دورية أكاديمية
p53- and ERK7-dependent ribosome surveillance response regulates Drosophila insulin-like peptide secretion.
العنوان: | p53- and ERK7-dependent ribosome surveillance response regulates Drosophila insulin-like peptide secretion. |
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المؤلفون: | Kiran Hasygar, Ville Hietakangas |
المصدر: | PLoS Genetics, Vol 10, Iss 11, p e1004764 (2014) |
بيانات النشر: | Public Library of Science (PLoS), 2014. |
سنة النشر: | 2014 |
المجموعة: | LCC:Genetics |
مصطلحات موضوعية: | Genetics, QH426-470 |
الوصف: | 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. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1553-7390 1553-7404 |
Relation: | http://europepmc.org/articles/PMC4230838?pdf=render; https://doaj.org/toc/1553-7390; https://doaj.org/toc/1553-7404 |
DOI: | 10.1371/journal.pgen.1004764 |
URL الوصول: | https://doaj.org/article/9a187b9d49064dbea14767a8b2c78198 |
رقم الأكسشن: | edsdoj.9a187b9d49064dbea14767a8b2c78198 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 15537390 15537404 |
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DOI: | 10.1371/journal.pgen.1004764 |