The Drosophila TNF receptor Grindelwald couples loss of cell polarity and neoplastic growth

Cell polarity is an important feature of many tissues and is often disrupted in cancer; the TNF receptor Grindelwald is now shown to have an important role in coordinating cell polarity and neoplastic growth in a Drosophila model. Linking cell polarity and neoplasia Cell polarity is an important fea...

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Vydáno v:	Nature (London) Ročník 522; číslo 7557; s. 482 - 486
Hlavní autoři:	Andersen, Ditte S., Colombani, Julien, Palmerini, Valentina, Chakrabandhu, Krittalak, Boone, Emilie, Röthlisberger, Michael, Toggweiler, Janine, Basler, Konrad, Mapelli, Marina, Hueber, Anne-Odile, Léopold, Pierre
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London Nature Publishing Group UK 25.06.2015 Nature Publishing Group
Témata:	631/80/304 Amino Acid Sequence Animals Apoptosis Apoptosis - genetics Biochemistry, Molecular Biology Cancer Cell Adhesion Molecules Cell Adhesion Molecules - metabolism Cell Division Cell Division - genetics Cell Polarity Cell Polarity - genetics Cell Transformation, Neoplastic Cell Transformation, Neoplastic - genetics Cloning Development Biology Disease Models, Animal Drosophila melanogaster Drosophila melanogaster - cytology Drosophila melanogaster - enzymology Drosophila melanogaster - genetics Drosophila melanogaster - metabolism Drosophila Proteins Drosophila Proteins - chemistry Drosophila Proteins - deficiency Drosophila Proteins - genetics Drosophila Proteins - metabolism Female Genes Genomics Genotype & phenotype Humanities and Social Sciences Humans Insects JNK Mitogen-Activated Protein Kinases JNK Mitogen-Activated Protein Kinases - metabolism letter Life Sciences Male MAP Kinase Signaling System Matrix Metalloproteinase 1 Matrix Metalloproteinase 1 - metabolism Membrane Proteins Membrane Proteins - chemistry Membrane Proteins - deficiency Membrane Proteins - genetics Membrane Proteins - metabolism Molecular Sequence Data multidisciplinary Neoplasm Invasiveness Neoplasm Invasiveness - genetics Neoplasms Neoplasms - enzymology Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Proteins ras Proteins ras Proteins - genetics ras Proteins - metabolism Receptors, Tumor Necrosis Factor Receptors, Tumor Necrosis Factor - chemistry Receptors, Tumor Necrosis Factor - genetics Receptors, Tumor Necrosis Factor - metabolism Science Tumors
ISSN:	0028-0836, 1476-4687, 1476-4687
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Abstract	Cell polarity is an important feature of many tissues and is often disrupted in cancer; the TNF receptor Grindelwald is now shown to have an important role in coordinating cell polarity and neoplastic growth in a Drosophila model. Linking cell polarity and neoplasia Cell polarity is an important feature of many tissues, and is often disrupted in cancer. This study demonstrates, in a Drosophila model, that the tumour necrosis factor receptor molecule Grindelwald plays an important role in coordinating cell polarity and neoplastic growth. The authors identify Grindelwald as the long-sought receptor for the apoptosis-inducing factor Eiger, and show that Grindelwald functions by integrating signals from Eiger as well as from cell polarity cues. Disruption of epithelial polarity is a key event in the acquisition of neoplastic growth. JNK signalling is known to play an important part in driving the malignant progression of many epithelial tumours, although the link between loss of polarity and JNK signalling remains elusive. In a Drosophila genome-wide genetic screen designed to identify molecules implicated in neoplastic growth 1 , we identified grindelwald ( grnd ), a gene encoding a transmembrane protein with homology to members of the tumour necrosis factor receptor (TNFR) superfamily. Here we show that Grnd mediates the pro-apoptotic functions of Eiger (Egr), the unique Drosophila TNF, and that overexpression of an active form of Grnd lacking the extracellular domain is sufficient to activate JNK signalling in vivo . Grnd also promotes the invasiveness of Ras V12 /scrib −/− tumours through Egr-dependent Matrix metalloprotease-1 (Mmp1) expression. Grnd localizes to the subapical membrane domain with the cell polarity determinant Crumbs (Crb) and couples Crb-induced loss of polarity with JNK activation and neoplastic growth through physical interaction with Veli (also known as Lin-7). Therefore, Grnd represents the first example of a TNFR that integrates signals from both Egr and apical polarity determinants to induce JNK-dependent cell death or tumour growth.
AbstractList	Cell polarity is an important feature of many tissues and is often disrupted in cancer; the TNF receptor Grindelwald is now shown to have an important role in coordinating cell polarity and neoplastic growth in a Drosophila model. Linking cell polarity and neoplasia Cell polarity is an important feature of many tissues, and is often disrupted in cancer. This study demonstrates, in a Drosophila model, that the tumour necrosis factor receptor molecule Grindelwald plays an important role in coordinating cell polarity and neoplastic growth. The authors identify Grindelwald as the long-sought receptor for the apoptosis-inducing factor Eiger, and show that Grindelwald functions by integrating signals from Eiger as well as from cell polarity cues. Disruption of epithelial polarity is a key event in the acquisition of neoplastic growth. JNK signalling is known to play an important part in driving the malignant progression of many epithelial tumours, although the link between loss of polarity and JNK signalling remains elusive. In a Drosophila genome-wide genetic screen designed to identify molecules implicated in neoplastic growth 1 , we identified grindelwald ( grnd ), a gene encoding a transmembrane protein with homology to members of the tumour necrosis factor receptor (TNFR) superfamily. Here we show that Grnd mediates the pro-apoptotic functions of Eiger (Egr), the unique Drosophila TNF, and that overexpression of an active form of Grnd lacking the extracellular domain is sufficient to activate JNK signalling in vivo . Grnd also promotes the invasiveness of Ras V12 /scrib −/− tumours through Egr-dependent Matrix metalloprotease-1 (Mmp1) expression. Grnd localizes to the subapical membrane domain with the cell polarity determinant Crumbs (Crb) and couples Crb-induced loss of polarity with JNK activation and neoplastic growth through physical interaction with Veli (also known as Lin-7). Therefore, Grnd represents the first example of a TNFR that integrates signals from both Egr and apical polarity determinants to induce JNK-dependent cell death or tumour growth. Disruption of epithelial polarity is a key event in the acquisition of neoplastic growth. JNK signalling is known to play an important part in driving the malignant progression of many epithelial tumours, although the link between loss of polarity and JNK signalling remains elusive. In a Drosophila genome-wide genetic screen designed to identify molecules implicated in neoplastic growth, we identified grindelwald (grnd), a gene encoding a transmembrane protein with homology to members of the tumour necrosis factor receptor (TNFR) superfamily. Here we show that Grnd mediates the pro-apoptotic functions of Eiger (Egr), the unique Drosophila TNF, and that overexpression of an active form of Grnd lacking the extracellular domain is sufficient to activate JNK signalling in vivo. Grnd also promotes the invasiveness of Ras(V12)/scrib(-/-) tumours through Egr-dependent Matrix metalloprotease-1 (Mmp1) expression. Grnd localizes to the subapical membrane domain with the cell polarity determinant Crumbs (Crb) and couples Crb-induced loss of polarity with JNK activation and neoplastic growth through physical interaction with Veli (also known as Lin-7). Therefore, Grnd represents the first example of a TNFR that integrates signals from both Egr and apical polarity determinants to induce JNK-dependent cell death or tumour growth. Disruption of epithelial polarity is a key event in the acquisition of neoplastic growth. JNK signalling is known to play an important part in driving the malignant progression of many epithelial tumours, although the link between loss of polarity and JNK signalling remains elusive. In a Drosophila genome-wide genetic screen designed to identify molecules implicated in neoplastic growth1, we identified grindelwald (grnd), a gene encoding a transmembrane protein with homology to members of the tumour necrosis factor receptor (TNFR) superfamily. Here we show that Grnd mediates the pro-apoptotic functions of Eiger (Egr), the unique Drosophila TNF, and that overexpression of an active form of Grnd lacking the extracellular domain is sufficient to activate JNK signalling in vivo. Grnd also promotes the invasiveness of Ras^sup V12^/scrib^sup -/-^ tumours through Egr-dependent Matrix metallo-protease- 1 (Mmp1) expression. Grnd localizes to the subapical membrane domain with the cell polarity determinant Crumbs (Crb) and couples Crb-induced loss of polarity with JNK activation and neoplastic growth through physical interaction with Veli (also known as Lin-7). Therefore, Grnd represents the first example of a TNFR that integrates signals from both Egr and apical polarity determinants to induce JNK-dependent cell death or tumour growth. Disruption of epithelial polarity is a key event in the acquisition of neoplastic growth. JNK signalling is known to play an important part in driving the malignant progression of many epithelial tumours, although the link between loss of polarity and JNK signalling remains elusive. In a Drosophila genome-wide genetic screen designed to identify molecules implicated in neoplastic growth, we identified grindelwald (grnd), a gene encoding a transmembrane protein with homology to members of the tumour necrosis factor receptor (TNFR) superfamily. Here we show that Grnd mediates the pro-apoptotic functions of Eiger (Egr), the unique Drosophila TNF, and that overexpression of an active form of Grnd lacking the extracellular domain is sufficient to activate JNK signalling in vivo. Grnd also promotes the invasiveness of Ras(V12)/scrib(-/-) tumours through Egr-dependent Matrix metalloprotease-1 (Mmp1) expression. Grnd localizes to the subapical membrane domain with the cell polarity determinant Crumbs (Crb) and couples Crb-induced loss of polarity with JNK activation and neoplastic growth through physical interaction with Veli (also known as Lin-7). Therefore, Grnd represents the first example of a TNFR that integrates signals from both Egr and apical polarity determinants to induce JNK-dependent cell death or tumour growth.Disruption of epithelial polarity is a key event in the acquisition of neoplastic growth. JNK signalling is known to play an important part in driving the malignant progression of many epithelial tumours, although the link between loss of polarity and JNK signalling remains elusive. In a Drosophila genome-wide genetic screen designed to identify molecules implicated in neoplastic growth, we identified grindelwald (grnd), a gene encoding a transmembrane protein with homology to members of the tumour necrosis factor receptor (TNFR) superfamily. Here we show that Grnd mediates the pro-apoptotic functions of Eiger (Egr), the unique Drosophila TNF, and that overexpression of an active form of Grnd lacking the extracellular domain is sufficient to activate JNK signalling in vivo. Grnd also promotes the invasiveness of Ras(V12)/scrib(-/-) tumours through Egr-dependent Matrix metalloprotease-1 (Mmp1) expression. Grnd localizes to the subapical membrane domain with the cell polarity determinant Crumbs (Crb) and couples Crb-induced loss of polarity with JNK activation and neoplastic growth through physical interaction with Veli (also known as Lin-7). Therefore, Grnd represents the first example of a TNFR that integrates signals from both Egr and apical polarity determinants to induce JNK-dependent cell death or tumour growth.
Author	Basler, Konrad Chakrabandhu, Krittalak Mapelli, Marina Boone, Emilie Palmerini, Valentina Röthlisberger, Michael Léopold, Pierre Toggweiler, Janine Colombani, Julien Andersen, Ditte S. Hueber, Anne-Odile
Author_xml	– sequence: 1 givenname: Ditte S. surname: Andersen fullname: Andersen, Ditte S. organization: University of Nice-Sophia Antipolis, Institute of Biology Valrose, CNRS, Institute of Biology Valrose, INSERM, Institute of Biology Valrose, Genetics and Physiology of Growth laboratory, Institute of Biology Valrose – sequence: 2 givenname: Julien surname: Colombani fullname: Colombani, Julien email: julien.colombani@unice.fr organization: University of Nice-Sophia Antipolis, Institute of Biology Valrose, CNRS, Institute of Biology Valrose, INSERM, Institute of Biology Valrose, Genetics and Physiology of Growth laboratory, Institute of Biology Valrose – sequence: 3 givenname: Valentina surname: Palmerini fullname: Palmerini, Valentina organization: Department of Experimental Oncology, European Institute of Oncology – sequence: 4 givenname: Krittalak surname: Chakrabandhu fullname: Chakrabandhu, Krittalak organization: University of Nice-Sophia Antipolis, Institute of Biology Valrose, CNRS, Institute of Biology Valrose, INSERM, Institute of Biology Valrose, Death receptors Signalling and Cancer Therapy laboratory, Institute of Biology Valrose – sequence: 5 givenname: Emilie surname: Boone fullname: Boone, Emilie organization: University of Nice-Sophia Antipolis, Institute of Biology Valrose, CNRS, Institute of Biology Valrose, INSERM, Institute of Biology Valrose, Genetics and Physiology of Growth laboratory, Institute of Biology Valrose – sequence: 6 givenname: Michael surname: Röthlisberger fullname: Röthlisberger, Michael organization: Institute of Molecular Life Sciences, University of Zurich – sequence: 7 givenname: Janine surname: Toggweiler fullname: Toggweiler, Janine organization: Institute of Molecular Life Sciences, University of Zurich – sequence: 8 givenname: Konrad surname: Basler fullname: Basler, Konrad organization: Institute of Molecular Life Sciences, University of Zurich – sequence: 9 givenname: Marina surname: Mapelli fullname: Mapelli, Marina organization: Department of Experimental Oncology, European Institute of Oncology – sequence: 10 givenname: Anne-Odile surname: Hueber fullname: Hueber, Anne-Odile organization: University of Nice-Sophia Antipolis, Institute of Biology Valrose, CNRS, Institute of Biology Valrose, INSERM, Institute of Biology Valrose, Death receptors Signalling and Cancer Therapy laboratory, Institute of Biology Valrose – sequence: 11 givenname: Pierre surname: Léopold fullname: Léopold, Pierre email: leopold@unice.fr organization: University of Nice-Sophia Antipolis, Institute of Biology Valrose, CNRS, Institute of Biology Valrose, INSERM, Institute of Biology Valrose, Genetics and Physiology of Growth laboratory, Institute of Biology Valrose
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Snippet	Cell polarity is an important feature of many tissues and is often disrupted in cancer; the TNF receptor Grindelwald is now shown to have an important role in... Disruption of epithelial polarity is a key event in the acquisition of neoplastic growth. JNK signalling is known to play an important part in driving the...
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SubjectTerms	631/80/304 Amino Acid Sequence Animals Apoptosis Apoptosis - genetics Biochemistry, Molecular Biology Cancer Cell Adhesion Molecules Cell Adhesion Molecules - metabolism Cell Division Cell Division - genetics Cell Polarity Cell Polarity - genetics Cell Transformation, Neoplastic Cell Transformation, Neoplastic - genetics Cloning Development Biology Disease Models, Animal Drosophila melanogaster Drosophila melanogaster - cytology Drosophila melanogaster - enzymology Drosophila melanogaster - genetics Drosophila melanogaster - metabolism Drosophila Proteins Drosophila Proteins - chemistry Drosophila Proteins - deficiency Drosophila Proteins - genetics Drosophila Proteins - metabolism Female Genes Genomics Genotype & phenotype Humanities and Social Sciences Humans Insects JNK Mitogen-Activated Protein Kinases JNK Mitogen-Activated Protein Kinases - metabolism letter Life Sciences Male MAP Kinase Signaling System Matrix Metalloproteinase 1 Matrix Metalloproteinase 1 - metabolism Membrane Proteins Membrane Proteins - chemistry Membrane Proteins - deficiency Membrane Proteins - genetics Membrane Proteins - metabolism Molecular Sequence Data multidisciplinary Neoplasm Invasiveness Neoplasm Invasiveness - genetics Neoplasms Neoplasms - enzymology Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Proteins ras Proteins ras Proteins - genetics ras Proteins - metabolism Receptors, Tumor Necrosis Factor Receptors, Tumor Necrosis Factor - chemistry Receptors, Tumor Necrosis Factor - genetics Receptors, Tumor Necrosis Factor - metabolism Science Tumors
Title	The Drosophila TNF receptor Grindelwald couples loss of cell polarity and neoplastic growth
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