東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Integration of EGFR and LIN-12/Notch...

Underwood, Ryan.

FindBook

Google Book

Amazon

博客來

Integration of EGFR and LIN-12/Notch Signaling in Vulval Precursor Cell fate Specification in Caenorhabditis elegans.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Integration of EGFR and LIN-12/Notch Signaling in Vulval Precursor Cell fate Specification in Caenorhabditis elegans./
作者:	Underwood, Ryan.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
面頁冊數:	158 p.
附註:	Source: Dissertations Abstracts International, Volume: 79-10, Section: B.
Contained By:	Dissertations Abstracts International79-10B.
標題:	Biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10749185
ISBN:	9780355828030

Integration of EGFR and LIN-12/Notch Signaling in Vulval Precursor Cell fate Specification in Caenorhabditis elegans.
Underwood, Ryan.

Integration of EGFR and LIN-12/Notch Signaling in Vulval Precursor Cell fate Specification in Caenorhabditis elegans. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 158 p.

Source: Dissertations Abstracts International, Volume: 79-10, Section: B.

Thesis (Ph.D.)--Columbia University, 2018.

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

Cellular differentiation is the cornerstone of metazoan development. Cell-cell signaling mechanisms are responsible for the specification of many cell fates. The response of a particular cell to a given signal is highly context dependent allowing signaling mechanisms to be reused to produce a variety of different outcomes. The EGFR and LIN-12/Notch signaling pathways are well-conserved across metazoan species and govern many fate-specification events. The specification of C. elegans Vulval Precursor Cells (VPCs) offers a powerful system to investigate how these signaling mechanisms specify cell-fates, and previous studies of VPC fate patterning have identified several forms of crosstalk between these two critical signaling mechanisms. In this thesis, I investigate how input from both the EGFR and LIN-12/Notch signaling pathways is integrated by the VPCs. I provide evidence that VPCs respond to the relative levels of LIN-12/Notch and EGFR signaling. I show that LIN-1/Elk1 is critical for VPCs to adopt discrete cell fates. In addition, I show that the Mediator components SUR-2/Med23 and the CDK-8 kinase module (CKM), in cooperation with LIN-1/Elk1, are required for an EGFR-mediated resistance to LIN-12/Notch activity. I also used CRISPR/Cas9 techniques to generate endogenous, fluorescently-tagged LAG-1 proteins. Characterization of tagged LAG-1 accumulation in the VPCs and in the somatic gonad show that LAG-1 is present in all VPCs at low levels in a lin-12/Notch independent manner. Activation of LIN-12/Notch is correlated with higher levels of LAG-1 accumulation compared to cells that do not have activated LIN-12/Notch. These findings suggest a potential autoregulation mechanism for lag-1 in certain contexts. They also suggest that endogenously tagged LAG-1 may be a useful molecular marker of LIN-12/Notch activation.

ISBN: 9780355828030Subjects--Topical Terms:

522710
Biology.
Subjects--Index Terms:

C. elegans

Integration of EGFR and LIN-12/Notch Signaling in Vulval Precursor Cell fate Specification in Caenorhabditis elegans.
LDR:03129nmm a2200409 4500 001 2272173
005 20201105105952.5
008 220629s2018 ||||||||||||||||| ||eng d
020 $a 9780355828030
035 $a (MiAaPQ)AAI10749185
035 $a (MiAaPQ)columbia:14487
035 $a AAI10749185
040 $a MiAaPQ $c MiAaPQ
100 1 $a Underwood, Ryan. $3 3549602
245 1 0 $a Integration of EGFR and LIN-12/Notch Signaling in Vulval Precursor Cell fate Specification in Caenorhabditis elegans.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2018
300 $a 158 p.
500 $a Source: Dissertations Abstracts International, Volume: 79-10, Section: B.
500 $a Publisher info.: Dissertation/Thesis.
500 $a Advisor: Greenwald, Iva.
502 $a Thesis (Ph.D.)--Columbia University, 2018.
506 $a This item must not be sold to any third party vendors.
520 $a Cellular differentiation is the cornerstone of metazoan development. Cell-cell signaling mechanisms are responsible for the specification of many cell fates. The response of a particular cell to a given signal is highly context dependent allowing signaling mechanisms to be reused to produce a variety of different outcomes. The EGFR and LIN-12/Notch signaling pathways are well-conserved across metazoan species and govern many fate-specification events. The specification of C. elegans Vulval Precursor Cells (VPCs) offers a powerful system to investigate how these signaling mechanisms specify cell-fates, and previous studies of VPC fate patterning have identified several forms of crosstalk between these two critical signaling mechanisms. In this thesis, I investigate how input from both the EGFR and LIN-12/Notch signaling pathways is integrated by the VPCs. I provide evidence that VPCs respond to the relative levels of LIN-12/Notch and EGFR signaling. I show that LIN-1/Elk1 is critical for VPCs to adopt discrete cell fates. In addition, I show that the Mediator components SUR-2/Med23 and the CDK-8 kinase module (CKM), in cooperation with LIN-1/Elk1, are required for an EGFR-mediated resistance to LIN-12/Notch activity. I also used CRISPR/Cas9 techniques to generate endogenous, fluorescently-tagged LAG-1 proteins. Characterization of tagged LAG-1 accumulation in the VPCs and in the somatic gonad show that LAG-1 is present in all VPCs at low levels in a lin-12/Notch independent manner. Activation of LIN-12/Notch is correlated with higher levels of LAG-1 accumulation compared to cells that do not have activated LIN-12/Notch. These findings suggest a potential autoregulation mechanism for lag-1 in certain contexts. They also suggest that endogenously tagged LAG-1 may be a useful molecular marker of LIN-12/Notch activation.
590 $a School code: 0054.
650 4 $a Biology. $3 522710
650 4 $a Genetics. $3 530508
650 4 $a Developmental biology. $3 592588
653 $a C. elegans
653 $a EGF receptor
653 $a LAG-1
653 $a Mediator
653 $a Notch
653 $a Vulva
690 $a 0306
690 $a 0369
690 $a 0758
710 2 $a Columbia University. $b Biochemistry and Molecular Biophysics. $3 3276398
773 0 $t Dissertations Abstracts International $g 79-10B.
790 $a 0054
791 $a Ph.D.
792 $a 2018
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10749185