Talk:Developmental Mechanism - Morphodynamics
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Cite this page: Hill, M.A. (2026, October 4) Embryology Developmental Mechanism - Morphodynamics. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Developmental_Mechanism_-_Morphodynamics |
2015
Mechanically patterning the embryonic airway epithelium
Proc Natl Acad Sci U S A. 2015 Jul 28;112(30):9230-5. doi: 10.1073/pnas.1504102112. Epub 2015 Jul 13.
Varner VD1, Gleghorn JP1, Miller E2, Radisky DC2, Nelson CM3.
Abstract
Collections of cells must be patterned spatially during embryonic development to generate the intricate architectures of mature tissues. In several cases, including the formation of the branched airways of the lung, reciprocal signaling between an epithelium and its surrounding mesenchyme helps generate these spatial patterns. Several molecular signals are thought to interact via reaction-diffusion kinetics to create distinct biochemical patterns, which act as molecular precursors to actual, physical patterns of biological structure and function. Here, however, we show that purely physical mechanisms can drive spatial patterning within embryonic epithelia. Specifically, we find that a growth-induced physical instability defines the relative locations of branches within the developing murine airway epithelium in the absence of mesenchyme. The dominant wavelength of this instability determines the branching pattern and is controlled by epithelial growth rates. These data suggest that physical mechanisms can create the biological patterns that underlie tissue morphogenesis in the embryo. KEYWORDS: buckling; instability; mechanical stress; morphodynamics; morphogenesis
PMID 26170292
2013
Apical constriction initiates new bud formation during monopodial branching of the embryonic chicken lung
Development. 2013 Aug;140(15):3146-55. doi: 10.1242/dev.093682. Epub 2013 Jul 3.
Kim HY, Varner VD, Nelson CM. Source Department of Chemical and Biological Engineering, Princeton University, Princeton, NJ 08544, USA.
Abstract Branching morphogenesis sculpts the airway epithelium of the lung into a tree-like structure to conduct air and promote gas exchange after birth. In the avian lung, a series of buds emerges from the dorsal surface of the primary bronchus via monopodial branching to form the conducting airways; anatomically, these buds are similar to those formed by domain branching in the mammalian lung. Here, we show that monopodial branching is initiated by apical constriction of the airway epithelium, and not by differential cell proliferation, using computational modeling and quantitative imaging of embryonic chicken lung explants. Both filamentous actin and phosphorylated myosin light chain were enriched at the apical surface of the airway epithelium during monopodial branching. Consistently, inhibiting actomyosin contractility prevented apical constriction and blocked branch initiation. Although cell proliferation was enhanced along the dorsal and ventral aspects of the primary bronchus, especially before branch formation, inhibiting proliferation had no effect on the initiation of branches. To test whether the physical forces from apical constriction alone are sufficient to drive the formation of new buds, we constructed a nonlinear, three-dimensional finite element model of the airway epithelium and used it to simulate apical constriction and proliferation in the primary bronchus. Our results suggest that, consistent with the experimental results, apical constriction is sufficient to drive the early stages of monopodial branching whereas cell proliferation is dispensable. We propose that initial folding of the airway epithelium is driven primarily by apical constriction during monopodial branching of the avian lung. KEYWORDS: Biomechanics, Mechanical stress, Morphodynamics, Patterning
PMID 23824575