ArticleThe EMBO journal2008
A Wingless and Notch double-repression mechanism regulates G1-S transition in the Drosophila wing.
Article in The EMBO journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 104 citations in OpenAlex.
- Remote ischemia precondition protects against renal IRI through apoptosis associated vesicles carrying MIF protein via modulating DUSP6/JNK signaling axis.Journal of nanobiotechnology · 2025Article
- Notch Signaling in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025Review
- Ribogenesis boosts controlled by HEATR1-MYC interplay promote transition into brain tumour growth.EMBO reports · 2024Article
- Regenerative growth is constrained by brain tumor to ensure proper patterning in Drosophila.PLoS genetics · 2023Article
- Myc-regulated miRNAs modulate p53 expression and impact animal survival under nutrient deprivation.PLoS genetics · 2023Article
- The wing imaginal disc.Genetics · 2022Article
- Misregulation of Nucleoporins 98 and 96 leads to defects in protein synthesis that promote hallmarks of tumorigenesis.Disease models & mechanisms · 2022Article
- Notch signaling regulates neural stem cell quiescence entry and exit in Drosophila.Development (Cambridge, England) · 2022Article
- Identification and profiling of stable microRNAs in hemolymph of young and oldCurrent research in insect science · 2022Article
- The fate of notch-1 transcript is linked to cell cycle dynamics by activity of a natural antisense transcript.Nucleic acids research · 2021Article
- Damage-responsive, maturity-silenced enhancers regulate multiple genes that direct regeneration ineLife · 2020Article
- Article
- RAL GTPases Drive Intestinal Stem Cell Function and Regeneration through Internalization of WNT Signalosomes.Cell stem cell · 2019Article
- MicroRNAs in Drosophila Cancer Models.Advances in experimental medicine and biology · 2019Review
- Article
- Imaginal disc regeneration takes flight.Current opinion in cell biology · 2017Review
- Notch-dependent epithelial fold determines boundary formation between developmental fields in the Drosophila antenna.PLoS genetics · 2017Article
- Study of bantam miRNA expression in brain tumour resulted due to loss of polarity modules in Drosophila melanogaster.Journal of genetics · 2017Article
- Controlling the Master: Chromatin Dynamics at the MYC Promoter Integrate Developmental Signaling.Genes · 2017Review
- JAK/STAT controls organ size and fate specification by regulating morphogen production and signalling.Nature communications · 2017Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The control of tissue growth and patterning is orchestrated in various multicellular tissues by the coordinated activity of the signalling molecules Wnt/Wingless (Wg) and Notch, and mutations in these pathways can cause cancer. The role of these molecules in the control of cell proliferation and the crosstalk between their corresponding pathways remain poorly understood. Crosstalk between Notch and Wg has been proposed to organize pattern and growth in the Drosophila wing primordium. Here we report that Wg and Notch act in a surprisingly linear pathway to control G1-S progression. We present evidence that these molecules exert their function by regulating the expression of the dmyc proto-oncogene and the bantam micro-RNA, which positively modulated the activity of the E2F transcription factor. Our results demonstrate that Notch acts in this cellular context as a repressor of cell-cycle progression and Wg has a permissive role in alleviating Notch-mediated repression of G1-S progression in wing cells.
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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.