ArticlePLoS genetics2017
Nutrient-Dependent Endocycling in Steroidogenic Tissue Dictates Timing of Metamorphosis in Drosophila melanogaster.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 91 citations in OpenAlex.
- Genetic and Molecular Regulation of Ecdysone Biosynthesis During Insect Metamorphosis.Insects · 2026Review
- Transcription factor Tono mediates histone H3K4 trimethylation to regulate endoreplication through transcriptional reprogramming.Science advances · 2026Article
- HR3/RORα-mediated cholesterol sensing regulates TOR signaling.Nature communications · 2026Article
- Endocrine gland growth as the developmental switch for insect diapause.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Single-cell transcriptomics of theProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Food absence is a cue for metamorphosis in the solitary beeProceedings of the National Academy of Sciences of the United States of America · 2026Article
- CDK2-Mediated Phosphorylation ofResearch (Washington, D.C.) · 2026Article
- Filopodia are essential for steroid release.Nature communications · 2025Article
- USP8 and Hsp70 regulate endoreplication by synergistically promoting Fzr deubiquitination and stabilization.Science advances · 2025Article
- Nutrient status alters developmental fates via a switch in mitochondrial homeodynamics.Nature communications · 2025Article
- Early attainment of 20-hydroxyecdysone threshold shapes mosquito sexual dimorphism in developmental timing.Nature communications · 2025Article
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- Cell cycle re-entry in the agingbioRxiv : the preprint server for biology · 2024Article
- Developmental analysis of Spalt function in the Drosophila prothoracic gland.Development (Cambridge, England) · 2024Article
- Hypoxia delays steroid-induced developmental maturation in Drosophila by suppressing EGF signaling.PLoS genetics · 2024Article
- A dynamical model of growth and maturation inProceedings of the National Academy of Sciences of the United States of America · 2023Article
- KDM5-mediated activation of genes required for mitochondrial biology is necessary for viability in Drosophila.Development (Cambridge, England) · 2023Article
- The macrophage genetic cassetteScience advances · 2023Article
- Starvation selection reduces and delays larval ecdysone production and signaling.The Journal of experimental biology · 2023Article
- Mammalian puberty: a fly perspective.The FEBS journal · 2023Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Many animals have an intrinsic growth checkpoint during juvenile development, after which an irreversible decision is made to upregulate steroidogenesis, triggering the metamorphic juvenile-to-adult transition. However, a molecular process underlying such a critical developmental decision remains obscure. Here we show that nutrient-dependent endocycling in steroidogenic cells provides the machinery necessary for irreversible activation of metamorphosis in Drosophila melanogaster. Endocycle progression in cells of the prothoracic gland (PG) is tightly coupled with the growth checkpoint, and block of endocycle in PG cells causes larval developmental arrest due to reduction in biosynthesis of the steroid hormone ecdysone. Moreover, inhibition of the nutrient sensor target of rapamycin (TOR) in the PG during the checkpoint period causes endocycle inhibition and developmental arrest, which can be rescued by inducing additional rounds of endocycles by Cyclin E. We propose that a TOR-mediated cell cycle checkpoint in steroidogenic tissue provides a systemic growth checkpoint for reproductive maturation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.