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The role of myb in regulating the ce...

Fung, Siau Min.

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The role of myb in regulating the cell cycle during Drosophila development.

Record Type:	Electronic resources : Monograph/item
Title/Author:	The role of myb in regulating the cell cycle during Drosophila development./
Author:	Fung, Siau Min.
Description:	222 p.
Notes:	Source: Dissertation Abstracts International, Volume: 64-03, Section: B, page: 1066.
Contained By:	Dissertation Abstracts International64-03B.
Subject:	Biology, Genetics. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3083942

The role of myb in regulating the cell cycle during Drosophila development.
Fung, Siau Min.

The role of myb in regulating the cell cycle during Drosophila development. - 222 p.

Source: Dissertation Abstracts International, Volume: 64-03, Section: B, page: 1066.

Thesis (Ph.D.)--University of Illinois at Chicago, Health Sciences Center, 2003.

The proto-oncogene <italic>myb</italic> has been implicated in human leukemias, breast cancer and colon carcinoma. In Dr. Katzen's lab, we use the <italic>Drosophila</italic> model system to study <italic>Drosophila myb </italic> (<italic>Dm myb</italic>) function and its regulation during cell cycle progression. <italic>Dm myb</italic> encodes a transcription factor that has been shown to be involved in the regulation of cell proliferation. We were therefore interested in looking for genetic interactions between <italic> Dm myb</italic> and other known cell cycle regulators. We performed a genetic screen in which we tested whether reduced levels of each “cell cycle gene” within a mutant <italic>myb</italic> background modified the <italic> myb</italic> phenotype. From the modifier screen, we were able to show genetic interactions between <italic>Dm myb</italic> and four cell cycle regulators: <italic> string</italic> (<italic>cdc25</italic> phosphatase), <italic>cyclin A, rux </italic> and <italic>cyclin E</italic>. The genetic interaction between <italic> cyclin A</italic> and <italic>myb</italic> appeared to be especially strong, with reduced levels of <italic>cyclin A</italic> enhancing all aspects of the mutant <italic>Dm myb</italic> phenotypes.Subjects--Topical Terms:

1017730
Biology, Genetics.

The role of myb in regulating the cell cycle during Drosophila development.
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100 1 $a Fung, Siau Min. $3 1943013
245 1 0 $a The role of myb in regulating the cell cycle during Drosophila development.
300 $a 222 p.
500 $a Source: Dissertation Abstracts International, Volume: 64-03, Section: B, page: 1066.
500 $a Adviser: Alisa Katzen.
502 $a Thesis (Ph.D.)--University of Illinois at Chicago, Health Sciences Center, 2003.
520 $a The proto-oncogene <italic>myb</italic> has been implicated in human leukemias, breast cancer and colon carcinoma. In Dr. Katzen's lab, we use the <italic>Drosophila</italic> model system to study <italic>Drosophila myb </italic> (<italic>Dm myb</italic>) function and its regulation during cell cycle progression. <italic>Dm myb</italic> encodes a transcription factor that has been shown to be involved in the regulation of cell proliferation. We were therefore interested in looking for genetic interactions between <italic> Dm myb</italic> and other known cell cycle regulators. We performed a genetic screen in which we tested whether reduced levels of each “cell cycle gene” within a mutant <italic>myb</italic> background modified the <italic> myb</italic> phenotype. From the modifier screen, we were able to show genetic interactions between <italic>Dm myb</italic> and four cell cycle regulators: <italic> string</italic> (<italic>cdc25</italic> phosphatase), <italic>cyclin A, rux </italic> and <italic>cyclin E</italic>. The genetic interaction between <italic> cyclin A</italic> and <italic>myb</italic> appeared to be especially strong, with reduced levels of <italic>cyclin A</italic> enhancing all aspects of the mutant <italic>Dm myb</italic> phenotypes.
520 $a The enhancement of the mutant <italic>myb</italic> phenotype caused by reduced levels of <italic>cyclin A</italic> was most dramatic in the abdomen. Since this aspect of the mutant <italic>myb</italic> phenotype had never been studied in detail, we investigated the cellular basis of the abdominal cuticular defects observed in <italic>Dm myb</italic> mutants. As the data in this thesis demonstrate, <italic>Dm myb</italic> is required to sustain the appropriate rate of proliferation, to suppress formation of supernumerary centrosomes, and to maintain genomic integrity.
520 $a Reduction of <italic>cyclin A</italic> levels in a mutant <italic>myb </italic> background results in slower proliferation and failure to replace larval polyploid cells. Mitotic progression through pre-prophase and anaphase is sluggish, and frequent mitotic defects are observed in anaphase. These findings correlate with the increased occurrence of multilobed and multinucleated cells m both wings and abdomens. At the molecular level, we have shown that <italic> cyclin A</italic> transcription is not regulated by the DMyb protein and we have been unable to detect a physical interaction between Cyclin A and DMyb. We are testing the hypothesis that DMyb is subject to activating phosphorylation(s) by CyclinA/Cdk1 complex.
590 $a School code: 0806.
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Biology, Cell. $3 1017686
650 4 $a Biology, Molecular. $3 1017719
690 $a 0369
690 $a 0379
690 $a 0307
710 2 0 $a University of Illinois at Chicago, Health Sciences Center. $3 1021703
773 0 $t Dissertation Abstracts International $g 64-03B.
790 1 0 $a Katzen, Alisa, $e advisor
790 $a 0806
791 $a Ph.D.
792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3083942