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Loss of TBX3 Enhances Pancreatic Pro...

Mukherjee, Somdutta.

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Loss of TBX3 Enhances Pancreatic Progenitor Generation from Human Pluripotent Stem Cells.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Loss of TBX3 Enhances Pancreatic Progenitor Generation from Human Pluripotent Stem Cells./
Author:	Mukherjee, Somdutta.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2021,
Description:	133 p.
Notes:	Source: Dissertations Abstracts International, Volume: 82-12, Section: B.
Contained By:	Dissertations Abstracts International82-12B.
Subject:	Developmental biology. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28416039
ISBN:	9798738646560

Loss of TBX3 Enhances Pancreatic Progenitor Generation from Human Pluripotent Stem Cells.
Mukherjee, Somdutta.

Loss of TBX3 Enhances Pancreatic Progenitor Generation from Human Pluripotent Stem Cells. - Ann Arbor : ProQuest Dissertations & Theses, 2021 - 133 p.

Source: Dissertations Abstracts International, Volume: 82-12, Section: B.

Thesis (Ph.D.)--University of Pennsylvania, 2021.

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

Tbx3 has been identified as a regulator of fate decisions during liver development in the mouse, but whether it function similarly in humans remains unclear. We generated TBX3 knockout human pluripotent stem cell (PSCs) lines using CRISPR/Cas9 genome editing technology. We differentiated TBX3 knockout lines to hepatocytes and found a decrease in hepatic markers and in hepatocyte function, demonstrating that TBX3 is also important for liver differentiation in humans. Surprisingly, we detected expression of pancreatic markers, including PDX1 in our TBX3 knockout hepatocytes, suggesting the possibility that TBX3 may regulate liver development by suppressing a pancreatic fate. We next differentiated the TBX3 knockout lines to pancreatic progenitors to determine whether the loss of TBX3 impacts pancreatic differentiation. We found that TBX3 knockout PSCs generated more pancreatic progenitors, and that these progenitors had an enhanced pancreatic gene expression signature at the expense of hepatic gene expression. We also found that epithelial-to-mesenchymal transition was commonly dysregulated in TBX3 mutant pancreas and hepatocyte cells. This suggests that TBX3 may function during EMT in both liver and pancreas development. These data highlight a potential role of TBX3 in distinguishing between hepatic and pancreatic domains during foregut patterning, with implications for enhancing the generation of pancreatic progenitors from PSCs.

ISBN: 9798738646560Subjects--Topical Terms:

592588
Developmental biology.
Subjects--Index Terms:

Endoderm patterning

Loss of TBX3 Enhances Pancreatic Progenitor Generation from Human Pluripotent Stem Cells.
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245 1 0 $a Loss of TBX3 Enhances Pancreatic Progenitor Generation from Human Pluripotent Stem Cells.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2021
300 $a 133 p.
500 $a Source: Dissertations Abstracts International, Volume: 82-12, Section: B.
500 $a Advisor: Gadue, Paul J.
502 $a Thesis (Ph.D.)--University of Pennsylvania, 2021.
506 $a This item must not be sold to any third party vendors.
506 $a This item must not be sold to any third party vendors.
520 $a Tbx3 has been identified as a regulator of fate decisions during liver development in the mouse, but whether it function similarly in humans remains unclear. We generated TBX3 knockout human pluripotent stem cell (PSCs) lines using CRISPR/Cas9 genome editing technology. We differentiated TBX3 knockout lines to hepatocytes and found a decrease in hepatic markers and in hepatocyte function, demonstrating that TBX3 is also important for liver differentiation in humans. Surprisingly, we detected expression of pancreatic markers, including PDX1 in our TBX3 knockout hepatocytes, suggesting the possibility that TBX3 may regulate liver development by suppressing a pancreatic fate. We next differentiated the TBX3 knockout lines to pancreatic progenitors to determine whether the loss of TBX3 impacts pancreatic differentiation. We found that TBX3 knockout PSCs generated more pancreatic progenitors, and that these progenitors had an enhanced pancreatic gene expression signature at the expense of hepatic gene expression. We also found that epithelial-to-mesenchymal transition was commonly dysregulated in TBX3 mutant pancreas and hepatocyte cells. This suggests that TBX3 may function during EMT in both liver and pancreas development. These data highlight a potential role of TBX3 in distinguishing between hepatic and pancreatic domains during foregut patterning, with implications for enhancing the generation of pancreatic progenitors from PSCs.
590 $a School code: 0175.
650 4 $a Developmental biology. $3 592588
650 4 $a Cellular biology. $3 3172791
653 $a Endoderm patterning
653 $a Pancreatic progentiors
653 $a Pluripotent stem cells
653 $a TBX3
690 $a 0758
690 $a 0379
710 2 $a University of Pennsylvania. $b Cell and Molecular Biology. $3 2101694
773 0 $t Dissertations Abstracts International $g 82-12B.
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791 $a Ph.D.
792 $a 2021
793 $a English
856 4 0 $u https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28416039