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A molecular and genetic analysis of ...

Stein, Jennifer Ann.

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A molecular and genetic analysis of novel genes controlling Drosophila cellularization and germ cell migration.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	A molecular and genetic analysis of novel genes controlling Drosophila cellularization and germ cell migration./
作者:	Stein, Jennifer Ann.
面頁冊數:	173 p.
附註:	Adviser: Ruth Lehmann.
Contained By:	Dissertation Abstracts International63-08B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3062848
ISBN:	0493809686

A molecular and genetic analysis of novel genes controlling Drosophila cellularization and germ cell migration.
Stein, Jennifer Ann.

A molecular and genetic analysis of novel genes controlling Drosophila cellularization and germ cell migration. - 173 p.

Adviser: Ruth Lehmann.

Thesis (Ph.D.)--New York University, 2002.

Germ cells migrate in a complex but stereotypic path to form the Drosophila gonad. One of the crucial steps in their migration is their transfer off the gut epithelium into the mesoderm to contact somatic gonadal precursors. In a zygotic mutagenesis screen of the second chromosome, two mutants were identified in which germ cells fail to move off the gut into the mesoderm. Both mutants have similar, strong and penetrant germ cell migration defects. Both genes also appear to have the same phenotype as and functionally overlap with <italic> HMG CoA Reductase</italic>, a gene known to be necessary and sufficient for germ cell attraction. These new genes probably act in at least one previously undescribed germ cell migration pathway.

ISBN: 0493809686Subjects--Topical Terms:

1017686
Biology, Cell.

A molecular and genetic analysis of novel genes controlling Drosophila cellularization and germ cell migration.
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245 1 0 $a A molecular and genetic analysis of novel genes controlling Drosophila cellularization and germ cell migration.
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502 $a Thesis (Ph.D.)--New York University, 2002.
520 $a Germ cells migrate in a complex but stereotypic path to form the Drosophila gonad. One of the crucial steps in their migration is their transfer off the gut epithelium into the mesoderm to contact somatic gonadal precursors. In a zygotic mutagenesis screen of the second chromosome, two mutants were identified in which germ cells fail to move off the gut into the mesoderm. Both mutants have similar, strong and penetrant germ cell migration defects. Both genes also appear to have the same phenotype as and functionally overlap with <italic> HMG CoA Reductase</italic>, a gene known to be necessary and sufficient for germ cell attraction. These new genes probably act in at least one previously undescribed germ cell migration pathway.
520 $a We identified the gene affected in one of these mutants as <italic>slam </italic>, and determined that <italic>slam</italic> is not only required for germ cell migration, but is also required in the early blastoderm for cellularization. In the blastoderm, Slam is involved in trafficking membrane bound vesicles to the basal surface of the epithelium. Surprisingly, Slam is expressed during blastoderm stage, but is not expressed when the germ cells are migrating. We believe that Slam deposits a hypothetical germ cell guidance cue on the basal surface of the primordial midgut epithelium which later enables germ cells to move off the gut into the mesoderm. This model would demonstrate a link between patterning of the epithelial cells of the blastoderm and germ cell migration.
520 $a We have also mapped and characterized the other mutant generated in the zygotic mutagenesis screen. This second gene, <italic>9.35</italic>, is defined by a single allele. The germ cell migration phenotype of <italic>9.35</italic> is just as strong as <italic>slam</italic>; however, there are no other developmental defects in <italic>9.35. 9.35</italic> is one of the most specific germ cell migration mutants known, and may even be the hypothetical guidance cue deposited by <italic>slam</italic>. We have narrowed <italic>9.35</italic> down to several promising candidates.
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