GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
Material
Publisher
Person/Organisation
Language
Years
FID
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    Erratum to: Relative utility of agronomic, phenological, and morphological traits for assessing genotype‐by‐environment interaction in maize inbreds
    Wiley ; 2022
    In:  Crop Science Vol. 62, No. 6 ( 2022-11), p. 2568-2569
    Details
    In: Crop Science, Wiley, Vol. 62, No. 6 ( 2022-11), p. 2568-2569
    Type of Medium: Online Resource
    ISSN: 0011-183X , 1435-0653
    URL: Issue
    URL: Article
    DOI: 10.1002/csc2.v62.6
    DOI: 10.1002/csc2.20860
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 1480918-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Relative utility of agronomic, phenological, and morphological traits for assessing genotype‐by‐environment interaction in maize inbreds
    Wiley ; 2020
    In:  Crop Science Vol. 60, No. 1 ( 2020-01), p. 62-81
    Details
    In: Crop Science, Wiley, Vol. 60, No. 1 ( 2020-01), p. 62-81
    Abstract: Plant breeders face the challenge of genotype × environment interaction (G × E) in comprehensively breeding for expanded geographic regions. An improved understanding of G × E sensitivity of traits and the environmental features that effectively discriminate among genotypes will enable more efficient breeding efforts. In this study of 31 maize ( Zea mays L.) inbreds grown in 36 environments that are part of the Genomes to Fields Initiative, we measured 14 traits, including flowering date, height, and yield components (i.e., ear and kernel dimensions) to (i) identify traits that are the most sensitive indicators of G × E; (ii) determine how geographic location and weather factors influence environments’ discriminability of inbreds; and (iii) detect patterns of stability in better and worse discriminating environments. Genotype × environment interaction explained between 9.0–20.4% of the phenotypic variance with greater effects in the yield‐component traits. Discriminability of environments varied by trait. Midwest locations (where 26 of the 31 inbreds were developed) were among the most discriminating environments for more traits, while environments in the West and East tended to be less discriminating. Weather factors during silking were significantly different between the most and least discriminating environments more often than average weather across the season or during the period from planting to silking. Stability of genotypes varied by trait, and performance was usually not correlated with stability. The dissection of complex traits, such as yield into component traits, appears to be a useful approach to understand how environmental factors differentially affect phenotype.
    Type of Medium: Online Resource
    ISSN: 0011-183X , 1435-0653
    URL: Issue
    URL: Article
    DOI: 10.1002/csc2.v60.1
    DOI: 10.1002/csc2.20035
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 1480918-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Human organoids: a new dimension in cell biology
    American Society for Cell Biology (ASCB) ; 2019
    In:  Molecular Biology of the Cell Vol. 30, No. 10 ( 2019-05), p. 1129-1137
    Details
    In: Molecular Biology of the Cell, American Society for Cell Biology (ASCB), Vol. 30, No. 10 ( 2019-05), p. 1129-1137
    Abstract: Organoids derived from stem cells or tissues in culture can develop into structures that resemble the in vivo anatomy and physiology of intact organs. Human organoid cultures provide the potential to study human development and model disease processes with the same scrutiny and depth of analysis customary for research with nonhuman model organisms. Resembling the complexity of the actual tissue or organ, patient-derived human organoid studies may accelerate medical research, creating new opportunities for tissue engineering and regenerative medicine, generating knowledge and tools for preclinical studies, including drug development and testing. Biologists are drawn to this system as a new “model organism” to study complex disease phenotypes and genetic variability among individuals using patient-derived tissues. The American Society for Cell Biology convened a task force to report on the potential, challenges, and limitations for human organoid research. The task force suggests ways to ease the entry for new researchers into the field and how to facilitate broader use of this new model organism within the research community. This includes guidelines for reproducibility, culturing, sharing of patient materials, patient consent, training, and communication with the public.
    Type of Medium: Online Resource
    ISSN: 1059-1524 , 1939-4586
    URL: Article
    DOI: 10.1091/mbc.E19-03-0135
    Language: English
    Publisher: American Society for Cell Biology (ASCB)
    Publication Date: 2019
    detail.hit.zdb_id: 1474922-1
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Transmural pressure signals through retinoic acid to regulate lung branching
    The Company of Biologists ; 2022
    In:  Development Vol. 149, No. 2 ( 2022-01-15)
    Details
    In: Development, The Company of Biologists, Vol. 149, No. 2 ( 2022-01-15)
    Abstract: During development, the mammalian lung undergoes several rounds of branching, the rate of which is tuned by the relative pressure of the fluid within the lumen of the lung. We carried out bioinformatics analysis of RNA-sequencing of embryonic mouse lungs cultured under physiologic or sub-physiologic transmural pressure and identified transcription factor-binding motifs near genes whose expression changes in response to pressure. Surprisingly, we found retinoic acid (RA) receptor binding sites significantly overrepresented in the promoters and enhancers of pressure-responsive genes. Consistently, increasing transmural pressure activates RA signaling, and pharmacologically inhibiting RA signaling decreases airway epithelial branching and smooth muscle wrapping. We found that pressure activates RA signaling through the mechanosensor Yap. A computational model predicts that mechanical signaling through Yap and RA affects lung branching by altering the balance between epithelial proliferation and smooth muscle wrapping, which we test experimentally. Our results reveal that transmural pressure signals through RA to balance the relative rates of epithelial growth and smooth muscle differentiation in the developing mouse lung and identify RA as a previously unreported component in the mechanotransduction machinery of embryonic tissues.
    Type of Medium: Online Resource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.199726
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2022
    detail.hit.zdb_id: 2007916-3
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Substratum stiffness tunes membrane voltage in mammary epithelial cells
    The Company of Biologists ; 2021
    In:  Journal of Cell Science Vol. 134, No. 13 ( 2021-07-01)
    Details
    In: Journal of Cell Science, The Company of Biologists, Vol. 134, No. 13 ( 2021-07-01)
    Abstract: Membrane voltage (Vm) plays a critical role in the regulation of several cellular behaviors, including proliferation, apoptosis and phenotypic plasticity. Many of these behaviors are affected by the stiffness of the underlying extracellular matrix, but the connections between Vm and the mechanical properties of the microenvironment are unclear. Here, we investigated the relationship between matrix stiffness and Vm by culturing mammary epithelial cells on synthetic substrata, the stiffnesses of which mimicked those of the normal mammary gland and breast tumors. Although proliferation is associated with depolarization, we surprisingly observed that cells are hyperpolarized when cultured on stiff substrata, a microenvironmental condition that enhances proliferation. Accordingly, we found that Vm becomes depolarized as stiffness decreases, in a manner dependent on intracellular Ca2+. Furthermore, inhibiting Ca2+-gated Cl− currents attenuates the effects of substratum stiffness on Vm. Specifically, we uncovered a role for cystic fibrosis transmembrane conductance regulator (CFTR) in the regulation of Vm by substratum stiffness. Taken together, these results suggest a novel role for CFTR and membrane voltage in the response of mammary epithelial cells to their mechanical microenvironment.
    Type of Medium: Online Resource
    ISSN: 0021-9533 , 1477-9137
    URL: Article
    DOI: 10.1242/jcs.256313
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2021
    detail.hit.zdb_id: 219171-4
    detail.hit.zdb_id: 1483099-1
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Vascular Endothelial-Cadherin Regulates Cytoskeletal Tension, Cell Spreading, and Focal Adhesions by Stimulating RhoA
    American Society for Cell Biology (ASCB) ; 2004
    In:  Molecular Biology of the Cell Vol. 15, No. 6 ( 2004-06), p. 2943-2953
    Details
    In: Molecular Biology of the Cell, American Society for Cell Biology (ASCB), Vol. 15, No. 6 ( 2004-06), p. 2943-2953
    Abstract: Changes in vascular endothelial (VE)-cadherin–mediated cell-cell adhesion and integrin-mediated cell-matrix adhesion coordinate to affect the physical and mechanical rearrangements of the endothelium, although the mechanisms for such cross talk remain undefined. Herein, we describe the regulation of focal adhesion formation and cytoskeletal tension by intercellular VE-cadherin engagement, and the molecular mechanism by which this occurs. Increasing the density of endothelial cells to increase cell-cell contact decreased focal adhesions by decreasing cell spreading. This contact inhibition of cell spreading was blocked by disrupting VE-cadherin engagement with an adenovirus encoding dominant negative VE-cadherin. When changes in cell spreading were prevented by culturing cells on a micropatterned substrate, VE-cadherin–mediated cell-cell contact paradoxically increased focal adhesion formation. We show that VE-cadherin engagement mediates each of these effects by inducing both a transient and sustained activation of RhoA. Both the increase and decrease in cell-matrix adhesion were blocked by disrupting intracellular tension and signaling through the Rho-ROCK pathway. In all, these findings demonstrate that VE-cadherin signals through RhoA and the actin cytoskeleton to cross talk with cell-matrix adhesion and thereby define a novel pathway by which cell-cell contact alters the global mechanical and functional state of cells.
    Type of Medium: Online Resource
    ISSN: 1059-1524 , 1939-4586
    URL: Article
    DOI: 10.1091/mbc.e03-10-0745
    Language: English
    Publisher: American Society for Cell Biology (ASCB)
    Publication Date: 2004
    detail.hit.zdb_id: 1474922-1
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Smooth muscle: a stiff sculptor of epithelial shapes
    The Royal Society ; 2018
    In:  Philosophical Transactions of the Royal Society B: Biological Sciences Vol. 373, No. 1759 ( 2018-11-05), p. 20170318-
    Details
    In: Philosophical Transactions of the Royal Society B: Biological Sciences, The Royal Society, Vol. 373, No. 1759 ( 2018-11-05), p. 20170318-
    Abstract: Smooth muscle is increasingly recognized as a key mechanical sculptor of epithelia during embryonic development. Smooth muscle is a mesenchymal tissue that surrounds the epithelia of organs including the gut, blood vessels, lungs, bladder, ureter, uterus, oviduct and epididymis. Smooth muscle is stiffer than its adjacent epithelium and often serves its morphogenetic function by physically constraining the growth of a proliferating epithelial layer. This constraint leads to mechanical instabilities and epithelial morphogenesis through buckling. Smooth muscle stiffness alone, without smooth muscle cell shortening, seems to be sufficient to drive epithelial morphogenesis. Fully understanding the development of organs that use smooth muscle stiffness as a driver of morphogenesis requires investigating how smooth muscle develops, a key aspect of which is distinguishing smooth muscle-like tissues from one another in vivo and in culture. This necessitates a comprehensive appreciation of the genetic, anatomical and functional markers that are used to distinguish the different subtypes of smooth muscle (for example, vascular versus visceral) from similar cell types (including myofibroblasts and myoepithelial cells). Here, we review how smooth muscle acts as a mechanical driver of morphogenesis and discuss ways of identifying smooth muscle, which is critical for understanding these morphogenetic events. This article is part of the Theo Murphy meeting issue ‘Mechanics of Development’.
    Type of Medium: Online Resource
    ISSN: 0962-8436 , 1471-2970
    URL: Article
    DOI: 10.1098/rstb.2017.0318
    RVK:
    WA 15000
    Language: English
    Publisher: The Royal Society
    Publication Date: 2018
    detail.hit.zdb_id: 1462620-2
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Mechanical tugging force regulates the size of cell–cell junctions
    Proceedings of the National Academy of Sciences ; 2010
    In:  Proceedings of the National Academy of Sciences Vol. 107, No. 22 ( 2010-06), p. 9944-9949
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 107, No. 22 ( 2010-06), p. 9944-9949
    Abstract: Actomyosin contractility affects cellular organization within tissues in part through the generation of mechanical forces at sites of cell–matrix and cell–cell contact. While increased mechanical loading at cell–matrix adhesions results in focal adhesion growth, whether forces drive changes in the size of cell–cell adhesions remains an open question. To investigate the responsiveness of adherens junctions (AJ) to force, we adapted a system of microfabricated force sensors to quantitatively report cell–cell tugging force and AJ size. We observed that AJ size was modulated by endothelial cell–cell tugging forces: AJs and tugging force grew or decayed with myosin activation or inhibition, respectively. Myosin-dependent regulation of AJs operated in concert with a Rac1, and this coordinated regulation was illustrated by showing that the effects of vascular permeability agents (S1P, thrombin) on junctional stability were reversed by changing the extent to which these agents coupled to the Rac and myosin-dependent pathways. Furthermore, direct application of mechanical tugging force, rather than myosin activity per se, was sufficient to trigger AJ growth. These findings demonstrate that the dynamic coordination of mechanical forces and cell–cell adhesive interactions likely is critical to the maintenance of multicellular integrity and highlight the need for new approaches to study tugging forces.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0914547107
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2010
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Matrix Pore Size Governs Escape of Human Breast Cancer Cells from a Microtumor to an Empty Cavity
    Elsevier BV ; 2020
    In:  iScience Vol. 23, No. 11 ( 2020-11), p. 101673-
    Details
    In: iScience, Elsevier BV, Vol. 23, No. 11 ( 2020-11), p. 101673-
    Type of Medium: Online Resource
    ISSN: 2589-0042
    URL: Article
    DOI: 10.1016/j.isci.2020.101673
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2020
    detail.hit.zdb_id: 2927064-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    Matrix degradation and cell proliferation are coupled to promote invasion and escape from an engineered human breast microtumor
    Oxford University Press (OUP) ; 2021
    In:  Integrative Biology Vol. 13, No. 1 ( 2021-02-03), p. 17-29
    Details
    In: Integrative Biology, Oxford University Press (OUP), Vol. 13, No. 1 ( 2021-02-03), p. 17-29
    Abstract: Metastasis, the leading cause of mortality in cancer patients, depends upon the ability of cancer cells to invade into the extracellular matrix that surrounds the primary tumor and to escape into the vasculature. To investigate the features of the microenvironment that regulate invasion and escape, we generated solid microtumors of MDA-MB-231 human breast carcinoma cells within gels of type I collagen. The microtumors were formed at defined distances adjacent to an empty cavity, which served as an artificial vessel into which the constituent tumor cells could escape. To define the relative contributions of matrix degradation and cell proliferation on invasion and escape, we used pharmacological approaches to block the activity of matrix metalloproteinases (MMPs) or to arrest the cell cycle. We found that blocking MMP activity prevents both invasion and escape of the breast cancer cells. Surprisingly, blocking proliferation increases the rate of invasion but has no effect on that of escape. We found that arresting the cell cycle increases the expression of MMPs, consistent with the increased rate of invasion. To gain additional insight into the role of cell proliferation in the invasion process, we generated microtumors from cells that express the fluorescent ubiquitination-based cell cycle indicator. We found that the cells that initiate invasions are preferentially quiescent, whereas cell proliferation is associated with the extension of invasions. These data suggest that matrix degradation and cell proliferation are coupled during the invasion and escape of human breast cancer cells and highlight the critical role of matrix proteolysis in governing tumor phenotype.
    Type of Medium: Online Resource
    ISSN: 1757-9708
    URL: Article
    DOI: 10.1093/intbio/zyaa026
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2480063-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...