ArticleFly2016
A triangular connection between Cyclin G, PP2A and Akt1 in the regulation of growth and metabolism in Drosophila.
Article in Fly, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Genome-wide screen for deficiencies modifying Cyclin G-induced developmental instability in Drosophila melanogaster.Genetics · 2026Article
- Gene model for the ortholog ofmicroPublication biology · 2025Article
- Review
- Genome annotation with long RNA reads reveals new patterns of gene expression and improves single-cell analyses in an ant brain.BMC biology · 2021Article
- Systemic signalling and local effectors in developmental stability, body symmetry, and size.Cell stress · 2018Review
- Cyclin G and the Polycomb Repressive complexes PRC1 and PR-DUB cooperate for developmental stability.PLoS genetics · 2018Article
- p53 and cyclin G cooperate in mediating genome stability in somatic cells of Drosophila.Scientific reports · 2017Article
- Germline-specific labeling of the somatic chromosomes by protein phosphatase 2A and histone H3S28 phosphorylation in Acricotopus lucidus.Protoplasma · 2017Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Size and weight control is a tightly regulated process, involving the highly conserved Insulin receptor/target of rapamycin (InR/TOR) signaling cascade. We recently identified Cyclin G (CycG) as an important modulator of InR/TOR signaling activity in Drosophila. cycG mutant flies are underweight and show a disturbed fat metabolism resembling TOR mutants. In fact, InR/TOR signaling activity is disturbed in cycG mutants at the level of Akt1, the central kinase linking InR and TORC1. Akt1 is negatively regulated by protein phosphatase PP2A. Notably the binding of the PP2A B'-regulatory subunit Widerborst (Wdb) to Akt1 is differentially regulated in cycG mutants, presumably by a direct interaction of CycG and Wdb. Since the metabolic defects of cycG mutant animals are abrogated by a concomitant loss of Wdb, CycG presumably influences Akt1 activity at the PP2A nexus. Here we show that Well rounded (Wrd), another B' subunit of PP2A in Drosophila, binds CycG similar to Wdb, and that its loss ameliorates some, but not all, of the metabolic defects of cycG mutants. We propose a model, whereby the binding of CycG to a particular B'-regulatory subunit influences the tissue specific activity of PP2A, required for the fine tuning of the InR/TOR signaling cascade in Drosophila.
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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.