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A Role for TORC1 in ER Stress-Induce...

Stauffer Culbertson, Bobbiejane.

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A Role for TORC1 in ER Stress-Induced Vacuolar Fragmentation in Saccharomyces cerevisiae.

Record Type:	Electronic resources : Monograph/item
Title/Author:	A Role for TORC1 in ER Stress-Induced Vacuolar Fragmentation in Saccharomyces cerevisiae./
Author:	Stauffer Culbertson, Bobbiejane.
Description:	140 p.
Notes:	Source: Dissertation Abstracts International, Volume: 77-08(E), Section: B.
Contained By:	Dissertation Abstracts International77-08B(E).
Subject:	Cellular biology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10036109
ISBN:	9781339542843

A Role for TORC1 in ER Stress-Induced Vacuolar Fragmentation in Saccharomyces cerevisiae.
Stauffer Culbertson, Bobbiejane.

A Role for TORC1 in ER Stress-Induced Vacuolar Fragmentation in Saccharomyces cerevisiae. - 140 p.

Source: Dissertation Abstracts International, Volume: 77-08(E), Section: B.

Thesis (Ph.D.)--University of California, Davis, 2015.

The yeast vacuole is known to undergo changes in size and number in response to hyperosmotic shock and changes in the cell cycle, in a process that remains poorly defined. In this work, we demonstrate that chemical or genetic perturbations of ER homeostasis that result in ER stress, or the accumulation of unfolded or misfolded proteins that overwhelms the functional capacity of the ER, initiates vacuolar fragmentation. We find that vacuoles fragment independently of known ER stress signaling pathways, but instead rely on the Target of Rapamycin signaling network (TOR) and its downstream components, Sch9 and Tap42/Sit4. We explore the relationship between ER stress and TORC1, and find evidence that they function in parallel pathways to influence vacuolar morphology. Furthermore, we perform an unbiased, in-vivo , genome-wide visual screen that identifies 315 genes required for efficient vacuolar fragmentation in response to ER stress. We identify known fission factors, validating this approach, as well as novel factors, demonstrating the specificity of this response. Furthermore, we show that ER stress alters distribution of the vacuolar ATPase (V-ATPase) assembly factor, Vph2, in a TORC1-dependent manner. Interestingly, we find that rescue of vacuolar acidification does not restore the defects in vacuolar fragmentation identified in Vph2 mutants, raising the possibility of a different role of the V-ATPase in vacuolar fragmentation.

ISBN: 9781339542843Subjects--Topical Terms:

3172791
Cellular biology.

A Role for TORC1 in ER Stress-Induced Vacuolar Fragmentation in Saccharomyces cerevisiae.
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020 $a 9781339542843
035 $a (MiAaPQ)AAI10036109
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100 1 $a Stauffer Culbertson, Bobbiejane. $3 3194769
245 1 2 $a A Role for TORC1 in ER Stress-Induced Vacuolar Fragmentation in Saccharomyces cerevisiae.
300 $a 140 p.
500 $a Source: Dissertation Abstracts International, Volume: 77-08(E), Section: B.
500 $a Adviser: Ted Powers.
502 $a Thesis (Ph.D.)--University of California, Davis, 2015.
520 $a The yeast vacuole is known to undergo changes in size and number in response to hyperosmotic shock and changes in the cell cycle, in a process that remains poorly defined. In this work, we demonstrate that chemical or genetic perturbations of ER homeostasis that result in ER stress, or the accumulation of unfolded or misfolded proteins that overwhelms the functional capacity of the ER, initiates vacuolar fragmentation. We find that vacuoles fragment independently of known ER stress signaling pathways, but instead rely on the Target of Rapamycin signaling network (TOR) and its downstream components, Sch9 and Tap42/Sit4. We explore the relationship between ER stress and TORC1, and find evidence that they function in parallel pathways to influence vacuolar morphology. Furthermore, we perform an unbiased, in-vivo , genome-wide visual screen that identifies 315 genes required for efficient vacuolar fragmentation in response to ER stress. We identify known fission factors, validating this approach, as well as novel factors, demonstrating the specificity of this response. Furthermore, we show that ER stress alters distribution of the vacuolar ATPase (V-ATPase) assembly factor, Vph2, in a TORC1-dependent manner. Interestingly, we find that rescue of vacuolar acidification does not restore the defects in vacuolar fragmentation identified in Vph2 mutants, raising the possibility of a different role of the V-ATPase in vacuolar fragmentation.
590 $a School code: 0029.
650 4 $a Cellular biology. $3 3172791
650 4 $a Biochemistry. $3 518028
650 4 $a Genetics. $3 530508
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690 $a 0369
710 2 $a University of California, Davis. $b Biochemistry Molecular Cellular and Developmental Biology. $3 3194770
773 0 $t Dissertation Abstracts International $g 77-08B(E).
790 $a 0029
791 $a Ph.D.
792 $a 2015
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10036109