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egl-32 acts through sperm to regulat...
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McGovern, Marie.
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egl-32 acts through sperm to regulate egg-laying in Caenorhabditis elegans.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
egl-32 acts through sperm to regulate egg-laying in Caenorhabditis elegans./
作者:
McGovern, Marie.
面頁冊數:
110 p.
附註:
Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0101.
Contained By:
Dissertation Abstracts International67-01B.
標題:
Biology, Molecular. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3205006
ISBN:
9780542510533
egl-32 acts through sperm to regulate egg-laying in Caenorhabditis elegans.
McGovern, Marie.
egl-32 acts through sperm to regulate egg-laying in Caenorhabditis elegans.
- 110 p.
Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0101.
Thesis (Ph.D.)--City University of New York, 2006.
A study of the egg-laying defective mutant, egl-32, in Caenorhabditis elegans has revealed that sperm have an active role in regulating egg-laying. Initially, our lab became interested in studying egl-32 because we believed it interacted directly with a TGF-beta pathway that regulates dauer development. In studying this mutant we hoped we would gain a better understanding of the role of the TGF-beta dauer pathway in egg-laying. We now believe that egl-32 and the TGF-beta pathway only interact indirectly. However, studying the egg-laying defective mutant, egl-32, has lead to the novel finding that sperm have an influence on egg-laying. In an attempt to determine the cellular and anatomical basis for the egl-32's egg laying defect it was found that egl-32 interacts with genes highly expressed in sperm. Here I present evidence that the cellular basis of the egl-32's egg-laying defective phenotype is due to a defect in sperm. I have investigated the possibility that sperm are playing an active role in egg-laying by performing simple mating experiments. These mating experiments have revealed the wild-type sperm can rescue the egg-laying defect of egl-32 mutant animals. Also, introduction of mutant egl-32 sperm into wild-type animals can induce an egg-laying defective phenotype. In an effort to determine the exact location of egl-32 a candidate gene, smn-1 was uncovered. A knockout of smn-1 was obtained and characterized. The knockout is homozygous lethal. Heterozygous animals are egg-laying defective and respond similarly to egl-32 in mating experiments. smn-1 was also determined to interact with the same sperm proteins as egl-32.
ISBN: 9780542510533Subjects--Topical Terms:
1017719
Biology, Molecular.
egl-32 acts through sperm to regulate egg-laying in Caenorhabditis elegans.
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A study of the egg-laying defective mutant, egl-32, in Caenorhabditis elegans has revealed that sperm have an active role in regulating egg-laying. Initially, our lab became interested in studying egl-32 because we believed it interacted directly with a TGF-beta pathway that regulates dauer development. In studying this mutant we hoped we would gain a better understanding of the role of the TGF-beta dauer pathway in egg-laying. We now believe that egl-32 and the TGF-beta pathway only interact indirectly. However, studying the egg-laying defective mutant, egl-32, has lead to the novel finding that sperm have an influence on egg-laying. In an attempt to determine the cellular and anatomical basis for the egl-32's egg laying defect it was found that egl-32 interacts with genes highly expressed in sperm. Here I present evidence that the cellular basis of the egl-32's egg-laying defective phenotype is due to a defect in sperm. I have investigated the possibility that sperm are playing an active role in egg-laying by performing simple mating experiments. These mating experiments have revealed the wild-type sperm can rescue the egg-laying defect of egl-32 mutant animals. Also, introduction of mutant egl-32 sperm into wild-type animals can induce an egg-laying defective phenotype. In an effort to determine the exact location of egl-32 a candidate gene, smn-1 was uncovered. A knockout of smn-1 was obtained and characterized. The knockout is homozygous lethal. Heterozygous animals are egg-laying defective and respond similarly to egl-32 in mating experiments. smn-1 was also determined to interact with the same sperm proteins as egl-32.
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