specific site may pave the way for the development of new strategies essential in the management of chemical use against resistant mosquitoes.

Project description:BackgroundEpigenetic modifications, particularly DNA methylation and posttranslational histone modifications regulate heritable changes in transcription without changes in the DNA sequence. Despite a number of studies showing clear links between environmental factors and DNA methylation, little is known about the effect of environmental factors on the recently identified histone lysine methylation. Since their identification numerous studies have establish critical role played by these enzymes in mammalian development.ObjectivesIdentification of the Jumonji (Jmj) domain containing histone lysine demethylase have added a new dimension to epigenetic control of gene expression by dynamic regulation of histone methylation marks. The objective of our study was to evaluate the effect of prohexadione and trinexapac, widely used plant growth regulators of the acylcyclohexanediones class, on the enzymatic activity of histone lysine demethylases and histone modifications during the neural stem/progenitor cell differentiation.MethodsHere we show that prohexadione, but not trinexapac, directly inhibits non-heme iron (II), 2-oxoglutarate-dependent histone lysine demethylase such as Jmjd2a. We used molecular modeling to show binding of prohexadione to Jmjd2a. We also performed in vitro demethylation assays to show the inhibitory effect of prohexadione on Jmjd2a. Further we tested this molecule in cell culture model of mouse hippocampal neural stem/progenitor cells to demonstrate its effect toward neuronal proliferation and differentiation.ResultsMolecular modeling studies suggest that prohexadione binds to the 2-oxoglutarate binding site of Jmjd2a demethylase. Treatment of primary neural stem/progenitor cells with prohexadione showed a concentration dependent reduction in their proliferation. Further, the prohexadione treated neurospheres were induced toward neurogenic lineage upon differentiation.ConclusionsOur results describe an important chemico-biological interaction of prohexadione, in light of critical roles played by histone lysine demethylases in human health and diseases.

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Fenoxycarb, a carbamate insect growth regulator, inhibits brassinosteroid action.

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Fenoxycarb, a carbamate insect growth regulator, inhibits brassinosteroid action.

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