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  • 1
    Online Resource
    Online Resource
    Targeted DamID reveals differential binding of mammalian pluripotency factors
    The Company of Biologists ; 2018
    In:  Development
    Details
    In: Development, The Company of Biologists
    Abstract: The precise control of gene expression by transcription factor networks is critical to organismal development. The predominant approach for mapping transcription factor-chromatin interactions has been chromatin immunoprecipitation (ChIP). However, ChIP requires a large number of homogeneous cells and antisera with high specificity. A second approach, DamID, has the drawback that high levels of Dam methylase are toxic. Here we modify our Targeted DamID approach (TaDa) to enable cell type-specific expression in mammalian systems, generating an inducible system (mammalian TaDa or MaTaDa) to identify protein/DNA interactions in 100 to 1000 times fewer cells than ChIP. We mapped the binding sites of key pluripotency factors, OCT4 and PRDM14, in mouse embryonic stem cells, epiblast-like cells and primordial germ cell-like cells (PGCLCs). PGCLCs are an important system to elucidate primordial germ cell development in mice. We monitored PRDM14 binding during the specification of PGCLCs, identifying direct targets of PRDM14 that are key to understanding its critical role in PGCLC development. We show that MaTaDa is a sensitive and accurate method to assess cell type specific transcription factor binding in limited numbers of cells.
    Type of Medium: Online Resource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.170209
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2018
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Rotation and asymmetry of the mitotic spindle direct asymmetric cell division in the developing central nervous system
    Springer Science and Business Media LLC ; 2000
    In:  Nature Cell Biology Vol. 2, No. 1 ( 2000-1), p. 7-12
    Details
    In: Nature Cell Biology, Springer Science and Business Media LLC, Vol. 2, No. 1 ( 2000-1), p. 7-12
    Type of Medium: Online Resource
    ISSN: 1465-7392 , 1476-4679
    URL: Article
    DOI: 10.1038/71323
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2000
    detail.hit.zdb_id: 1494945-3
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    The vasculature as a neural stem cell niche
    Elsevier BV ; 2017
    In:  Neurobiology of Disease Vol. 107 ( 2017-11), p. 4-14
    Details
    In: Neurobiology of Disease, Elsevier BV, Vol. 107 ( 2017-11), p. 4-14
    Type of Medium: Online Resource
    ISSN: 0969-9961
    URL: Article
    DOI: 10.1016/j.nbd.2017.01.010
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
    detail.hit.zdb_id: 1471408-5
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    A Novel Strategy to Isolate Ubiquitin Conjugates Reveals Wide Role for Ubiquitination during Neural Development
    Elsevier BV ; 2011
    In:  Molecular & Cellular Proteomics Vol. 10, No. 5 ( 2011-05), p. M110.002188-
    Details
    In: Molecular & Cellular Proteomics, Elsevier BV, Vol. 10, No. 5 ( 2011-05), p. M110.002188-
    Type of Medium: Online Resource
    ISSN: 1535-9476
    URL: Article
    DOI: 10.1074/mcp.M110.002188
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2011
    detail.hit.zdb_id: 2071375-7
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    The Fes/Fer non-receptor tyrosine kinase cooperates with Src42A to regulate dorsal closure in Drosophila
    The Company of Biologists ; 2006
    In:  Development Vol. 133, No. 16 ( 2006-08-15), p. 3063-3073
    Details
    In: Development, The Company of Biologists, Vol. 133, No. 16 ( 2006-08-15), p. 3063-3073
    Abstract: Fes/Fer non-receptor tyrosine kinases regulate cell adhesion and cytoskeletal reorganisation through the modification of adherens junctions. Unregulated Fes/Fer kinase activity has been shown to lead to tumours in vivo. Here, we show that Drosophila Fer localises to adherens junctions in the dorsal epidermis and regulates a major morphological event, dorsal closure. Mutations in Src42A cause defects in dorsal closure similar to those seen in dfer mutant embryos. Furthermore, Src42Amutations enhance the dfer mutant phenotype, suggesting that Src42A and DFer act in the same cellular process. We show that DFer is required for the formation of the actin cable in leading edge cells and for normal rates of dorsal closure. We have isolated a gain-of-function mutation in dfer(dfergof) that expresses an N-terminally fused form of the protein, similar to oncogenic forms of vertebrate Fer. dfergof blocks dorsal closure and causes axon misrouting. We find that in dfer loss-of-function mutants β-catenin is hypophosphorylated, whereas in dfergof β-catenin is hyperphosphorylated. Phosphorylated β-catenin is removed from adherens junctions and degraded, thus implicating DFer in the regulation of adherens junctions.
    Type of Medium: Online Resource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.02467
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2006
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Targeted gene expression as a means of altering cell fates and generating dominant phenotypes
    The Company of Biologists ; 1993
    In:  Development Vol. 118, No. 2 ( 1993-06-01), p. 401-415
    Details
    In: Development, The Company of Biologists, Vol. 118, No. 2 ( 1993-06-01), p. 401-415
    Abstract: We have designed a system for targeted gene expression that allows the selective activation of any cloned gene in a wide variety of tissueand cell-specific patterns. The gene encoding the yeast transcriptional activator GAL4 is inserted randomly into the Drosophila genome to drive GAL4 expression from one of a diverse array of genomic enhancers. It is then possible to introduce a gene containing GAL4 binding sites within its promoter, to activate it in those cells where GAL4 is expressed, and to observe the effect of this directed misexpression on development. We have used GAL4-directed transcription to expand the domain of embryonic expression of the homeobox protein even-skipped. We show that even-skipped represses wingless and transforms cells that would normally secrete naked cuticle into denticle secreting cells. The GAL4 system can thus be used to study regulatory interactions during embryonic development. In adults, targeted expression can be used to generate dominant phenotypes for use in genetic screens. We have directed expression of an activated form of the Dras2 protein, resulting in dominant eye and wing defects that can be used in screens to identify other members of the Dras2 signal transduction pathway.
    Type of Medium: Online Resource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.118.2.401
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 1993
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Notch regulates the switch from symmetric to asymmetric neural stem cell division in the Drosophila optic lobe
    The Company of Biologists ; 2010
    In:  Development Vol. 137, No. 18 ( 2010-09-15), p. 2981-2987
    Details
    In: Development, The Company of Biologists, Vol. 137, No. 18 ( 2010-09-15), p. 2981-2987
    Abstract: The proper balance between symmetric and asymmetric stem cell division is crucial both to maintain a population of stem cells and to prevent tumorous overgrowth. Neural stem cells in the Drosophila optic lobe originate within a polarised neuroepithelium, where they divide symmetrically. Neuroepithelial cells are transformed into asymmetrically dividing neuroblasts in a precisely regulated fashion. This cell fate transition is highly reminiscent of the switch from neuroepithelial cells to radial glial cells in the developing mammalian cerebral cortex. To identify the molecules that mediate the transition, we microdissected neuroepithelial cells and compared their transcriptional profile with similarly obtained optic lobe neuroblasts. We find genes encoding members of the Notch pathway expressed in neuroepithelial cells. We show that Notch mutant clones are extruded from the neuroepithelium and undergo premature neurogenesis. A wave of proneural gene expression is thought to regulate the timing of the transition from neuroepithelium to neuroblast. We show that the proneural wave transiently suppresses Notch activity in neuroepithelial cells, and that inhibition of Notch triggers the switch from symmetric, proliferative division, to asymmetric, differentiative division.
    Type of Medium: Online Resource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.051250
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2010
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    The Drosophila homologue of CTIP1 (Bcl11a) and CTIP2 (Bcl11b) regulates neural stem cell temporal patterning
    The Company of Biologists ; 2022
    In:  Development Vol. 149, No. 17 ( 2022-09-01)
    Details
    In: Development, The Company of Biologists, Vol. 149, No. 17 ( 2022-09-01)
    Abstract: In the developing nervous system, neural stem cells (NSCs) use temporal patterning to generate a wide variety of different neuronal subtypes. In Drosophila, the temporal transcription factors, Hunchback, Kruppel, Pdm and Castor, are sequentially expressed by NSCs to regulate temporal identity during neurogenesis. Here, we identify a new temporal transcription factor that regulates the transition from the Pdm to Castor temporal windows. This factor, which we call Chronophage (or ‘time-eater’), is homologous to mammalian CTIP1 (Bcl11a) and CTIP2 (Bcl11b). We show that Chronophage binds upstream of the castor gene and regulates its expression. Consistent with Chronophage promoting a temporal switch, chronophage mutants generate an excess of Pdm-specified neurons and are delayed in generating neurons associated with the Castor temporal window. In addition to promoting the Pdm to Castor transition, Chronophage also represses the production of neurons generated during the earlier Hunchback and Kruppel temporal windows. Genetic interactions with Hunchback and Kruppel indicate that Chronophage regulates NSC competence to generate Hunchback- and Kruppel-specified neurons. Taken together, our results suggest that Chronophage has a conserved role in temporal patterning and neuronal subtype specification.
    Type of Medium: Online Resource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.200677
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2022
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    folded gastrulation , cell shape change and the control of myosin localization
    The Company of Biologists ; 2005
    In:  Development Vol. 132, No. 18 ( 2005-09-15), p. 4165-4178
    Details
    In: Development, The Company of Biologists, Vol. 132, No. 18 ( 2005-09-15), p. 4165-4178
    Abstract: The global cell movements that shape an embryo are driven by intricate changes to the cytoarchitecture of individual cells. In a developing embryo,these changes are controlled by patterning genes that confer cell identity. However, little is known about how patterning genes influence cytoarchitecture to drive changes in cell shape. In this paper, we analyze the function of the folded gastrulation gene (fog), a known target of the patterning gene twist. Our analysis of fog function therefore illuminates a molecular pathway spanning all the way from patterning gene to physical change in cell shape. We show that secretion of Fog protein is apically polarized, making this the earliest polarized component of a pathway that ultimately drives myosin to the apical side of the cell. We demonstrate that fog is both necessary and sufficient to drive apical myosin localization through a mechanism involving activation of myosin contractility with actin. We determine that this contractility driven form of localization involves RhoGEF2 and the downstream effector Rho kinase. This distinguishes apical myosin localization from basal myosin localization, which we find not to require actinomyosin contractility or FOG/RhoGEF2/Rho-kinase signaling. Furthermore, we demonstrate that once localized apically, myosin continues to contract. The force generated by continued myosin contraction is translated into a flattening and constriction of the cell surface through a tethering of the actinomyosin cytoskeleton to the apical adherens junctions. Our analysis of fog function therefore provides a direct link from patterning to cell shape change.
    Type of Medium: Online Resource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.01938
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2005
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Insulin Finds Its Niche
    American Association for the Advancement of Science (AAAS) ; 2013
    In:  Science Vol. 340, No. 6134 ( 2013-05-17), p. 817-818
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 340, No. 6134 ( 2013-05-17), p. 817-818
    Abstract: Coordination of organ growth and metabolism in response to changing environmental conditions is essential for physiological homeostasis. A central metabolic control mechanism in multicellular organisms is insulin signaling. Under conditions of elevated blood sugar, insulin promotes the storage of glucose in tissues such as muscle, fat, and liver. Classically, the role of insulin signaling is systemic. In mammals, insulin is produced by pancreatic beta cells and released into the bloodstream in response to increased concentrations of blood glucose, inducing global changes in growth and metabolism. Intriguingly, recent studies have demonstrated that insulin signaling can also occur locally, over a short range. Why have local insulin signaling? Local signals allow organ-specific, rather than organismal responses to changing environmental conditions (see the figure). This allows the modulation of the growth and development of individual tissues to be separately controlled, and raises the question of whether this phenomenon could be exploited for therapeutic strategies. Many of these recent findings have arisen from research in invertebrates; however, there are striking parallels in mammals.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.1238525
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2013
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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