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  • 1
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    Blocking PGE2-induced tumour repopulation abrogates bladder cancer chemoresistance (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-12-04
    Description: Cytotoxic chemotherapy is effective in debulking tumour masses initially; however, in some patients tumours become progressively unresponsive after multiple treatment cycles. Previous studies have demonstrated that cancer stem cells (CSCs) are selectively enriched after chemotherapy through enhanced survival. Here we reveal a new mechanism by which bladder CSCs actively contribute to therapeutic resistance via an unexpected proliferative response to repopulate residual tumours between chemotherapy cycles, using human bladder cancer xenografts. Further analyses demonstrate the recruitment of a quiescent label-retaining pool of CSCs into cell division in response to chemotherapy-induced damages, similar to mobilization of normal stem cells during wound repair. While chemotherapy effectively induces apoptosis, associated prostaglandin E2 (PGE2) release paradoxically promotes neighbouring CSC repopulation. This repopulation can be abrogated by a PGE2-neutralizing antibody and celecoxib drug-mediated blockade of PGE2 signalling. In vivo administration of the cyclooxygenase-2 (COX2) inhibitor celecoxib effectively abolishes a PGE2- and COX2-mediated wound response gene signature, and attenuates progressive manifestation of chemoresistance in xenograft tumours, including primary xenografts derived from a patient who was resistant to chemotherapy. Collectively, these findings uncover a new underlying mechanism that models the progressive development of clinical chemoresistance, and implicate an adjunctive therapy to enhance chemotherapeutic response of bladder urothelial carcinomas by abrogating early tumour repopulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465385/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465385/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurtova, Antonina V -- Xiao, Jing -- Mo, Qianxing -- Pazhanisamy, Senthil -- Krasnow, Ross -- Lerner, Seth P -- Chen, Fengju -- Roh, Terrence T -- Lay, Erica -- Ho, Philip Levy -- Chan, Keith Syson -- AI036211/AI/NIAID NIH HHS/ -- CA125123/CA/NCI NIH HHS/ -- CA129640/CA/NCI NIH HHS/ -- CA175397/CA/NCI NIH HHS/ -- R00 CA129640/CA/NCI NIH HHS/ -- R01 CA175397/CA/NCI NIH HHS/ -- RR024574/RR/NCRR NIH HHS/ -- England -- Nature. 2015 Jan 8;517(7533):209-13. doi: 10.1038/nature14034. Epub 2014 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular &Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA [2] Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; Department of Molecular &Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; Dan L Duncan Cancer Center and Center for Cell Gene &Therapy, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; Scott Department of Urology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; 1] Department of Molecular &Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA [2] Summer Medical and Research Training (SMART) Program, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; 1] Department of Molecular &Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA [2] Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA [3] Dan L Duncan Cancer Center and Center for Cell Gene &Therapy, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA [4] Scott Department of Urology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25470039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Neutralizing/immunology/pharmacology ; Apoptosis/drug effects ; Celecoxib ; Cell Proliferation/drug effects ; Cyclooxygenase 2/metabolism ; Cyclooxygenase 2 Inhibitors/pharmacology ; Dinoprostone/*antagonists & inhibitors/immunology/metabolism/secretion ; Drug Resistance, Neoplasm/*drug effects ; Female ; Humans ; Male ; Mice ; Neoplastic Stem Cells/*drug effects/metabolism/*pathology ; Pyrazoles/pharmacology ; Signal Transduction/drug effects ; Sulfonamides/pharmacology ; Urinary Bladder Neoplasms/*drug therapy/*pathology ; Wound Healing/genetics ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Topology of feather melanocyte progenitor niche allows complex pigment patterns to emerge (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-04-27
    Description: Color patterns of bird plumage affect animal behavior and speciation. Diverse patterns are present in different species and within the individual. Here, we study the cellular and molecular basis of feather pigment pattern formation. Melanocyte progenitors are distributed as a horizontal ring in the proximal follicle, sending melanocytes vertically up into the epithelial cylinder, which gradually emerges as feathers grow. Different pigment patterns form by modulating the presence, arrangement, or differentiation of melanocytes. A layer of peripheral pulp further regulates pigmentation via patterned agouti expression. Lifetime feather cyclic regeneration resets pigment patterns for physiological needs. Thus, the evolution of stem cell niche topology allows complex pigment patterning through combinatorial co-option of simple regulatory mechanisms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4144997/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4144997/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, S J -- Foley, J -- Jiang, T X -- Yeh, C Y -- Wu, P -- Foley, A -- Yen, C M -- Huang, Y C -- Cheng, H C -- Chen, C F -- Reeder, B -- Jee, S H -- Widelitz, R B -- Chuong, C M -- AR060306/AR/NIAMS NIH HHS/ -- AR42177/AR/NIAMS NIH HHS/ -- AR47364/AR/NIAMS NIH HHS/ -- R01 AR042177/AR/NIAMS NIH HHS/ -- R01 AR047364/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Jun 21;340(6139):1442-5. doi: 10.1126/science.1230374. Epub 2013 Apr 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23618762" target="_blank"〉PubMed〈/a〉
    Keywords: Agouti Signaling Protein/metabolism ; Animals ; Birds/*anatomy & histology/physiology ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Chickens/anatomy & histology/physiology ; Columbidae/anatomy & histology/physiology ; Feathers/*cytology/growth & development ; Female ; Galliformes/anatomy & histology/physiology ; Male ; Melanocytes/*cytology/physiology ; Models, Biological ; *Pigmentation ; Regeneration ; *Stem Cell Niche ; Stem Cells/*cytology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Ascaris suum draft genome (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-10-28
    Description: Parasitic diseases have a devastating, long-term impact on human health, welfare and food production worldwide. More than two billion people are infected with geohelminths, including the roundworms Ascaris (common roundworm), Necator and Ancylostoma (hookworms), and Trichuris (whipworm), mainly in developing or impoverished nations of Asia, Africa and Latin America. In humans, the diseases caused by these parasites result in about 135,000 deaths annually, with a global burden comparable with that of malaria or tuberculosis in disability-adjusted life years. Ascaris alone infects around 1.2 billion people and, in children, causes nutritional deficiency, impaired physical and cognitive development and, in severe cases, death. Ascaris also causes major production losses in pigs owing to reduced growth, failure to thrive and mortality. The Ascaris-swine model makes it possible to study the parasite, its relationship with the host, and ascariasis at the molecular level. To enable such molecular studies, we report the 273 megabase draft genome of Ascaris suum and compare it with other nematode genomes. This genome has low repeat content (4.4%) and encodes about 18,500 protein-coding genes. Notably, the A. suum secretome (about 750 molecules) is rich in peptidases linked to the penetration and degradation of host tissues, and an assemblage of molecules likely to modulate or evade host immune responses. This genome provides a comprehensive resource to the scientific community and underpins the development of new and urgently needed interventions (drugs, vaccines and diagnostic tests) against ascariasis and other nematodiases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jex, Aaron R -- Liu, Shiping -- Li, Bo -- Young, Neil D -- Hall, Ross S -- Li, Yingrui -- Yang, Linfeng -- Zeng, Na -- Xu, Xun -- Xiong, Zijun -- Chen, Fangyuan -- Wu, Xuan -- Zhang, Guojie -- Fang, Xiaodong -- Kang, Yi -- Anderson, Garry A -- Harris, Todd W -- Campbell, Bronwyn E -- Vlaminck, Johnny -- Wang, Tao -- Cantacessi, Cinzia -- Schwarz, Erich M -- Ranganathan, Shoba -- Geldhof, Peter -- Nejsum, Peter -- Sternberg, Paul W -- Yang, Huanming -- Wang, Jun -- Wang, Jian -- Gasser, Robin B -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Oct 26;479(7374):529-33. doi: 10.1038/nature10553.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Veterinary Science, The University of Melbourne, Parkville, Victoria 3010, Australia. ajex@unimelb.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22031327" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antinematodal Agents ; Ascariasis/drug therapy/parasitology ; Ascaris suum/drug effects/*genetics ; Drug Design ; Genes, Helminth/genetics ; Genome, Helminth/*genetics ; Genomics ; Molecular Sequence Annotation ; Molecular Targeted Therapy
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    DHODH modulates transcriptional elongation in the neural crest and melanoma (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-25
    Description: Melanoma is a tumour of transformed melanocytes, which are originally derived from the embryonic neural crest. It is unknown to what extent the programs that regulate neural crest development interact with mutations in the BRAF oncogene, which is the most commonly mutated gene in human melanoma. We have used zebrafish embryos to identify the initiating transcriptional events that occur on activation of human BRAF(V600E) (which encodes an amino acid substitution mutant of BRAF) in the neural crest lineage. Zebrafish embryos that are transgenic for mitfa:BRAF(V600E) and lack p53 (also known as tp53) have a gene signature that is enriched for markers of multipotent neural crest cells, and neural crest progenitors from these embryos fail to terminally differentiate. To determine whether these early transcriptional events are important for melanoma pathogenesis, we performed a chemical genetic screen to identify small-molecule suppressors of the neural crest lineage, which were then tested for their effects on melanoma. One class of compound, inhibitors of dihydroorotate dehydrogenase (DHODH), for example leflunomide, led to an almost complete abrogation of neural crest development in zebrafish and to a reduction in the self-renewal of mammalian neural crest stem cells. Leflunomide exerts these effects by inhibiting the transcriptional elongation of genes that are required for neural crest development and melanoma growth. When used alone or in combination with a specific inhibitor of the BRAF(V600E) oncogene, DHODH inhibition led to a marked decrease in melanoma growth both in vitro and in mouse xenograft studies. Taken together, these studies highlight developmental pathways in neural crest cells that have a direct bearing on melanoma formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759979/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759979/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, Richard Mark -- Cech, Jennifer -- Ratanasirintrawoot, Sutheera -- Lin, Charles Y -- Rahl, Peter B -- Burke, Christopher J -- Langdon, Erin -- Tomlinson, Matthew L -- Mosher, Jack -- Kaufman, Charles -- Chen, Frank -- Long, Hannah K -- Kramer, Martin -- Datta, Sumon -- Neuberg, Donna -- Granter, Scott -- Young, Richard A -- Morrison, Sean -- Wheeler, Grant N -- Zon, Leonard I -- K08 AR055368/AR/NIAMS NIH HHS/ -- R01 CA103846/CA/NCI NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- R01 HG002668-08/HG/NHGRI NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Mar 24;471(7339):518-22. doi: 10.1038/nature09882.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Program and Hematology/Oncology, Children's Hospital Boston, Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430780" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Animals, Genetically Modified ; Cell Differentiation/drug effects ; Cell Line, Tumor ; Cell Lineage/drug effects ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic ; Genes, p53/genetics ; Humans ; Isoxazoles/pharmacology/therapeutic use ; Melanoma/drug therapy/enzymology/*genetics/*pathology ; Mice ; Neural Crest/drug effects/*enzymology/metabolism/pathology ; Oxidoreductases Acting on CH-CH Group Donors/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins B-raf/antagonists & ; inhibitors/chemistry/genetics/metabolism ; Rats ; Stem Cells/cytology/drug effects/pathology ; *Transcription, Genetic/drug effects/physiology ; Xenograft Model Antitumor Assays ; Zebrafish/embryology/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Molecular regulation of sexual preference revealed by genetic studies of 5-HT in the brains of male mice (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-29
    Description: Although the question of to whom a male directs his mating attempts is a critical one in social interactions, little is known about the molecular and cellular mechanisms controlling mammalian sexual preference. Here we report that the neurotransmitter 5-hydroxytryptamine (5-HT) is required for male sexual preference. Wild-type male mice preferred females over males, but males lacking central serotonergic neurons lost sexual preference although they were not generally defective in olfaction or in pheromone sensing. A role for 5-HT was demonstrated by the phenotype of mice lacking tryptophan hydroxylase 2 (Tph2), which is required for the first step of 5-HT synthesis in the brain. Thirty-five minutes after the injection of the intermediate 5-hydroxytryptophan (5-HTP), which circumvented Tph2 to restore 5-HT to the wild-type level, adult Tph2 knockout mice also preferred females over males. These results indicate that 5-HT and serotonergic neurons in the adult brain regulate mammalian sexual preference.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4094133/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4094133/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Yan -- Jiang, Yun'ai -- Si, Yunxia -- Kim, Ji-Young -- Chen, Zhou-Feng -- Rao, Yi -- R01 AR056318/AR/NIAMS NIH HHS/ -- England -- Nature. 2011 Apr 7;472(7341):95-9. doi: 10.1038/nature09822. Epub 2011 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Biological Sciences, Beijing 102206, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21441904" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Hydroxytryptophan/metabolism/pharmacology ; Animals ; Brain/*metabolism/physiology ; Brain Chemistry ; Estrous Cycle/physiology ; Female ; Heterosexuality/physiology ; Homosexuality, Male/genetics ; Housing, Animal ; Male ; Mating Preference, Animal/*physiology ; Mice ; Mice, Knockout ; Neurons/metabolism/physiology ; Odors/analysis ; Serotonin/biosynthesis/*metabolism ; Sex Attractants/analysis ; *Sex Characteristics ; Smell ; Tryptophan Hydroxylase/deficiency/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Metagenomic discovery of biomass-degrading genes and genomes from cow rumen (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-29
    Description: The paucity of enzymes that efficiently deconstruct plant polysaccharides represents a major bottleneck for industrial-scale conversion of cellulosic biomass into biofuels. Cow rumen microbes specialize in degradation of cellulosic plant material, but most members of this complex community resist cultivation. To characterize biomass-degrading genes and genomes, we sequenced and analyzed 268 gigabases of metagenomic DNA from microbes adherent to plant fiber incubated in cow rumen. From these data, we identified 27,755 putative carbohydrate-active genes and expressed 90 candidate proteins, of which 57% were enzymatically active against cellulosic substrates. We also assembled 15 uncultured microbial genomes, which were validated by complementary methods including single-cell genome sequencing. These data sets provide a substantially expanded catalog of genes and genomes participating in the deconstruction of cellulosic biomass.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hess, Matthias -- Sczyrba, Alexander -- Egan, Rob -- Kim, Tae-Wan -- Chokhawala, Harshal -- Schroth, Gary -- Luo, Shujun -- Clark, Douglas S -- Chen, Feng -- Zhang, Tao -- Mackie, Roderick I -- Pennacchio, Len A -- Tringe, Susannah G -- Visel, Axel -- Woyke, Tanja -- Wang, Zhong -- Rubin, Edward M -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):463-7. doi: 10.1126/science.1200387.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Energy, Joint Genome Institute, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21273488" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bacteria/enzymology/*genetics/isolation & purification/metabolism ; Bacterial Proteins/chemistry/genetics/metabolism ; *Biomass ; Carbohydrate Metabolism ; Cattle/*microbiology ; Cellulase/genetics/metabolism ; Cellulases/chemistry/*genetics/metabolism ; Cellulose/*metabolism ; Cellulose 1,4-beta-Cellobiosidase/genetics/metabolism ; Genes, Bacterial ; Genome, Bacterial ; *Metagenome ; Metagenomics/methods ; Molecular Sequence Annotation ; Molecular Sequence Data ; Poaceae/microbiology ; Rumen/metabolism/*microbiology ; Sequence Analysis, DNA
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Progenitor outgrowth from the niche in Drosophila trachea is guided by FGF from decaying branches (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-01-11
    Description: Although there has been progress identifying adult stem and progenitor cells and the signals that control their proliferation and differentiation, little is known about the substrates and signals that guide them out of their niche. By examining Drosophila tracheal outgrowth during metamorphosis, we show that progenitors follow a stereotyped path out of the niche, tracking along a subset of tracheal branches destined for destruction. The embryonic tracheal inducer branchless FGF (fibroblast growth factor) is expressed dynamically just ahead of progenitor outgrowth in decaying branches. Knockdown of branchless abrogates progenitor outgrowth, whereas misexpression redirects it. Thus, reactivation of an embryonic tracheal inducer in decaying branches directs outgrowth of progenitors that replace them. This explains how the structure of a newly generated tissue is coordinated with that of the old.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966907/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966907/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Feng -- Krasnow, Mark A -- T32 GM007790/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Jan 10;343(6167):186-9. doi: 10.1126/science.1241442.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305-5307, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24408434" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Drosophila Proteins/genetics/*physiology ; Drosophila melanogaster/*embryology ; Fibroblast Growth Factors/genetics/*physiology ; Gene Knockdown Techniques ; *Metamorphosis, Biological ; Receptors, Fibroblast Growth Factor/genetics/physiology ; Stem Cell Niche/*physiology ; Trachea/*embryology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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