ArticlePLoS genetics2014
p53- and ERK7-dependent ribosome surveillance response regulates Drosophila insulin-like peptide secretion.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
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- Climate change-induced stress in the honey beeFrontiers in physiology · 2025Review
- Atypical MAP kinases - new insights and directions from amoeba.Journal of cell science · 2023Review
- An atypical MAPK regulates translocation of a GATA transcription factor in response to chemoattractant stimulation.Journal of cell science · 2022Article
- Genetic variation of macronutrient tolerance in Drosophila melanogaster.Nature communications · 2022Article
- Coordinated control of adiposity and growth by anti-anabolic kinase ERK7.EMBO reports · 2021Article
- Fat Body p53 Regulates Systemic Insulin Signaling and Autophagy under Nutrient Stress via Drosophila Upd2 Repression.Cell reports · 2020Article
- Impact of Conventional and Atypical MAPKs on the Development of Metabolic Diseases.Biomolecules · 2020Review
- A Neuronal Relay Mediates a Nutrient Responsive Gut/Fat Body Axis Regulating Energy Homeostasis in Adult Drosophila.Cell metabolism · 2019Article
- Transcriptional response of honey bee (Apis mellifera) to differential nutritional status and Nosema infection.BMC genomics · 2018Article
- Modulation of the secretory pathway by amino-acid starvation.The Journal of cell biology · 2018Review
- Dictyostelium Erk2 is an atypical MAPK required for chemotaxis.Cellular signalling · 2018Article
- dTBC1D7 regulates systemic growth independently of TSC through insulin signaling.The Journal of cell biology · 2018Article
- MAPK15 upregulation promotes cell proliferation and prevents DNA damage in male germ cell tumors.Oncotarget · 2016Article
- Growth-Blocking Peptides As Nutrition-Sensitive Signals for Insulin Secretion and Body Size Regulation.PLoS biology · 2016Article
- Characterization of Reproductive Dormancy in MaleFrontiers in physiology · 2016Article
- Genome-Wide Analysis of Drosophila RBf2 Protein Highlights the Diversity of RB Family Targets and Possible Role in Regulation of Ribosome Biosynthesis.G3 (Bethesda, Md.) · 2015Article
- MAPK15 mediates BCR-ABL1-induced autophagy and regulates oncogene-dependent cell proliferation and tumor formation.Autophagy · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin-like signalling is a conserved mechanism that coordinates animal growth and metabolism with nutrient status. In Drosophila, insulin-producing median neurosecretory cells (IPCs) regulate larval growth by secreting insulin-like peptides (dILPs) in a diet-dependent manner. Previous studies have shown that nutrition affects dILP secretion through humoral signals derived from the fat body. Here we uncover a novel mechanism that operates cell autonomously in the IPCs to regulate dILP secretion. We observed that impairment of ribosome biogenesis specifically in the IPCs strongly inhibits dILP secretion, which consequently leads to reduced body size and a delay in larval development. This response is dependent on p53, a known surveillance factor for ribosome biogenesis. A downstream effector of this growth inhibitory response is an atypical MAP kinase ERK7 (ERK8/MAPK15), which is upregulated in the IPCs following impaired ribosome biogenesis as well as starvation. We show that ERK7 is sufficient and essential to inhibit dILP secretion upon impaired ribosome biogenesis, and it acts epistatically to p53. Moreover, we provide evidence that p53 and ERK7 contribute to the inhibition of dILP secretion upon starvation. Thus, we conclude that a cell autonomous ribosome surveillance response, which leads to upregulation of ERK7, inhibits dILP secretion to impede tissue growth under limiting dietary conditions.
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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.