ArticleGenetics2014
Mei-P26 mediates tissue-specific responses to the Brat tumor suppressor and the dMyc proto-oncogene in Drosophila.
Article in Genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- The RNA-binding activity of theRNA biology · 2026Article
- Orb2 RNA-binding activity promotes neural stem cell development and brain growth in Drosophila larvae.Cell reports · 2026Article
- RNA-binding is the essential biological function of thebioRxiv : the preprint server for biology · 2026Article
- Divergent functions of the RNA-binding protein, Mei-P26 in germline and somatic lineages ofFrontiers in cell and developmental biology · 2026Article
- The TRIM-NHL RNA-binding protein MEI-P26 modulates the size of Drosophila Type I neuroblast lineages.Genetics · 2025Article
- Regenerative growth is constrained by brain tumor to ensure proper patterning in Drosophila.PLoS genetics · 2023Article
- Wolbachia endosymbionts manipulate the self-renewal and differentiation of germline stem cells to reinforce fertility of their fruit fly host.PLoS biology · 2023Article
- Myc-regulated miRNAs modulate p53 expression and impact animal survival under nutrient deprivation.PLoS genetics · 2023Article
- FOXO-mediated repression of Dicer1 regulates metabolism, stress resistance, and longevity inProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Molecular insights into RNA recognition and gene regulation by the TRIM-NHL protein Mei-P26.Life science alliance · 2022Article
- Molecular and biological functions of TRIM-NHL RNA-binding proteins.Wiley interdisciplinary reviews. RNA · 2021Review
- WD40 protein Wuho controls germline homeostasis via TRIM-NHL tumor suppressor Mei-p26 inDevelopment (Cambridge, England) · 2020Article
- MicroRNAs in Drosophila Cancer Models.Advances in experimental medicine and biology · 2019Review
- Controlling the Master: Chromatin Dynamics at the MYC Promoter Integrate Developmental Signaling.Genes · 2017Review
- Article
- Screening of suppressors of bax-induced cell death identifies glycerophosphate oxidase-1 as a mediator of debcl-induced apoptosis in Drosophila.Genes & cancer · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TRIM-NHL proteins are a family of translational regulators that control cell growth, proliferation, and differentiation during development. Drosophila Brat and Mei-P26 TRIM-NHL proteins serve as tumor suppressors in stem cell lineages and have been proposed to exert this action, in part, via the repression of the protooncogene dMyc. Here we analyze the role of Brat, Mei-P26, and dMyc in regulating growth in Drosophila imaginal discs. As in stem cell lineages, Brat and Mei-P26 repress dMyc in epithelial cells by acting at the post-transcriptional and protein level, respectively. Analysis of cell and organ size unravel that Mei-P26 mediates tissue-specific responses to Brat and dMyc activities. Loss-of-function of brat and overexpression of dMyc induce overgrowth in stem cell lineages and eventually can participate in tumor formation. In contrast, an increase in Mei-P26 levels inhibits growth of epithelial cells in these two conditions. Upon depletion of Brat, Mei-P26 up-regulation prevents an increase in dMyc protein levels and leads to tissue undergrowth. This mechanism appears to be tissue-specific since Mei-P26 is not upregulated in brain tumors resulting from brat loss-of-function. Driving Mei-P26 expression in these tumors -mimicking the situation in epithelial cells- is sufficient to prevent dMyc accumulation, thus rescuing the overgrowth. Finally, we show that Mei-P26 upregulation mediates dMyc-induced apoptosis and limits dMyc growth potential in epithelial cells. These findings shed light on the tumor suppressor roles of TRIM-NHL proteins and underscore a new mechanism that maintains tissue homeostasis upon dMyc deregulation.
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