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The Role of Cell Mechanics in Embryo...

Coarasa, Teresa Zulueta.

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The Role of Cell Mechanics in Embryonic Wound Repair: Staggered Contraction at the Leading Edge.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The Role of Cell Mechanics in Embryonic Wound Repair: Staggered Contraction at the Leading Edge./
作者:	Coarasa, Teresa Zulueta.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
面頁冊數:	172 p.
附註:	Source: Dissertations Abstracts International, Volume: 80-06, Section: B.
Contained By:	Dissertations Abstracts International80-06B.
標題:	Bioengineering. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10814544
ISBN:	9780438681996

The Role of Cell Mechanics in Embryonic Wound Repair: Staggered Contraction at the Leading Edge.
Coarasa, Teresa Zulueta.

The Role of Cell Mechanics in Embryonic Wound Repair: Staggered Contraction at the Leading Edge. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 172 p.

Source: Dissertations Abstracts International, Volume: 80-06, Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2018.

This item must not be sold to any third party vendors.

Epithelia are physical barriers against pathogens. Therefore, the ability of multicellular organisms to self-repair epithelial wounds is critical for survival. In embryos, wound repair is mediated by the assembly of a contractile supracellular cable at the wound margin composed of filamentous actin and the molecular motor non-muscle myosin II. It has been proposed that the contraction of the actomyosin cable acts as a "purse-string" to coordinate the movement of cells into the damaged area. Here, I analyze the physical basis of the "purse string" in Drosophila embryos. Using quantitative image analysis I found that, opposing the idea of a uniform "purse string", the distribution of cytoskeletal molecules at the wound margin is heterogeneous with areas of high and low protein density. Furthermore, I showed that mutants for the non-receptor tyrosine kinase Abelson (Abl) display a homogeneous distribution of actin at the wound margin that results in slow wound repair. To investigate the role of actomyosin heterogeneity in wound healing I used biophysical tools to quantify that forces around wounds are also heterogeneous, and patches of the wound edge with heterogeneous actomyosin levels contract faster than homogeneous patches. I developed a mathematical model of wound repair that predicted that actomyosin heterogeneity benefits wound closure if myosin dynamics are directed by tension and strain. To test this idea in vivo, I inhibited stretch-activated ion channels during wound closure, which resulted in disrupted myosin dynamics and impaired tissue repair. Together these results suggest that, instead of a "purse-string", staggered contractility regulates myosin dynamics to coordinate cell movements and to drive fast wound healing.

ISBN: 9780438681996Subjects--Topical Terms:

657580
Bioengineering.
Subjects--Index Terms:

Cell mechanics

The Role of Cell Mechanics in Embryonic Wound Repair: Staggered Contraction at the Leading Edge.
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520 $a Epithelia are physical barriers against pathogens. Therefore, the ability of multicellular organisms to self-repair epithelial wounds is critical for survival. In embryos, wound repair is mediated by the assembly of a contractile supracellular cable at the wound margin composed of filamentous actin and the molecular motor non-muscle myosin II. It has been proposed that the contraction of the actomyosin cable acts as a "purse-string" to coordinate the movement of cells into the damaged area. Here, I analyze the physical basis of the "purse string" in Drosophila embryos. Using quantitative image analysis I found that, opposing the idea of a uniform "purse string", the distribution of cytoskeletal molecules at the wound margin is heterogeneous with areas of high and low protein density. Furthermore, I showed that mutants for the non-receptor tyrosine kinase Abelson (Abl) display a homogeneous distribution of actin at the wound margin that results in slow wound repair. To investigate the role of actomyosin heterogeneity in wound healing I used biophysical tools to quantify that forces around wounds are also heterogeneous, and patches of the wound edge with heterogeneous actomyosin levels contract faster than homogeneous patches. I developed a mathematical model of wound repair that predicted that actomyosin heterogeneity benefits wound closure if myosin dynamics are directed by tension and strain. To test this idea in vivo, I inhibited stretch-activated ion channels during wound closure, which resulted in disrupted myosin dynamics and impaired tissue repair. Together these results suggest that, instead of a "purse-string", staggered contractility regulates myosin dynamics to coordinate cell movements and to drive fast wound healing.
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653 $a Quantitative image analysis
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