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10.1371/journal.pbio.1002239 http://scihub22266oqcxt.onion/10.1371/journal.pbio.1002239 C4551486!4551486 !26313758     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26313758 &cmd=llinks): Failed to open stream: HTTP request failed! 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Dally Proteoglycan Mediates the Autonomous and Nonautonomous Effects on Tissue Growth Caused by Activation of the PI3K and TOR Pathways |pdf=|usr=}}{{26313758 }} gab.com Text Dally Proteoglycan Mediates the Autonomous and Nonautonomous Effects on Tissue Growth Caused by Activation of the PI3K and TOR Pathways JO: PLoS Biol http://www.kidney.de/pget.php?&tw=1&pmid=26313758 #FOAvip How cells acquiring mutations in tumor suppressor genes outcompete neighboring wild-type cells is poorly understood. The phosphatidylinositol 3-kinase (PI3K)-phosphatase with tensin homology (PTEN) and tuberous sclerosis complex (TSC)-target of rapamycin (TOR) pathways are frequently activated in human cancer, and this activation is often causative of tumorigenesis. We utilized the Gal4-UAS system in Drosophila imaginal primordia, highly proliferative and growing tissues, to analyze the impact of restricted activation of these pathways on neighboring wild-type cell populations. Activation of these pathways leads to an autonomous induction of tissue overgrowth and to a remarkable nonautonomous reduction in growth and proliferation rates of adjacent cell populations. This nonautonomous response occurs independently of where these pathways are activated, is functional all throughout development, takes place across compartments, and is distinct from cell competition. The observed autonomous and nonautonomous effects on tissue growth rely on the up-regulation of the proteoglycan Dally, a major element involved in modulating the spreading, stability, and activity of the growth promoting Decapentaplegic (Dpp)/transforming growth factor ?(TGF-?) signaling molecule. Our findings indicate that a reduction in the amount of available growth factors contributes to the outcompetition of wild-type cells by overgrowing cell populations. During normal development, the PI3K/PTEN and TSC/TOR pathways play a major role in sensing nutrient availability and modulating the final size of any developing organ. We present evidence that Dally also contributes to integrating nutrient sensing and organ scaling, the fitting of pattern to size. Twit Text FOAVip Dally Proteoglycan Mediates the Autonomous and Nonautonomous Effects on Tissue Growth Caused by Activation of the PI3K and TOR Pathways ????PLoS Biol http://www.kidney.de/pget.php?&tw=1&pmid=26313758 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26313758 #FOAvip English Wikipedia <ref>{{Cite pmid|26313758 }}</ref> Dally Proteoglycan Mediates the Autonomous and Nonautonomous Effects on Tissue Growth Caused by Activation of the PI3K and TOR Pathways #MMPMID26313758 Ferreira A ; Milán M PLoS Biol 2015[Aug]; 13 (8 ): e1002239 PMID26313758 show ga How cells acquiring mutations in tumor suppressor genes outcompete neighboring wild-type cells is poorly understood. The phosphatidylinositol 3-kinase (PI3K)-phosphatase with tensin homology (PTEN) and tuberous sclerosis complex (TSC)-target of rapamycin (TOR) pathways are frequently activated in human cancer, and this activation is often causative of tumorigenesis. We utilized the Gal4-UAS system in Drosophila imaginal primordia, highly proliferative and growing tissues, to analyze the impact of restricted activation of these pathways on neighboring wild-type cell populations. Activation of these pathways leads to an autonomous induction of tissue overgrowth and to a remarkable nonautonomous reduction in growth and proliferation rates of adjacent cell populations. This nonautonomous response occurs independently of where these pathways are activated, is functional all throughout development, takes place across compartments, and is distinct from cell competition. The observed autonomous and nonautonomous effects on tissue growth rely on the up-regulation of the proteoglycan Dally, a major element involved in modulating the spreading, stability, and activity of the growth promoting Decapentaplegic (Dpp)/transforming growth factor ?(TGF-?) signaling molecule. Our findings indicate that a reduction in the amount of available growth factors contributes to the outcompetition of wild-type cells by overgrowing cell populations. During normal development, the PI3K/PTEN and TSC/TOR pathways play a major role in sensing nutrient availability and modulating the final size of any developing organ. We present evidence that Dally also contributes to integrating nutrient sensing and organ scaling, the fitting of pattern to size. |Animals [MESH] |Carcinogenesis/genetics/metabolism [MESH] |Cell Proliferation/*physiology [MESH] |Drosophila Proteins/genetics/*metabolism [MESH] |Drosophila/embryology/genetics/metabolism/*physiology [MESH] |Gene Expression Regulation, Developmental [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Imaginal Discs/physiology [MESH] |Male [MESH] |Membrane Glycoproteins/genetics/*metabolism [MESH] |Organ Size/physiology [MESH] |Phosphatidylinositol 3-Kinase/*metabolism [MESH] |Proteoglycans/genetics/*metabolism [MESH] |Signal Transduction/physiology [MESH] |TOR Serine-Threonine Kinases/*metabolism [MESH] |Up-Regulation [MESH]Dally Proteoglycan Mediates the Autonomous and Nonautonomous Effects o(epmc).pdf DeepDyve Pubget Overpricing