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Defining the Role of the Apelin Rece...

Deshwar, Ashish Ranjeet.

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Defining the Role of the Apelin Receptor and Mesp in Zebrafish Cardiac Progenitor Development.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Defining the Role of the Apelin Receptor and Mesp in Zebrafish Cardiac Progenitor Development./
Author:	Deshwar, Ashish Ranjeet.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2016,
Description:	129 p.
Notes:	Source: Dissertation Abstracts International, Volume: 78-08(E), Section: B.
Contained By:	Dissertation Abstracts International78-08B(E).
Subject:	Developmental biology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10190051
ISBN:	9781369669688

Defining the Role of the Apelin Receptor and Mesp in Zebrafish Cardiac Progenitor Development.
Deshwar, Ashish Ranjeet.

Defining the Role of the Apelin Receptor and Mesp in Zebrafish Cardiac Progenitor Development. - Ann Arbor : ProQuest Dissertations & Theses, 2016 - 129 p.

Source: Dissertation Abstracts International, Volume: 78-08(E), Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2016.

Formation of the vertebrate heart requires a complex series of transcriptional and epigenetic events. The building blocks of this organ, cardiac progenitor cells, must be specified, migrate to the correct embryonic location and remain plastic for a period of time in order to form a number of different cell types. The molecular events responsible for these phenomena remain poorly understood. In this thesis I examine the role of the apelin receptor (aplnr) and the mesp family of transcription factors in cardiac progenitor development. I find evidence that the Aplnr is required to enhance Nodal signaling in order to activate appropriate transcriptional targets at the right time. In the absence of this receptor cardiac progenitor gene expression displays delayed induction kinetics and these cells do not migrate to the correct location in the embryo. I also find that the Aplnr regulates Nodal signaling in a non-cell autonomous manner and may do so by an effect on Nodal ligand cleavage. Finally, I find that a recently discovered ligand for the Apelin Receptor, Apela, may in fact act as an antagonist in this process. When investigating the role of mesp family transcription factors in zebrafish I find that only one of four family members possesses potent cardiogenic activity: mespaa. Surprisingly, the mesp transcription factors are not required for the proper specification of the heart, however they do appear to regulate left-right asymmetry. Finally, using mespaa over-expressing cells to model cardiac progenitor development, I find that the activation of gata5 (a critical downstream target in cardiac development) does not occur in the embryo until after the start of gastrulation, challenging previous views on the timing of this process. Altogether I have discovered a number of novel insights into the mechanisms of cardiac progenitor development. These have broad ramifications in the field of developmental and stem cell biology and will be critical in order to harness the potential of these cells towards treatment of congenital and adult heart disease.

ISBN: 9781369669688Subjects--Topical Terms:

592588
Developmental biology.

Defining the Role of the Apelin Receptor and Mesp in Zebrafish Cardiac Progenitor Development.
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520 $a Formation of the vertebrate heart requires a complex series of transcriptional and epigenetic events. The building blocks of this organ, cardiac progenitor cells, must be specified, migrate to the correct embryonic location and remain plastic for a period of time in order to form a number of different cell types. The molecular events responsible for these phenomena remain poorly understood. In this thesis I examine the role of the apelin receptor (aplnr) and the mesp family of transcription factors in cardiac progenitor development. I find evidence that the Aplnr is required to enhance Nodal signaling in order to activate appropriate transcriptional targets at the right time. In the absence of this receptor cardiac progenitor gene expression displays delayed induction kinetics and these cells do not migrate to the correct location in the embryo. I also find that the Aplnr regulates Nodal signaling in a non-cell autonomous manner and may do so by an effect on Nodal ligand cleavage. Finally, I find that a recently discovered ligand for the Apelin Receptor, Apela, may in fact act as an antagonist in this process. When investigating the role of mesp family transcription factors in zebrafish I find that only one of four family members possesses potent cardiogenic activity: mespaa. Surprisingly, the mesp transcription factors are not required for the proper specification of the heart, however they do appear to regulate left-right asymmetry. Finally, using mespaa over-expressing cells to model cardiac progenitor development, I find that the activation of gata5 (a critical downstream target in cardiac development) does not occur in the embryo until after the start of gastrulation, challenging previous views on the timing of this process. Altogether I have discovered a number of novel insights into the mechanisms of cardiac progenitor development. These have broad ramifications in the field of developmental and stem cell biology and will be critical in order to harness the potential of these cells towards treatment of congenital and adult heart disease.
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