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Genetic analysis of hematopoiesis in...

Liao, Chien-Wei Eric.

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Genetic analysis of hematopoiesis in zebrafish: Hemangioblast, stem cell, and erythroid differentiation in the cloche, bloodless, and riesling mutants.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Genetic analysis of hematopoiesis in zebrafish: Hemangioblast, stem cell, and erythroid differentiation in the cloche, bloodless, and riesling mutants./
Author:	Liao, Chien-Wei Eric.
Description:	237 p.
Notes:	Adviser: Leonard I. Zon.
Contained By:	Dissertation Abstracts International63-04B.
Subject:	Biology, Genetics. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3051220
ISBN:	0493657525

Genetic analysis of hematopoiesis in zebrafish: Hemangioblast, stem cell, and erythroid differentiation in the cloche, bloodless, and riesling mutants.
Liao, Chien-Wei Eric.

Genetic analysis of hematopoiesis in zebrafish: Hemangioblast, stem cell, and erythroid differentiation in the cloche, bloodless, and riesling mutants. - 237 p.

Adviser: Leonard I. Zon.

Thesis (Ph.D.)--Harvard University, 2002.

SCL is a basic helix-loop-helix (bHLH) transcription factor identified by its involvement in chromosomal translocations associated with acute lymphoblastic leukemia. Targeted disruption of SCL gene in ES cells has established an essential role in hematopoiesis, acting at the stem cell level to specify all blood lineages. Although SCL is also expressed in endothelial and neural progenitors, SCL function in these cells remains unknown. In the zebrafish mutant <italic> cloche</italic> (<italic>clo</italic>), SCL expression is abolished in hematopoietic and vascular tissues. Correspondingly, it was previously shown that <italic> clo</italic> fails to differentiate blood and angioblasts. Genetic analysis demonstrates that the <italic>clo</italic> mutation is not linked to the SCL locus. Forced expression of SCL in <italic>clo</italic> embryos rescues the blood and vascular defects, suggesting that SCL acts downstream of <italic> clo</italic> to specify hematopoietic and vascular differentiation. These results corroborate recent <italic>in vivo</italic> and <italic>in vitro</italic> data in, mice that also demonstrate a role for SCL to specify both hematopoietic and endothelial lineages, putatively acting at the hemangioblast level. Moreover, we find that SCL variants unable to bind DNA rescue hematopoiesis from gene-targeted SCL<super>−/−</super> embryonic stem cells and complement hematopoietic and vascular deficits in the zebrafish mutant <italic>clo</italic>. These results challenge widely accepted dogma that bHLH transcription factors exert their biological function by direct binding to cognate DNA sequences in critical targets genes.

ISBN: 0493657525Subjects--Topical Terms:

1017730
Biology, Genetics.

Genetic analysis of hematopoiesis in zebrafish: Hemangioblast, stem cell, and erythroid differentiation in the cloche, bloodless, and riesling mutants.
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100 1 $a Liao, Chien-Wei Eric. $3 1258423
245 1 0 $a Genetic analysis of hematopoiesis in zebrafish: Hemangioblast, stem cell, and erythroid differentiation in the cloche, bloodless, and riesling mutants.
300 $a 237 p.
500 $a Adviser: Leonard I. Zon.
500 $a Source: Dissertation Abstracts International, Volume: 63-04, Section: B, page: 1672.
502 $a Thesis (Ph.D.)--Harvard University, 2002.
520 $a SCL is a basic helix-loop-helix (bHLH) transcription factor identified by its involvement in chromosomal translocations associated with acute lymphoblastic leukemia. Targeted disruption of SCL gene in ES cells has established an essential role in hematopoiesis, acting at the stem cell level to specify all blood lineages. Although SCL is also expressed in endothelial and neural progenitors, SCL function in these cells remains unknown. In the zebrafish mutant <italic> cloche</italic> (<italic>clo</italic>), SCL expression is abolished in hematopoietic and vascular tissues. Correspondingly, it was previously shown that <italic> clo</italic> fails to differentiate blood and angioblasts. Genetic analysis demonstrates that the <italic>clo</italic> mutation is not linked to the SCL locus. Forced expression of SCL in <italic>clo</italic> embryos rescues the blood and vascular defects, suggesting that SCL acts downstream of <italic> clo</italic> to specify hematopoietic and vascular differentiation. These results corroborate recent <italic>in vivo</italic> and <italic>in vitro</italic> data in, mice that also demonstrate a role for SCL to specify both hematopoietic and endothelial lineages, putatively acting at the hemangioblast level. Moreover, we find that SCL variants unable to bind DNA rescue hematopoiesis from gene-targeted SCL<super>−/−</super> embryonic stem cells and complement hematopoietic and vascular deficits in the zebrafish mutant <italic>clo</italic>. These results challenge widely accepted dogma that bHLH transcription factors exert their biological function by direct binding to cognate DNA sequences in critical targets genes.
590 $a School code: 0084.
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710 2 0 $a Harvard University. $3 528741
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