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

Regulatory genes involved in Cauloba...

Hung, Dean Yuin.

FindBook

Google Book

Amazon

博客來

Regulatory genes involved in Caulobacter cell cycle progression.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Regulatory genes involved in Caulobacter cell cycle progression./
作者:	Hung, Dean Yuin.
面頁冊數:	141 p.
附註:	Adviser: Lucy Shapiro.
Contained By:	Dissertation Abstracts International64-03B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3085302

Regulatory genes involved in Caulobacter cell cycle progression.
Hung, Dean Yuin.

Regulatory genes involved in Caulobacter cell cycle progression. - 141 p.

Adviser: Lucy Shapiro.

Thesis (Ph.D.)--Stanford University, 2003.

Regulation of cell cycle progression is a complex process in which a cell must analyze information about internal and external conditions, and make decisions on how to respond. <italic>Caulobacter crescentus</italic> possesses a network of signal transduction molecules that regulate its cell cycle. One central cell cycle protein is the global regulator, CtrA, a transcription factor that is activated by phosphorylation and targets numerous downstream genes. My interest in the signal transduction network regulating the <italic> Caulobacter</italic> cell cycle led me to investigate whether CtrA is present in other species, described in Chapter 2.Subjects--Topical Terms:

1017734
Biology, Microbiology.

Regulatory genes involved in Caulobacter cell cycle progression.
LDR:03365nam 2200289 a 45 001 929782
005 20110427
008 110427s2003 eng d
035 $a (UnM)AAI3085302
035 $a AAI3085302
040 $a UnM $c UnM
100 1 $a Hung, Dean Yuin. $3 1253268
245 1 0 $a Regulatory genes involved in Caulobacter cell cycle progression.
300 $a 141 p.
500 $a Adviser: Lucy Shapiro.
500 $a Source: Dissertation Abstracts International, Volume: 64-03, Section: B, page: 1078.
502 $a Thesis (Ph.D.)--Stanford University, 2003.
520 $a Regulation of cell cycle progression is a complex process in which a cell must analyze information about internal and external conditions, and make decisions on how to respond. <italic>Caulobacter crescentus</italic> possesses a network of signal transduction molecules that regulate its cell cycle. One central cell cycle protein is the global regulator, CtrA, a transcription factor that is activated by phosphorylation and targets numerous downstream genes. My interest in the signal transduction network regulating the <italic> Caulobacter</italic> cell cycle led me to investigate whether CtrA is present in other species, described in Chapter 2.
520 $a Chapter 3 discusses my work to identify new cell cycle regulators, and describes the cloning, and characterization of a novel gene, <italic>divT </italic>. The <italic>divT</italic> mutant exhibits a strong cell division phenotype. DivT is not a two-component system protein, and shows no homology to known proteins, but homologs are present in other α-proteobacteria. DivT has a cell cycle pattern of protein expression, and is regulated transcriptionally by CtrA.
520 $a DivK is an essential single-domain response regulator. Previous work identified and cloned <italic>divK</italic>, but elucidation of its role in <italic> Caulobacter</italic> cell cycle regulation remained an unanswered question. The main part of my thesis work was to identify DivK's role in <italic>Caulobacter </italic>. Chapter 4 presents work showing that DivK is present and phosphorylated throughout the cell cycle and exhibits a cell cycle-dependent pattern of protein localization. Chapter 5 describes experiments showing that DivK regulates proteolytic events critical to cell cycle progression. A <italic>divK-cs</italic> mutant displays phenotypes characteristic of a G1-arrest induced by the presence of active CtrA in the stalked cell. The CtrA protein is stable in a <italic> divK-cs</italic> mutant at the restrictive temperature, and upon shift to the permissive temperature, CtrA is rapidly degraded. The mutant phenotypes observed in <italic>divK-cs</italic> are not due to a defect in phosphorylation, and microarray analysis shows that the normal order of gene expression resumes after release from G1-arrest. The <italic>divK</italic> promoter contains a strong CtrA consensus binding motif where purified CtrA binds. Thus DivK cues the proteolysis of the global regulator, CtrA, allowing cell cycle progression to continue, and is itself regulated by CtrA.
590 $a School code: 0212.
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Biology, Molecular. $3 1017719
690 $a 0307
690 $a 0410
710 2 0 $a Stanford University. $3 754827
773 0 $t Dissertation Abstracts International $g 64-03B.
790 $a 0212
790 1 0 $a Shapiro, Lucy, $e advisor
791 $a Ph.D.
792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3085302