Please use this identifier to cite or link to this item: https://doi.org/10.1111/j.1440-169X.2011.01251.x
Title: Apoptotic force: Active mechanical function of cell death during morphogenesis
Authors: Teng, X.
Toyama, Y. 
Keywords: Actomyosin
Apoptosis
Biomechanics
Embryonic development
Morphogenesis
Issue Date: Feb-2011
Citation: Teng, X., Toyama, Y. (2011-02). Apoptotic force: Active mechanical function of cell death during morphogenesis. Development Growth and Differentiation 53 (2) : 269-276. ScholarBank@NUS Repository. https://doi.org/10.1111/j.1440-169X.2011.01251.x
Abstract: Apoptosis, or programmed cell death, is an essential process for the elimination of unnecessary cells during embryonic development, tissue homeostasis, and certain pathological conditions. Recently, an active mechanical function of apoptosis called apoptotic force has been demonstrated during a tissue fusion process of Drosophila embryogenesis. The mechanical force produced during apoptosis is used not only to force dying cells out from tissues in order to keep tissue integrity, but also to change the morphology of neighboring cells to fill the space originally occupied by the dying cell. Furthermore, the occurrence of apoptosis correlates with tissue movement and tension of the tissue. This finding suggests that apoptotic forces might be harnessed throughout cell death-related morphogenesis; however, this concept remains to be fully investigated. While the investigation of this active mechanical function of apoptosis has just begun, here we summarize the current understandings of this novel function of apoptosis, and discuss some possible developmental processes in which apoptosis may play a mechanical role. The concept of apoptotic force prompts a necessity to rethink the role of programmed cell death during morphogenesis. © 2011 The Authors. Journal compilation © 2011 Japanese Society of Developmental Biologists.
Source Title: Development Growth and Differentiation
URI: http://scholarbank.nus.edu.sg/handle/10635/102407
ISSN: 00121592
DOI: 10.1111/j.1440-169X.2011.01251.x
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