Talk:Developmental Mechanism - Tube Formation: Difference between revisions
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==2013== | |||
===Effects of nanostructures and mouse embryonic stem cells on in vitro morphogenesis of rat testicular cords=== | |||
PLoS One. 2013;8(3):e60054. doi: 10.1371/journal.pone.0060054. Epub 2013 Mar 28. | |||
Pan F, Chi L, Schlatt S. | |||
Source | |||
Institute of Physics, University Münster, Münster, Germany. | |||
Abstract | |||
Morphogenesis of tubular structures is a common event during embryonic development. The signals providing cells with topographical cues to define a cord axis and to form new compartments surrounded by a basement membrane are poorly understood. Male gonadal differentiation is a late event during organogenesis and continues into postnatal life. The cellular changes resemble the mechanisms during embryonic life leading to tubular structures in other organs. Testicular cord formation is dependent on and first recognized by SRY-dependent aggregation of Sertoli cells leading to the appearance of testis-specific cord-like structures. Here we explored whether testicular cells use topographical cues in the form of nanostructures to direct or stimulate cord formation and whether embryonic stem cells (ES) or soluble factors released from those cells have an impact on this process. Using primary cell cultures of immature rats we first revealed that variable nanogratings exerted effects on peritubular cells and on Sertoli cells (at less than <1000 cells/mm(2)) by aligning the cell bodies towards the direction of the nanogratings. After two weeks of culture testicular cells assembled into a network of cord-like structures. We revealed that Sertoli cells actively migrate towards existing clusters. Contractions of peritubular cells lead to the transformation of isolated clusters into cord-like structures. The addition of mouse ES cells or conditioned medium from ES cells accelerated this process. Our studies show that epithelial (Sertoli cell) and mesenchymal (peritubular cells) cells crosstalk and orchestrate the formation of cords in response to physical features of the underlying matrix as well as secretory factors from ES cells. We consider these data on testicular morphogenesis relevant for the better understanding of mechanisms in cord formation also in other organs which may help to create optimized in vitro tools for artificial organogenesis. | |||
PMID 23555881 | |||
==2011== | ==2011== | ||
Revision as of 22:15, 3 December 2013
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Cite this page: Hill, M.A. (2024, April 16) Embryology Developmental Mechanism - Tube Formation. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Developmental_Mechanism_-_Tube_Formation |
2013
Effects of nanostructures and mouse embryonic stem cells on in vitro morphogenesis of rat testicular cords
PLoS One. 2013;8(3):e60054. doi: 10.1371/journal.pone.0060054. Epub 2013 Mar 28.
Pan F, Chi L, Schlatt S. Source Institute of Physics, University Münster, Münster, Germany.
Abstract
Morphogenesis of tubular structures is a common event during embryonic development. The signals providing cells with topographical cues to define a cord axis and to form new compartments surrounded by a basement membrane are poorly understood. Male gonadal differentiation is a late event during organogenesis and continues into postnatal life. The cellular changes resemble the mechanisms during embryonic life leading to tubular structures in other organs. Testicular cord formation is dependent on and first recognized by SRY-dependent aggregation of Sertoli cells leading to the appearance of testis-specific cord-like structures. Here we explored whether testicular cells use topographical cues in the form of nanostructures to direct or stimulate cord formation and whether embryonic stem cells (ES) or soluble factors released from those cells have an impact on this process. Using primary cell cultures of immature rats we first revealed that variable nanogratings exerted effects on peritubular cells and on Sertoli cells (at less than <1000 cells/mm(2)) by aligning the cell bodies towards the direction of the nanogratings. After two weeks of culture testicular cells assembled into a network of cord-like structures. We revealed that Sertoli cells actively migrate towards existing clusters. Contractions of peritubular cells lead to the transformation of isolated clusters into cord-like structures. The addition of mouse ES cells or conditioned medium from ES cells accelerated this process. Our studies show that epithelial (Sertoli cell) and mesenchymal (peritubular cells) cells crosstalk and orchestrate the formation of cords in response to physical features of the underlying matrix as well as secretory factors from ES cells. We consider these data on testicular morphogenesis relevant for the better understanding of mechanisms in cord formation also in other organs which may help to create optimized in vitro tools for artificial organogenesis.
PMID 23555881
2011
MIM regulates vertebrate neural tube closure
Development. 2011 May;138(10):2035-47. Epub 2011 Apr 6.
Liu W, Komiya Y, Mezzacappa C, Khadka DK, Runnels L, Habas R. Source Department of Biology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA.
Abstract
Neural tube closure is a critical morphogenetic event that is regulated by dynamic changes in cell shape and behavior. Although previous studies have uncovered a central role for the non-canonical Wnt signaling pathway in neural tube closure, the underlying mechanism remains poorly resolved. Here, we show that the missing in metastasis (MIM; Mtss1) protein, previously identified as a Hedgehog response gene and actin and membrane remodeling protein, specifically binds to Daam1 and couples non-canonical Wnt signaling to neural tube closure. MIM binds to a conserved domain within Daam1, and this interaction is positively regulated by Wnt stimulation. Spatial expression of MIM is enriched in the anterior neural plate and neural folds, and depletion of MIM specifically inhibits anterior neural fold closure without affecting convergent extension movements or mesoderm cell fate specification. Particularly, we find that MIM is required for neural fold elevation and apical constriction along with cell polarization and elongation in both the superficial and deep layers of the anterior neural plate. The function of MIM during neural tube closure requires both its membrane-remodeling domain and its actin-binding domain. Finally, we show that the effect of MIM on neural tube closure is not due to modulation of Hedgehog signaling in the Xenopus embryo. Together, our studies define a morphogenetic pathway involving Daam1 and MIM that transduces non-canonical Wnt signaling for the cytoskeletal changes and membrane dynamics required for vertebrate neural tube closure.
PMID 21471152
2010
Kidney development: two tales of tubulogenesis
Curr Top Dev Biol. 2010;90:193-229.
Little M, Georgas K, Pennisi D, Wilkinson L. Source Institute for Molecular Bioscience, The University of Queensland, St. Lucia, Australia.
Abstract
The mammalian kidney may well be one of the most complex organs of postnatal life. Each adult human kidney contains on average more than one million functional filtration units, the nephrons, residing within a specialized cellular interstitium. Each kidney also contains over 25 distinct cell types, each of which must be specifically aligned with respect to each other to ensure both normal development and ultimately, normal renal function. Despite this complexity, the development of the kidney can be simplistically described as the coordinate formation of two distinct sets of tubules. These tubules develop cooperatively with each other in time and space, yet represent two distinct but classical types of tubulogenesis. The first of these tubules, the ureteric bud, forms as an outgrowth of another epithelial tube, the nephric duct, and undergoes extensive branching morphogenesis to create the collecting system of the kidney. The second tubules are the nephrons themselves which arise via a mesenchyme-to-epithelial transition induced by the first set of tubules. These tubules never branch, but must elongate to become intricately patterned and functionally segmented tubules. The molecular drivers for these two tales of tubulogenesis include many gene families regulating tubulogenesis and branching morphogenesis in other organs; however, the individual players and codependent interrelationships between a branched and non-branched tubular network make organogenesis in the kidney unique. Here we review both what is known and remains to be understood in kidney tubulogenesis.
Copyright 2010 Elsevier Inc. All rights reserved.
PMID 20691850
Molecular aspects of respiratory and vascular tube development
Respir Physiol Neurobiol. 2010 Aug 31;173 Suppl:S33-6. Epub 2010 Apr 18.
Behr M.
Source
Life & Medical Sciences Institute, Program Unit Development, Genetics & Molecular Physiology, Laboratory for Molecular Developmental Biology, University of Bonn, Carl-Troll-Strasse 31, Bonn, Germany. mbehr@uni-bonn.de
Abstract
Lung, cardiovascular system, liver and kidney are some examples for organs that develop ramified three-dimensional networks of epithelial tubes. The tube morphology affects flow rates of transported materials, such as liquids and gases. Therefore, it is important to understand how tube morphology is controlled. In Drosophila melanogaster many evolutionarily conserved genetic pathways have been shown to be involved in airway patterning. Recent studies identified a number of conserved mechanisms that drive Drosophila airway maturation, such as controlling tube size, barrier formation and lumen clearance. Genetically highly ordered branching modes previously have been found, also for mouse lung development. The understanding of tube patterning, outgrowth, ramification and maturation also is of clinical relevance, since many factors are evolutionarily conserved and may have similar functions in humans. This meeting report highlights novel findings concerning tube development in the fruit fly (D. melanogaster), the zebrafish (Danio rerio) and the laboratory mouse (Mus musculus).
Copyright (c) 2010 Elsevier B.V. All rights reserved.
PMID 20403463
Apical constriction: a cell shape change that can drive morphogenesis
Dev Biol. 2010 May 1;341(1):5-19. Epub 2009 Sep 12. Sawyer JM, Harrell JR, Shemer G, Sullivan-Brown J, Roh-Johnson M, Goldstein B. Source Biology Department, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Abstract
Biologists have long recognized that dramatic bending of a cell sheet may be driven by even modest shrinking of the apical sides of cells. Cell shape changes and tissue movements like these are at the core of many of the morphogenetic movements that shape animal form during development, driving processes such as gastrulation, tube formation, and neurulation. The mechanisms of such cell shape changes must integrate developmental patterning information in order to spatially and temporally control force production-issues that touch on fundamental aspects of both cell and developmental biology and on birth defects research. How does developmental patterning regulate force-producing mechanisms, and what roles do such mechanisms play in development? Work on apical constriction from multiple systems including Drosophila, Caenorhabditis elegans, sea urchin, Xenopus, chick, and mouse has begun to illuminate these issues. Here, we review this effort to explore the diversity of mechanisms of apical constriction, the diversity of roles that apical constriction plays in development, and the common themes that emerge from comparing systems.
Copyright 2009 Elsevier Inc. All rights reserved.
PMID 19751720
