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Involvement of Methoprene‐tolerant and Krüppel homolog 1 in juvenile hormone‐mediated vitellogenesis of female Liposcelis entomophila (End.) (Psocoptera: Liposcelididae)

Methoprene‐tolerant (Met) as an intracellular receptor of juvenile hormone (JH) and the Krüppel‐homolog 1 (Kr‐h1) as a JH‐inducible transcription factor had been proved to contribute to insect reproduction. Their functions vary in different insect orders, however, they are not clear in Psocoptera. I...

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Autores principales: Yang, Bin‐Bin, Miao, Shi‐Yuan, Lu, Yu‐Jie, Wang, Sui‐Sui, Wang, Zheng‐Yan, Zhao, Ya‐Ru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10078567/
https://www.ncbi.nlm.nih.gov/pubmed/36193599
http://dx.doi.org/10.1002/arch.21973
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author Yang, Bin‐Bin
Miao, Shi‐Yuan
Lu, Yu‐Jie
Wang, Sui‐Sui
Wang, Zheng‐Yan
Zhao, Ya‐Ru
author_facet Yang, Bin‐Bin
Miao, Shi‐Yuan
Lu, Yu‐Jie
Wang, Sui‐Sui
Wang, Zheng‐Yan
Zhao, Ya‐Ru
author_sort Yang, Bin‐Bin
collection PubMed
description Methoprene‐tolerant (Met) as an intracellular receptor of juvenile hormone (JH) and the Krüppel‐homolog 1 (Kr‐h1) as a JH‐inducible transcription factor had been proved to contribute to insect reproduction. Their functions vary in different insect orders, however, they are not clear in Psocoptera. In this study, LeMet and LeKr‐h1 were identified and their roles in vitellogenesis and ovarian development were investigated in Liposcelis entomophila (Enderlein). Treatment with exogenous JH III significantly induced the expression of LeKr‐h1, LeVg, and LeVgR. Furthermore, silencing LeMet and LeKr‐h1 remarkably reduced the transcription of LeVg and LeVgR, disrupted the production of Vg in fat body and the uptake of Vg by oocytes, and ultimately led to a decline in fecundity. The results indicated that the JH signaling pathway was essential to the reproductive process of this species. Interestingly, knockdown of LeMet or LeKr‐h1 also resulted in fluctuations in the expression of FoxO, indicating the complex regulatory interactions between different hormone factors. Besides, knockdown of both LeMet and LeKr‐h1 significantly increased L. entomophila mortality. Our study provides initial insight into the roles of JH signaling in the female reproduction of psocids and provided evidence that RNAi‐mediated knockdown of Met or Kr‐h1 is a potential pest control strategy.
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spelling pubmed-100785672023-04-07 Involvement of Methoprene‐tolerant and Krüppel homolog 1 in juvenile hormone‐mediated vitellogenesis of female Liposcelis entomophila (End.) (Psocoptera: Liposcelididae) Yang, Bin‐Bin Miao, Shi‐Yuan Lu, Yu‐Jie Wang, Sui‐Sui Wang, Zheng‐Yan Zhao, Ya‐Ru Arch Insect Biochem Physiol Research Articles Methoprene‐tolerant (Met) as an intracellular receptor of juvenile hormone (JH) and the Krüppel‐homolog 1 (Kr‐h1) as a JH‐inducible transcription factor had been proved to contribute to insect reproduction. Their functions vary in different insect orders, however, they are not clear in Psocoptera. In this study, LeMet and LeKr‐h1 were identified and their roles in vitellogenesis and ovarian development were investigated in Liposcelis entomophila (Enderlein). Treatment with exogenous JH III significantly induced the expression of LeKr‐h1, LeVg, and LeVgR. Furthermore, silencing LeMet and LeKr‐h1 remarkably reduced the transcription of LeVg and LeVgR, disrupted the production of Vg in fat body and the uptake of Vg by oocytes, and ultimately led to a decline in fecundity. The results indicated that the JH signaling pathway was essential to the reproductive process of this species. Interestingly, knockdown of LeMet or LeKr‐h1 also resulted in fluctuations in the expression of FoxO, indicating the complex regulatory interactions between different hormone factors. Besides, knockdown of both LeMet and LeKr‐h1 significantly increased L. entomophila mortality. Our study provides initial insight into the roles of JH signaling in the female reproduction of psocids and provided evidence that RNAi‐mediated knockdown of Met or Kr‐h1 is a potential pest control strategy. John Wiley and Sons Inc. 2022-10-03 2023-01 /pmc/articles/PMC10078567/ /pubmed/36193599 http://dx.doi.org/10.1002/arch.21973 Text en © 2022 The Authors. Archives of Insect Biochemistry and Physiology published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Yang, Bin‐Bin
Miao, Shi‐Yuan
Lu, Yu‐Jie
Wang, Sui‐Sui
Wang, Zheng‐Yan
Zhao, Ya‐Ru
Involvement of Methoprene‐tolerant and Krüppel homolog 1 in juvenile hormone‐mediated vitellogenesis of female Liposcelis entomophila (End.) (Psocoptera: Liposcelididae)
title Involvement of Methoprene‐tolerant and Krüppel homolog 1 in juvenile hormone‐mediated vitellogenesis of female Liposcelis entomophila (End.) (Psocoptera: Liposcelididae)
title_full Involvement of Methoprene‐tolerant and Krüppel homolog 1 in juvenile hormone‐mediated vitellogenesis of female Liposcelis entomophila (End.) (Psocoptera: Liposcelididae)
title_fullStr Involvement of Methoprene‐tolerant and Krüppel homolog 1 in juvenile hormone‐mediated vitellogenesis of female Liposcelis entomophila (End.) (Psocoptera: Liposcelididae)
title_full_unstemmed Involvement of Methoprene‐tolerant and Krüppel homolog 1 in juvenile hormone‐mediated vitellogenesis of female Liposcelis entomophila (End.) (Psocoptera: Liposcelididae)
title_short Involvement of Methoprene‐tolerant and Krüppel homolog 1 in juvenile hormone‐mediated vitellogenesis of female Liposcelis entomophila (End.) (Psocoptera: Liposcelididae)
title_sort involvement of methoprene‐tolerant and krüppel homolog 1 in juvenile hormone‐mediated vitellogenesis of female liposcelis entomophila (end.) (psocoptera: liposcelididae)
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10078567/
https://www.ncbi.nlm.nih.gov/pubmed/36193599
http://dx.doi.org/10.1002/arch.21973
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