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Molecular and cellular mechanisms of...

Nechiporuk, Alex.

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Molecular and cellular mechanisms of zebrafish fin regeneration.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Molecular and cellular mechanisms of zebrafish fin regeneration./
作者:	Nechiporuk, Alex.
面頁冊數:	155 p.
附註:	Adviser: Mark T. Keating.
Contained By:	Dissertation Abstracts International63-06B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3056879
ISBN:	0493722076

Molecular and cellular mechanisms of zebrafish fin regeneration.
Nechiporuk, Alex.

Molecular and cellular mechanisms of zebrafish fin regeneration. - 155 p.

Adviser: Mark T. Keating.

Thesis (Ph.D.)--The University of Utah, 2002.

According to the National Center for Medical Rehabilitation Research, each year in the United States more than 100,000 individuals lose a limb due to traumatic injury or disease; 7,800 are paralyzed due to spinal cord injury. It is conceivable that these conditions could be treated by activating the body's own genetic instructions to reproduce missing structures or organs. A few vertebrate animals, including urodele amphibians and teleost fish, have an exceptional ability to regenerate various structures, such as limbs, spinal cord, and optic nerve. Limb regeneration in urodeles and fin regeneration in teleosts both appear to include the stages of wound healing and establishment of wound epithelium, recruitment of the blastema, which is defined as a mass of pluripotent mesenchyme cells, and differentiation and outgrowth of the regenerate. Here molecular biological and genetic approaches were applied to study cellular and molecular mechanisms of zebrafish fin regeneration. A classical genetic approach was used to identify four mutants defective in fin regeneration. Histological and molecular analysis shows that these mutants blocked during various stages of fin regeneration. One of these mutations, <italic> emmental</italic> (<italic>emm</italic>), prevents formation of a functional blastema through defective cell proliferation and increased apoptosis. Positional cloning revealed that mutation of a zebrafish homologue of yeast <italic> sly1</italic> causes the <italic>emm</italic> phenotype. <italic>sly1</italic> is upregulated in blastemal cells during blastema formation and regenerative outgrowth. The data indicate that sly1 is essential for enhanced proliferation that occurs in blastema during regeneration. Another mutant, <italic>nightcap </italic> (<italic>ncp</italic>), is specifically blocked during regenerative outgrowth. Positional cloning revealed that <italic>ncp</italic> encodes a zebrafish homologue of <italic>mps1</italic>, a gene required for the mitotic checkpoint in yeast. Further analysis revealed that <italic>ncp</italic> regenerates have severe proliferative defects and decreased checkpoint activity in most rapidly proliferating proximal blastemal cells. Our results indicate that <italic> mps1</italic> and its checkpoint activity is necessary to maintain this zone of rapidly proliferating cells. <italic>sly1</italic> and <italic>mps1</italic> are the first genes required for vertebrate organ regeneration that have been isolated using a genetic approach.

ISBN: 0493722076Subjects--Topical Terms:

1017686
Biology, Cell.

Molecular and cellular mechanisms of zebrafish fin regeneration.
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