scholarly journals Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Eduardo Pulgar ◽  
Cornelia Schwayer ◽  
Néstor Guerrero ◽  
Loreto López ◽  
Susana Márquez ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Progenitor Cell ◽  
Terminal Differentiation ◽  
Cell Contact ◽  
Epithelial Layer ◽  
Apical Constriction ◽  
Embryonic Tissues ◽  
Vegetal Pole ◽  
Dependent Cell ◽  
Contact Mechanism

The developmental strategies used by progenitor cells to allow a safe journey from their induction place towards the site of terminal differentiation are still poorly understood. Here, we uncovered a mechanism of progenitor cell allocation that stems from an incomplete process of epithelial delamination that allows progenitors to coordinate their movement with adjacent extra-embryonic tissues. Progenitors of the zebrafish laterality organ originate from the superficial epithelial enveloping layer by an apical constriction process of cell delamination. During this process, progenitors retain long-lasting apical contacts that enable the epithelial layer to pull a subset of progenitors on their way to the vegetal pole. The remaining delaminated cells follow the movement of apically attached progenitors by a protrusion-dependent cell-cell contact mechanism, avoiding sequestration by the adjacent endoderm, ensuring their collective fate and allocation at the site of differentiation. Thus, we reveal that incomplete delamination serves as a cellular platform for coordinated tissue movements during development.

scholarly journals Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism

2021 ◽  
Author(s):  
Eduardo Pulgar ◽  
Cornelia Schwayer ◽  
Néstor Guerrero ◽  
Loreto López ◽  
Susana Márquez ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Progenitor Cell ◽  
Terminal Differentiation ◽  
Epithelial Layer ◽  
Allocation Mechanism ◽  
Apical Constriction ◽  
Embryonic Tissues ◽  
Cell Groups ◽  
Vegetal Pole

AbstractThe developmental strategies used by progenitor cells to endure a safe journey from their induction place towards the site of terminal differentiation are still poorly understood. Here we uncovered a progenitor cell allocation mechanism that stems from an incomplete process of epithelial delamination that allows progenitors to coordinate their movement with adjacent extra-embryonic tissues. Progenitors of the zebrafish laterality organ originate from the surface epithelial enveloping layer by an apical constriction process of cell delamination. During this process, progenitors retain long-term apical contacts that enable the epithelial layer to pull a subset of progenitors along their way towards the vegetal pole. The remaining delaminated progenitors follow apically-attached progenitors’ movement by a co-attraction mechanism, avoiding sequestration by the adjacent endoderm, ensuring their fate and collective allocation at the differentiation site. Thus, we reveal that incomplete delamination serves as a cellular platform for coordinated tissue movements during development.Impact StatementIncomplete delamination serves as a cellular platform for coordinated tissue movements during development, guiding newly formed progenitor cell groups to the differentiation site.

scholarly journals In vitro regulation of human hematopoiesis by natural killer cells: analysis at a clonal level

Blood ◽  
1987 ◽  
Vol 69 (1) ◽  
pp. 246-254 ◽  
Author(s):  
F Herrmann ◽  
RE Schmidt ◽  
J Ritz ◽  
JD Griffin
Keyword(s):  
Natural Killer ◽  
Progenitor Cells ◽  
Colony Formation ◽  
Progenitor Cell ◽  
Nk Cell ◽  
Colony Growth ◽  
Hematopoietic Progenitor Cells ◽  
Cell Contact ◽  
Hematopoietic Progenitor

We studied the effects of a series of well-characterized clones of human natural killer (NK) cells on the proliferation of highly purified normal marrow hematopoietic progenitor cells. Individual NK clones suppressed granulocyte, monocyte, erythroid, or mixed colony formation in a heterogeneous but clonally stable manner. Inhibition of colony growth required a period of close cell contact between NK cell and progenitor cell with maximum inhibition occurring after 8 to 18 hours of preincubation time. The mechanism of killing was at least partially humoral, however, as cell-free supernatants generated by NK clones “activated” by contact with a target cell also inhibited progenitor cell growth. One of the possible humoral mediators was identified as gamma-interferon by studies with specific neutralizing monoclonal antibodies. These results show that clonal NK lines can be further activated by coming in contact with hematopoietic progenitor cells, resulting in substantial inhibition of colony formation in vitro.

scholarly journals In vitro regulation of human hematopoiesis by natural killer cells: analysis at a clonal level

Blood ◽  
1987 ◽  
Vol 69 (1) ◽  
pp. 246-254 ◽  
Author(s):  
F Herrmann ◽  
RE Schmidt ◽  
J Ritz ◽  
JD Griffin
Keyword(s):  
Natural Killer ◽  
Progenitor Cells ◽  
Colony Formation ◽  
Progenitor Cell ◽  
Nk Cell ◽  
Colony Growth ◽  
Hematopoietic Progenitor Cells ◽  
Cell Contact ◽  
Hematopoietic Progenitor

Abstract We studied the effects of a series of well-characterized clones of human natural killer (NK) cells on the proliferation of highly purified normal marrow hematopoietic progenitor cells. Individual NK clones suppressed granulocyte, monocyte, erythroid, or mixed colony formation in a heterogeneous but clonally stable manner. Inhibition of colony growth required a period of close cell contact between NK cell and progenitor cell with maximum inhibition occurring after 8 to 18 hours of preincubation time. The mechanism of killing was at least partially humoral, however, as cell-free supernatants generated by NK clones “activated” by contact with a target cell also inhibited progenitor cell growth. One of the possible humoral mediators was identified as gamma-interferon by studies with specific neutralizing monoclonal antibodies. These results show that clonal NK lines can be further activated by coming in contact with hematopoietic progenitor cells, resulting in substantial inhibition of colony formation in vitro.

scholarly journals Mechanisms of vertebrate neural plate internalization

2020 ◽  
Vol 52 ◽  
Author(s):  
Claudio Araya ◽  
Daniela Carrasco
Keyword(s):  
Neural Tube ◽  
Molecular Mechanisms ◽  
Tube Formation ◽  
Neural Plate ◽  
Cell Contact ◽  
Apical Constriction ◽  
Mechanical Coupling ◽  
Dependent Cell ◽  
Clinical Conditions ◽  
Cell Cell

The internalization of multi-cellular tissues is a key morphogenetic process during animal development and organ formation. A good example of this is the initial stages of vertebrate central nervous system formation whereby a transient embryonic structure called the neural plate is able to undergo collective cell rearrangements within the dorsal midline. Despite that defects in neural plate midline internalization may result in a series of severe clinical conditions such as spina bifida and anencephaly, the biochemical and biomechanical details of this process remain only partially characterized. Here we review the main cellular and molecular mechanisms underlying midline cell and tissue internalization during vertebrate neural tube formation. We discuss the contribution of collective cell mechanisms including convergent and extension as well as apical constriction facilitating midline neural plate shaping. Furthermore, we summarize recent studies that shed light on how the interplay of signaling pathways and cell biomechanics modulate neural plate internalization. In addition, we discuss how adhesion-dependent cell-cell contact appears to be a critical component during midline cell convergence and surface cell contraction via cell-cell mechanical coupling. We envision that more detailed high-resolution quantitative data at both cell and tissue levels will be required to properly model mechanisms of vertebrate neural plate internalization with the hope to prevent human neural tube defects.

Bone Marrow Niches for Skeletal Progenitor Cells and their Inhabitants in Health and Disease

2019 ◽  
Vol 14 (4) ◽  
pp. 305-319 ◽  
Author(s):  
Marietta Herrmann ◽  
Franz Jakob
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Adult Stem Cells ◽  
Current Knowledge ◽  
Cell Populations ◽  
Surface Markers ◽  
Bone Marrow Niches

The bone marrow hosts skeletal progenitor cells which have most widely been referred to as Mesenchymal Stem or Stromal Cells (MSCs), a heterogeneous population of adult stem cells possessing the potential for self-renewal and multilineage differentiation. A consensus agreement on minimal criteria has been suggested to define MSCs in vitro, including adhesion to plastic, expression of typical surface markers and the ability to differentiate towards the adipogenic, osteogenic and chondrogenic lineages but they are critically discussed since the differentiation capability of cells could not always be confirmed by stringent assays in vivo. However, these in vitro characteristics have led to the notion that progenitor cell populations, similar to MSCs in bone marrow, reside in various tissues. MSCs are in the focus of numerous (pre)clinical studies on tissue regeneration and repair.Recent advances in terms of genetic animal models enabled a couple of studies targeting skeletal progenitor cells in vivo. Accordingly, different skeletal progenitor cell populations could be identified by the expression of surface markers including nestin and leptin receptor. While there are still issues with the identity of, and the overlap between different cell populations, these studies suggested that specific microenvironments, referred to as niches, host and maintain skeletal progenitor cells in the bone marrow. Dynamic mutual interactions through biological and physical cues between niche constituting cells and niche inhabitants control dormancy, symmetric and asymmetric cell division and lineage commitment. Niche constituting cells, inhabitant cells and their extracellular matrix are subject to influences of aging and disease e.g. via cellular modulators. Protective niches can be hijacked and abused by metastasizing tumor cells, and may even be adapted via mutual education. Here, we summarize the current knowledge on bone marrow skeletal progenitor cell niches in physiology and pathophysiology. We discuss the plasticity and dynamics of bone marrow niches as well as future perspectives of targeting niches for therapeutic strategies.

FLT3 expression initiates in fully multipotent mouse hematopoietic progenitor cells

Blood ◽  
2011 ◽  
Vol 118 (6) ◽  
pp. 1544-1548 ◽  
Author(s):  
Natalija Buza-Vidas ◽  
Petter Woll ◽  
Anne Hultquist ◽  
Sara Duarte ◽  
Michael Lutteropp ◽  
...  
Keyword(s):  
Cell Surface ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Hematopoietic Progenitor ◽  
Cell Compartment ◽  
Multipotent Progenitors ◽  
Flt3 Mutations ◽  
Flt3 Expression

Abstract Lymphoid-primed multipotent progenitors with down-regulated megakaryocyte-erythroid (MkE) potential are restricted to cells with high levels of cell-surface FLT3 expression, whereas HSCs and MkE progenitors lack detectable cell-surface FLT3. These findings are compatible with FLT3 cell-surface expression not being detectable in the fully multipotent stem/progenitor cell compartment in mice. If so, this process could be distinct from human hematopoiesis, in which FLT3 already is expressed in multipotent stem/progenitor cells. The expression pattern of Flt3 (mRNA) and FLT3 (protein) in multipotent progenitors is of considerable relevance for mouse models in which prognostically important Flt3 mutations are expressed under control of the endogenous mouse Flt3 promoter. Herein, we demonstrate that mouse Flt3 expression initiates in fully multipotent progenitors because in addition to lymphoid and granulocyte-monocyte progenitors, FLT3− Mk- and E-restricted downstream progenitors are also highly labeled when Flt3-Cre fate mapping is applied.

scholarly journals Elevated Mcl-1 perturbs lymphopoiesis, promotes transformation of hematopoietic stem/progenitor cells, and enhances drug resistance

Blood ◽  
2010 ◽  
Vol 116 (17) ◽  
pp. 3197-3207 ◽  
Author(s):  
Kirsteen J. Campbell ◽  
Mary L. Bath ◽  
Marian L. Turner ◽  
Cassandra J. Vandenberg ◽  
Philippe Bouillet ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Progenitor Cell ◽  
Fetal Liver ◽  
Cytotoxic Agents ◽  
Hematopoietic Stem ◽  
Stem And Progenitor Cells ◽  
Fetal Liver Cells ◽  
Follicular Lymphomas ◽  
The Impact

Abstract Diverse human cancers with poor prognosis, including many lymphoid and myeloid malignancies, exhibit high levels of Mcl-1. To explore the impact of Mcl-1 overexpression on the hematopoietic compartment, we have generated vavP-Mcl-1 transgenic mice. Their lymphoid and myeloid cells displayed increased resistance to a variety of cytotoxic agents. Myelopoiesis was relatively normal, but lymphopoiesis was clearly perturbed, with excess mature B and T cells accumulating. Rather than the follicular lymphomas typical of vavP-BCL-2 mice, aging vavP-Mcl-1 mice were primarily susceptible to lymphomas having the phenotype of a stem/progenitor cell (11 of 30 tumors) or pre-B cell (12 of 30 tumors). Mcl-1 overexpression dramatically accelerated Myc-driven lymphomagenesis. Most vavP-Mcl-1/ Eμ-Myc mice died around birth, and transplantation of blood from bitransgenic E18 embryos into unirradiated mice resulted in stem/progenitor cell tumors. Furthermore, lethally irradiated mice transplanted with E13 fetal liver cells from Mcl-1/Myc bitransgenic mice uniformly died of stem/progenitor cell tumors. When treated in vivo with cyclophosphamide, tumors coexpressing Mcl-1 and Myc transgenes were significantly more resistant than conventional Eμ-Myc lymphomas. Collectively, these results demonstrate that Mcl-1 overexpression renders hematopoietic cells refractory to many cytotoxic insults, perturbs lymphopoiesis and promotes malignant transformation of hematopoietic stem and progenitor cells.

scholarly journals Liver X receptor β regulates the development of the dentate gyrus and autistic-like behavior in the mouse

2018 ◽  
Vol 115 (12) ◽  
pp. E2725-E2733 ◽  
Author(s):  
Yulong Cai ◽  
Xiaotong Tang ◽  
Xi Chen ◽  
Xin Li ◽  
Ying Wang ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Neural Progenitor Cells ◽  
Repetitive Behavior ◽  
Autism Spectrum ◽  
Liver X Receptor ◽  
Self Renewal ◽  
Spectrum Disorders ◽  
Deficient Mice

The dentate gyrus (DG) of the hippocampus is a laminated brain region in which neurogenesis begins during early embryonic development and continues until adulthood. Recent studies have implicated that defects in the neurogenesis of the DG seem to be involved in the genesis of autism spectrum disorders (ASD)-like behaviors. Liver X receptor β (LXRβ) has recently emerged as an important transcription factor involved in the development of laminated CNS structures, but little is known about its role in the development of the DG. Here, we show that deletion of the LXRβ in mice causes hypoplasia in the DG, including abnormalities in the formation of progenitor cells and granule cell differentiation. We also found that expression of Notch1, a central mediator of progenitor cell self-renewal, is reduced in LXRβ-null mice. In addition, LXRβ deletion in mice results in autistic-like behaviors, including abnormal social interaction and repetitive behavior. These data reveal a central role for LXRβ in orchestrating the timely differentiation of neural progenitor cells within the DG, thereby providing a likely explanation for its association with the genesis of autism-related behaviors in LXRβ-deficient mice.

scholarly journals Extracellular Electron Transfer to Fe(III) Oxides by the Hyperthermophilic Archaeon Geoglobus ahangari via a Direct Contact Mechanism

2013 ◽  
Vol 79 (15) ◽  
pp. 4694-4700 ◽  
Author(s):  
Michael P. Manzella ◽  
Gemma Reguera ◽  
Kazem Kashefi
Keyword(s):  
Electron Acceptor ◽  
Direct Contact ◽  
Alginate Beads ◽  
Hydrothermal Systems ◽  
Microbial Reduction ◽  
Extracellular Electron Transfer ◽  
Cell Contact ◽  
Content Type ◽  
Chemical Conditions ◽  
Contact Mechanism

ABSTRACTThe microbial reduction of Fe(III) plays an important role in the geochemistry of hydrothermal systems, yet it is poorly understood at the mechanistic level. Here we show that the obligate Fe(III)-reducing archaeonGeoglobus ahangariuses a direct-contact mechanism for the reduction of Fe(III) oxides to magnetite at 85°C. Alleviating the need to directly contact the mineral with the addition of a chelator or the electron shuttle anthraquinone-2,6-disulfonate (AQDS) stimulated Fe(III) reduction. In contrast, entrapment of the oxides within alginate beads to prevent cell contact with the electron acceptor prevented Fe(III) reduction and cell growth unless AQDS was provided. Furthermore, filtered culture supernatant fluids had no effect on Fe(III) reduction, ruling out the secretion of an endogenous mediator too large to permeate the alginate beads. Consistent with a direct contact mechanism, electron micrographs showed cells in intimate association with the Fe(III) mineral particles, which once dissolved revealed abundant curled appendages. The cells also produced several heme-containing proteins. Some of them were detected among proteins sheared from the cell's outer surface and were required for the reduction of insoluble Fe(III) oxides but not for the reduction of the soluble electron acceptor Fe(III) citrate. The results thus support a mechanism in which the cells directly attach and transfer electrons to the Fe(III) oxides using redox-active proteins exposed on the cell surface. This strategy confers onG. ahangaria competitive advantage for accessing and reducing Fe(III) oxides under the extreme physical and chemical conditions of hot ecosystems.

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