ArticlePLoS genetics2010
Combined inactivation of pRB and hippo pathways induces dedifferentiation in the Drosophila retina.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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
33 citing papers in PubMed, 48 citations in OpenAlex.
- Single-Cell RNA Sequencing Reveals Lactylation Modifications in Neuroblastoma and the Construction of a Prognostic Model.Molecules (Basel, Switzerland) · 2026Article
- Tumor heterogeneity in retinoblastoma: a literature review.Cancer metastasis reviews · 2025Review
- Osmolar Modulation Drives Reversible Cell Cycle Exit and Human Pluripotent Cell Differentiation via NF-κВ and WNT Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Combined inactivation of RB and Hippo converts differentiating Drosophila photoreceptors into eye progenitor cells through derepression of homothorax.Developmental cell · 2023Article
- Maintenance of neuronal fate and transcriptional identity.Biology open · 2023Review
- Transcriptional Repression by FoxM1 Suppresses Tumor Differentiation and Promotes Metastasis of Breast Cancer.Cancer research · 2022Article
- Abrogation of Rb Tumor Suppression Initiates GBM in Differentiated Astrocytes by Driving a Progenitor Cell Program.Frontiers in oncology · 2022Article
- Cross-species identification of PIP5K1-, splicing- and ubiquitin-related pathways as potential targets for RB1-deficient cells.PLoS genetics · 2021Article
- Yorkie and JNK revert syncytial muscles into myoblasts during Org-1-dependent lineage reprogramming.The Journal of cell biology · 2019Article
- Changes in chromatin accessibility ensure robust cell cycle exit in terminally differentiated cells.PLoS biology · 2019Article
- Regulation of cell polarity determinants by the Retinoblastoma tumor suppressor protein.Scientific reports · 2016Article
- Protein phosphatase 2A promotes the transition to G0 during terminal differentiation in Drosophila.Development (Cambridge, England) · 2015Article
- mTORC1 maintains the tumorigenicity of SSEA-4(+) high-grade osteosarcoma.Scientific reports · 2015Article
- Drosophila as a Potential Model for Ocular Tumors.Ocular oncology and pathology · 2015Review
- How the cell cycle impacts chromatin architecture and influences cell fate.Frontiers in genetics · 2015Article
- Regulators of pluripotency and their implications in regenerative medicine.Stem cells and cloning : advances and applications · 2015Review
- Organ size control is dominant over Rb family inactivation to restrict proliferation in vivo.Cell reports · 2014Article
- Involvement of YAP, TAZ and HSP90 in contact guidance and intercellular junction formation in corneal epithelial cells.PloS one · 2014Article
- Defining a new vision for the retinoblastoma gene: report from the 3rd International Rb Meeting.Cell division · 2013Article
- What do mechanotransduction, Hippo, Wnt, and TGFβ have in common? YAP and TAZ as key orchestrating molecules in ocular health and disease.Experimental eye research · 2013Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Functional inactivation of the Retinoblastoma (pRB) pathway is an early and obligatory event in tumorigenesis. The importance of pRB is usually explained by its ability to promote cell cycle exit. Here, we demonstrate that, independently of cell cycle exit control, in cooperation with the Hippo tumor suppressor pathway, pRB functions to maintain the terminally differentiated state. We show that mutations in the Hippo signaling pathway, wts or hpo, trigger widespread dedifferentiation of rbf mutant cells in the Drosophila eye. Initially, rbf wts or rbf hpo double mutant cells are morphologically indistinguishable from their wild-type counterparts as they properly differentiate into photoreceptors, form axonal projections, and express late neuronal markers. However, the double mutant cells cannot maintain their neuronal identity, dedifferentiate, and thus become uncommitted eye specific cells. Surprisingly, this dedifferentiation is fully independent of cell cycle exit defects and occurs even when inappropriate proliferation is fully blocked by a de2f1 mutation. Thus, our results reveal the novel involvement of the pRB pathway during the maintenance of a differentiated state and suggest that terminally differentiated Rb mutant cells are intrinsically prone to dedifferentiation, can be converted to progenitor cells, and thus contribute to cancer advancement.
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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.