Embryonic development involves a fundamental biomechanical process that constructs complicated three-dimensional tissue structures through massive cellular movements. During early gastrulation stages, polarized cell intercalation movements drive the dramatic extension of the Xenopus laevis frog embryo in the anterior-posterior direction. How those individual cellular protrusive forces integrate to produce the bulk force at the tissue level remains unknown. Furthermore, the embryo is shaped not only by active forces, but also by the mechanical properties such as the viscoelastic properties of the constituent tissues. Although rapid progresses have been made to identify the genes or proteins involved in this process, there is much less known about mechanical roles of the genes and proteins in the process. By investigating the contribution of subcellular-, cellular-, and tissue-level structures to the tissue mechanical properties, we found that, on the tissue-level, there were large temporal and spatial variation in tissue stiffness of dorsal isolates and the stiffness was largely dependent on paraxial mesoderm tissues, while notochord tissue, which has been proposed to support the early embryos, was not a major contributor to the tissue mechanics. On the cellular-level, the mechanical properties of dorsal isolates were mainly dependent on cells, but not their ECM. On the subcellular-level, the mechanical properties of the embryonic cells were determined by actin and myosin II contractility, while microtubules indirectly controlled the tissue stiffness by regulating actomyosin network through a Rho-GEF mediated signaling pathway. In order to measure the tissue extension forces, we developed a high throughput technique combining imaging techniques and finite element models. Using this technique, we identified two cases of mechanical adaptation. In the first case we found that dorsal axial tissues generated less force to compensate for their own lower mechanical resistance. In the second we found that dorsal axial tissues encountering a stiffer environment were capable of generating nearly 2-fold greater force. These cases of adaptation demonstrate that force production is quantitatively balanced during CE and that the mechanisms responsible for this adaptation are able to ensure robust morphogenesis against environmental and genetic variation in physical force production and tissue stiffness.
| Identifer | oai:union.ndltd.org:PITT/oai:PITTETD:etd-01142010-110450 |
| Date | 25 June 2010 |
| Creators | Zhou, Jian |
| Contributors | Kris Noel Dahl, James H-C. Wang, Michael S. Sacks, Lance Davidson |
| Publisher | University of Pittsburgh |
| Source Sets | University of Pittsburgh |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.library.pitt.edu/ETD/available/etd-01142010-110450/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Pittsburgh or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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