Amplifying Cell

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Ben Scheres - One of the best experts on this subject based on the ideXlab platform.

  • members of the gcn5 histone acetyltransferase complex regulate plethora mediated root stem Cell niche maintenance and transit Amplifying Cell proliferation in arabidopsis
    The Plant Cell, 2009
    Co-Authors: Noortje Kornet, Ben Scheres
    Abstract:

    The PLETHORA (PLT) stem Cell transcription factors form a developmentally instructive protein gradient in Arabidopsis thaliana roots. Histone acetylation is known to facilitate gene transcription and plays an important role in developmental processes. Here, we show that histone acetyltransferase GCN5 (for general control nonderepressible 5) attenuates the PLT gradient. Based on genetic evidence, we establish that GCN5 is essential for root stem Cell niche maintenance and acts in the PLT pathway. The GCN5-associated factor ADA2b (for alteration/deficiency in activation 2b) is also positioned in the PLT pathway and regulates PLT expression, similar to GCN5. Both GCN5 and ADA2b mediate proliferation of the transit Amplifying Cells, but ADA2b does not affect stem Cell niche maintenance. Overexpression of PLT2 rescues the stem Cell niche defect of gcn5 mutants, indicating that GCN5 regulation of PLT expression is essential for maintenance of the root stem Cell niche. We conclude that histone acetylation complexes play an important role in shaping a developmentally instructive gradient in the root.

Fiona M Watt - One of the best experts on this subject based on the ideXlab platform.

  • sic transit gloria farewell to the epidermal transit Amplifying Cell
    Cell Stem Cell, 2007
    Co-Authors: Philip H Jones, Benjamin D Simons, Fiona M Watt
    Abstract:

    For the past 30 years, the prevailing model of epidermal homeostasis has been that epidermal stem Cells give rise to transit Amplifying Cells, which undergo a limited number of Cell divisions before initiating terminal differentiation. Recent studies challenge the existence of a transit Amplifying Cell compartment and suggest a new paradigm for epidermal homeostasis.

  • the spatial relationship between stem Cells and their progeny in the basal layer of human epidermis a new view based on whole mount labelling and lineage analysis
    Development, 1999
    Co-Authors: Uffe Birk Jensen, Sally Lowell, Fiona M Watt
    Abstract:

    In order to examine the spatial organisation of stem Cells and their progeny in human epidermis, we developed a method for whole-mount epidermal immunofluorescence labelling using high surface beta1 integrin expression as a stem Cell marker. We confirmed that there are clusters of high beta1 integrin-expressing Cells at the tips of the dermal papillae in epidermis from several body sites, whereas alpha6 integrin expression is more uniform. The majority of actively cycling Cells detected by Ki67 or bromodeoxyuridine labelling were found in the beta1 integrin-dull, transit Amplifying population and integrin-negative, keratin 10-positive Cells left the basal layer exclusively from this compartment. When we examined p53-positive clones in sun-exposed epidermis, we found two types of clone that differed in size and position in a way that was consistent with the founder Cell being a stem or transit Amplifying Cell. The patterning of the basal layer implies that transit Amplifying Cells migrate over the basement membrane away from the stem Cell clusters. In support of this, isolated beta1 integrin-dull keratinocytes were more motile on type IV collagen than beta1 integrin-bright keratinocytes and EGFP-labelled stem Cell clones in confluent cultured sheets were compact, whereas transit Amplifying clones were dispersed. The combination of whole-mount labelling and lineage marking thus reveals features of epidermal organisation that were previously unrecognised.

Christelle Coraux - One of the best experts on this subject based on the ideXlab platform.

  • basal Cells of the human adult airway surface epithelium retain transit Amplifying Cell properties
    Stem Cells, 2007
    Co-Authors: R Hajj, T Baranek, Richard Le Naour, P Lesimple, Edith Puchelle, Christelle Coraux
    Abstract:

    In numerous airway diseases, such as cystic fibrosis, the epithelium is severely damaged and must regenerate to restore its defense functions. Although the human airway epithelial stem Cells have not been identified yet, we have suggested recently that epithelial stem/progenitor Cells exist among both human fetal basal and suprabasal Cell subsets in the tracheal epithelium. In this study, we analyzed the capacity of human adult basal Cells isolated from human adult airway tissues to restore a well-differentiated and functional airway epithelium. To this end, we used the human-specific basal Cell markers tetraspanin CD151 and tissue factor (TF) to separate positive basal Cells from negative columnar Cells with a FACSAria Cell sorter. Sorted epithelial Cells were seeded into epithelium-denuded rat tracheae that were grafted subcutaneously in nude mice and on collagen-coated porous membranes, where they were grown at the air-liquid interface. Sorted basal and columnar populations were also analyzed for their telomerase activity, a specific transit-Amplifying Cell marker, by the telomeric repeat amplification protocol assay. After Cell sorting, the pure and viable CD151/TF-positive basal Cell population proliferated on plastic and adhered on epithelium-denuded rat tracheae, as well as on collagen-coated porous membranes, where it was able to restore a fully differentiated mucociliary and functional airway epithelium, whereas viable columnar negative Cells did not. Telomerase activity was detected in the CD151/TF-positive basal Cell population, but not in CD151/TF-negative columnar Cells. These results demonstrate that human adult basal Cells are at least airway surface transit-Amplifying epithelial Cells.

  • Basal Cells of the Human Adult Airway Surface Epithelium Retain Transit‐Amplifying Cell Properties
    Stem Cells, 2006
    Co-Authors: R Hajj, T Baranek, Richard Le Naour, P Lesimple, Edith Puchelle, Christelle Coraux
    Abstract:

    In numerous airway diseases, such as cystic fibrosis, the epithelium is severely damaged and must regenerate to restore its defense functions. Although the human airway epithelial stem Cells have not been identified yet, we have suggested recently that epithelial stem/progenitor Cells exist among both human fetal basal and suprabasal Cell subsets in the tracheal epithelium. In this study, we analyzed the capacity of human adult basal Cells isolated from human adult airway tissues to restore a well-differentiated and functional airway epithelium. To this end, we used the human-specific basal Cell markers tetraspanin CD151 and tissue factor (TF) to separate positive basal Cells from negative columnar Cells with a FACSAria Cell sorter. Sorted epithelial Cells were seeded into epithelium-denuded rat tracheae that were grafted subcutaneously in nude mice and on collagen-coated porous membranes, where they were grown at the air-liquid interface. Sorted basal and columnar populations were also analyzed for their telomerase activity, a specific transit-Amplifying Cell marker, by the telomeric repeat amplification protocol assay. After Cell sorting, the pure and viable CD151/TF-positive basal Cell population proliferated on plastic and adhered on epithelium-denuded rat tracheae, as well as on collagen-coated porous membranes, where it was able to restore a fully differentiated mucociliary and functional airway epithelium, whereas viable columnar negative Cells did not. Telomerase activity was detected in the CD151/TF-positive basal Cell population, but not in CD151/TF-negative columnar Cells. These results demonstrate that human adult basal Cells are at least airway surface transit-Amplifying epithelial Cells.

Noortje Kornet - One of the best experts on this subject based on the ideXlab platform.

  • members of the gcn5 histone acetyltransferase complex regulate plethora mediated root stem Cell niche maintenance and transit Amplifying Cell proliferation in arabidopsis
    The Plant Cell, 2009
    Co-Authors: Noortje Kornet, Ben Scheres
    Abstract:

    The PLETHORA (PLT) stem Cell transcription factors form a developmentally instructive protein gradient in Arabidopsis thaliana roots. Histone acetylation is known to facilitate gene transcription and plays an important role in developmental processes. Here, we show that histone acetyltransferase GCN5 (for general control nonderepressible 5) attenuates the PLT gradient. Based on genetic evidence, we establish that GCN5 is essential for root stem Cell niche maintenance and acts in the PLT pathway. The GCN5-associated factor ADA2b (for alteration/deficiency in activation 2b) is also positioned in the PLT pathway and regulates PLT expression, similar to GCN5. Both GCN5 and ADA2b mediate proliferation of the transit Amplifying Cells, but ADA2b does not affect stem Cell niche maintenance. Overexpression of PLT2 rescues the stem Cell niche defect of gcn5 mutants, indicating that GCN5 regulation of PLT expression is essential for maintenance of the root stem Cell niche. We conclude that histone acetylation complexes play an important role in shaping a developmentally instructive gradient in the root.

Robert M Lavker - One of the best experts on this subject based on the ideXlab platform.

  • strategies of epithelial repair modulation of stem Cell and transit Amplifying Cell proliferation
    Journal of Cell Science, 1998
    Co-Authors: Michael S Lehrer, Robert M Lavker
    Abstract:

    Using double labeling techniques, we studied the replication of corneal epithelial stem Cells that reside exclusively in the limbal zone, and their progeny transit Amplifying Cells. We show that corneal epithelial stem Cells can be induced to enter DNA synthesis by wounding and by TPA. We demonstrate the existence of a hierarchy of TA Cells; those of peripheral cornea undergo at least two rounds of DNA synthesis before they become post-mitotic, whereas those of central cornea are capable of only one round of division. However, the Cell cycle time of these TA Cells can be shortened and the number of times these TA Cells can replicate is increased in response to wounding. These results thus demonstrate three strategies of epithelial repair: (i) stem Cell replication, (ii) the unleashing of additional rounds of Cell proliferation that remain as an untapped reserve under normal circumstances, and (iii) enhancement of TA Cell proliferation via a shortening of the cycling time.