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Mechanisms of Cell Cycle Control.

Asfaha, Jonathan.

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Mechanisms of Cell Cycle Control.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Mechanisms of Cell Cycle Control./
作者:	Asfaha, Jonathan.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2021,
面頁冊數:	55 p.
附註:	Source: Dissertations Abstracts International, Volume: 82-10, Section: B.
Contained By:	Dissertations Abstracts International82-10B.
標題:	Cellular biology. -
電子資源:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28320705
ISBN:	9798708727725

Mechanisms of Cell Cycle Control.
Asfaha, Jonathan.

Mechanisms of Cell Cycle Control. - Ann Arbor : ProQuest Dissertations & Theses, 2021 - 55 p.

Source: Dissertations Abstracts International, Volume: 82-10, Section: B.

Thesis (Ph.D.)--University of California, San Francisco, 2021.

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

Ordered phosphorylation of cyclin-dependent kinase (CDK) substrates leads to the sequential transcriptional activation and inhibition of hundreds of cell cycle-regulated genes. We find that Ndd1, an activator of genes required for mitotic progression, is both positively and negatively regulated by CDK activity. CDK activity initially stimulates Ndd1-dependent transcription as cells enter mitosis, but prolonged high CDK activity in a mitotic arrest inhibits transcription. The result is a time-delayed negative feedback circuit that generates a pulse of mitotic gene expression. Our results suggest that high CDK activity catalyzes the formation of multiple weak phosphodegrons on Ndd1, leading to its destabilization. Cyclin specificity and phosphorylation kinetics contribute to the timing of Ndd1 destruction. Failure to degrade Ndd1 in a mitotic arrest leads to elevated mitotic gene expression. We conclude that a combination of positive and negative Ndd1 regulation by CDKs governs the timing and magnitude of the mitotic transcriptional program.

ISBN: 9798708727725Subjects--Topical Terms:

3172791
Cellular biology.
Subjects--Index Terms:

Cell division

Mechanisms of Cell Cycle Control.
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300 $a 55 p.
500 $a Source: Dissertations Abstracts International, Volume: 82-10, Section: B.
500 $a Advisor: Morgan, David O.
502 $a Thesis (Ph.D.)--University of California, San Francisco, 2021.
506 $a This item must not be sold to any third party vendors.
520 $a Ordered phosphorylation of cyclin-dependent kinase (CDK) substrates leads to the sequential transcriptional activation and inhibition of hundreds of cell cycle-regulated genes. We find that Ndd1, an activator of genes required for mitotic progression, is both positively and negatively regulated by CDK activity. CDK activity initially stimulates Ndd1-dependent transcription as cells enter mitosis, but prolonged high CDK activity in a mitotic arrest inhibits transcription. The result is a time-delayed negative feedback circuit that generates a pulse of mitotic gene expression. Our results suggest that high CDK activity catalyzes the formation of multiple weak phosphodegrons on Ndd1, leading to its destabilization. Cyclin specificity and phosphorylation kinetics contribute to the timing of Ndd1 destruction. Failure to degrade Ndd1 in a mitotic arrest leads to elevated mitotic gene expression. We conclude that a combination of positive and negative Ndd1 regulation by CDKs governs the timing and magnitude of the mitotic transcriptional program.
590 $a School code: 0034.
650 4 $a Cellular biology. $3 3172791
650 4 $a Molecular biology. $3 517296
650 4 $a Biochemistry. $3 518028
653 $a Cell division
653 $a Cyclin Dependent Kinase
653 $a Cyclins
653 $a Multisite phosphorylation
653 $a Phosphodegrons
653 $a Protein degradation
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690 $a 0487
690 $a 0307
710 2 $a University of California, San Francisco. $b Biochemistry and Molecular Biology. $3 1263088
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793 $a English
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