ArticleInsect biochemistry and molecular biology2008
Overexpression of Methoprene-tolerant, a Drosophila melanogaster gene that is critical for juvenile hormone action and insecticide resistance.
Article in Insect biochemistry and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Mechanisms and Genetic Drivers of Resistance of Insect Pests to Insecticides and Approaches to Its Control.Toxics · 2025Review
- The intrinsically disordered region of GCE protein adopts a more fixed structure by interacting with the LBD of the nuclear receptor FTZ-F1.Cell communication and signaling : CCS · 2020Article
- A plant diterpene counteracts juvenile hormone-mediated gene regulation during Drosophila melanogaster larval development.PloS one · 2018Article
- Genetic tools to study juvenile hormone action in Drosophila.Scientific reports · 2017Article
- Mitochondrial ferritin, a new target for inhibiting neuronal tumor cell proliferation.Cellular and molecular life sciences : CMLS · 2015Article
- Juvenile hormone regulates body size and perturbs insulin signaling in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The molecular genetics of insecticide resistance.Genetics · 2013Review
- Juvenile hormone and insulin suppress lipolysis between periods of lactation during tsetse fly pregnancy.Molecular and cellular endocrinology · 2013Article
- Article
- Suppressed production of methyl farnesoid hormones yields developmental defects and lethality in Drosophila larvae.General and comparative endocrinology · 2010Article
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Authors and funding
3 authors.
Funding
Abstract
The Methoprene-tolerant (Met) gene of Drosophila melanogaster is involved in both juvenile hormone (JH) action and resistance to JH insecticides, such as methoprene. Although the consequences of Met mutations on development and methoprene resistance are known, no studies have examined Met+ overexpression. Met+ was overexpressed in transgenic lines with various promoters that drive overexpression to different levels. Flies expressing either genomic or cDNA Met+ transgenes showed higher susceptibility to both the morphogenetic and toxic effects of methoprene, consistent with the hormone-binding property of MET. Both the sensitive period and lethal period were the same as seen for non-overexpressing Met+ flies. However, continual exposure of high-overexpressing Met+ larvae to borderline-toxic or higher methoprene doses advanced the sensitive period from prepupae to first instar and the lethal period from pharate adults to larvae and early pupae. When expression of transgenic UAS-Met+ was driven to high levels by either an actin-GAL4 or tubulin-GAL4 promoter, larvae showed high mortality in the absence of methoprene, indicating that high MET titer is lethal, perhaps resulting from expression in an inappropriate tissue. Adults overexpressing Met+ did not show enhanced oogenesis, ruling out MET as a limiting factor for this hormone-driven physiology.
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