ArticleBMC biology2014
Notch signaling during development requires the function of awd, the Drosophila homolog of human metastasis suppressor gene Nm23.
Article in BMC biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Metastasis suppressor NME1 in exosomes or liposomes conveys motility and migration inhibition in breast cancer model systems.Clinical & experimental metastasis · 2022Article
- Endocytosis: a pivotal pathway for regulating metastasis.British journal of cancer · 2021Review
- The Impact ofInternational journal of molecular sciences · 2020Article
- Characterization of Nme5-Like Gene/Protein from the Red AlgaMarine drugs · 2019Article
- Metastasis Suppressors NME1 and NME2 Promote Dynamin 2 Oligomerization and Regulate Tumor Cell Endocytosis, Motility, and Metastasis.Cancer research · 2019Article
- Notch and breast cancer metastasis: Current knowledge, new sights and targeted therapy.Oncology letters · 2019Review
- AWD regulates timed activation of BMP signaling in intestinal stem cells to maintain tissue homeostasis.Nature communications · 2019Article
- Vps28 Is Involved in the Intracellular Trafficking of Awd, theFrontiers in physiology · 2019Article
- Comparative Expression Profiling of Wild TypeFrontiers in physiology · 2019Article
- Modulation of small GTPase activity by NME proteins.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Article
- Extracellular NME proteins: a player or a bystander?Laboratory investigation; a journal of technical methods and pathology · 2018Review
- The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Metastasis suppressors: functional pathways.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Evidence for a novel function of Awd in maintenance of genomic stability.Scientific reports · 2017Article
- Dynamin controls extracellular level of Awd/Nme1 metastasis suppressor protein.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- Nucleoside diphosphate kinases (NDPKs) in animal development.Cellular and molecular life sciences : CMLS · 2015Review
- Interaction between Nm23 and the tumor suppressor VHL.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Progress on Nme (NDP kinase/Nm23/Awd) gene family-related functions derived from animal model systems: studies on development, cardiovascular disease, and cancer metastasis exemplified.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Article
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundThe Drosophila abnormal wing discs (awd) belongs to a highly conserved family of genes implicated in metastasis suppression, metabolic homeostasis and epithelial morphogenesis. The cellular function of the mammalian members of this family, the Nm23 proteins, has not yet been clearly defined. Previous awd genetic analyses unraveled its endocytic role that is required for proper internalization of receptors controlling different signaling pathways. In this study, we analyzed the role of Awd in controlling Notch signaling during development.
resultsTo study the awd gene function we used genetic mosaic approaches to obtain cells homozygous for a loss of function allele. In awd mutant follicle cells and wing disc cells, Notch accumulates in enlarged early endosomes, resulting in defective Notch signaling. Our results demonstrate that awd function is required before γ-secretase mediated cleavage since over-expression of the constitutively active form of the Notch receptor in awd mutant follicle cells allows rescue of the signaling. By using markers of different endosomal compartments we show that Notch receptor accumulates in early endosomes in awd mutant follicle cells. A trafficking assay in living wing discs also shows that Notch accumulates in early endosomes. Importantly, constitutively active Rab5 cannot rescue the awd phenotype, suggesting that awd is required for Rab5 function in early endosome maturation.
conclusionsIn this report we demonstrate that awd is essential for Notch signaling via its endocytic role. In addition, we identify the endocytic step at which Awd function is required for Notch signaling and we obtain evidence indicating that Awd is necessary for Rab5 function. These findings provide new insights into the developmental and pathophysiological function of this important gene family.
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