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The brain tumor gene product acts po...
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Gee, Christopher C.
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The brain tumor gene product acts positively on decapentaplegic signaling.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
The brain tumor gene product acts positively on decapentaplegic signaling./
作者:
Gee, Christopher C.
面頁冊數:
127 p.
附註:
Adviser: Allen Shearn.
Contained By:
Dissertation Abstracts International62-10B.
標題:
Biology, Genetics. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3028272
ISBN:
049340323X
The brain tumor gene product acts positively on decapentaplegic signaling.
Gee, Christopher C.
The brain tumor gene product acts positively on decapentaplegic signaling.
- 127 p.
Adviser: Allen Shearn.
Thesis (Ph.D.)--The Johns Hopkins University, 2002.
Mutations in the tumor suppressor gene <italic>brain tumor</italic> (<italic> brat</italic>) act recessively, yield overgrowth of <italic>Drosophila melanogaster </italic> larval brain lobes, and cause late third instar to early pupal lethality (Hankins GR 1991). Though not reported in earlier studies, <italic>brat</italic> heterozygotes exhibit wing vein defects at low frequencies. To gain a greater understanding of the role that the <italic>brat</italic> gene plays in fly development, I undertook a second chromosome deficiency screen using the deficiency kit provided by the Bloomington Stock Center. I scored wing vein defects in adult flies bearing one <italic>brat</italic> mutation and a second chromosome deficiency for evidence of intergenic noncomplementation. Three regions of the second chromosome exhibited intergenic noncomplementation with <italic> brat</italic> causing vein thickening or ectopic vein formation. Surprisingly, intergenic noncomplementation affected females and males differently. Closer examination of one of these regions identified <italic>thickveins</italic> (<italic>tkv</italic>) as a source of intergenic noncomplementation with <italic> brat</italic>. Because <italic>tkv </italic> is a Type I Transforming Growth Factor-β (TGF-β) receptor, these results link <italic>brat</italic> to signal transduction.
ISBN: 049340323XSubjects--Topical Terms:
1017730
Biology, Genetics.
The brain tumor gene product acts positively on decapentaplegic signaling.
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Mutations in the tumor suppressor gene <italic>brain tumor</italic> (<italic> brat</italic>) act recessively, yield overgrowth of <italic>Drosophila melanogaster </italic> larval brain lobes, and cause late third instar to early pupal lethality (Hankins GR 1991). Though not reported in earlier studies, <italic>brat</italic> heterozygotes exhibit wing vein defects at low frequencies. To gain a greater understanding of the role that the <italic>brat</italic> gene plays in fly development, I undertook a second chromosome deficiency screen using the deficiency kit provided by the Bloomington Stock Center. I scored wing vein defects in adult flies bearing one <italic>brat</italic> mutation and a second chromosome deficiency for evidence of intergenic noncomplementation. Three regions of the second chromosome exhibited intergenic noncomplementation with <italic> brat</italic> causing vein thickening or ectopic vein formation. Surprisingly, intergenic noncomplementation affected females and males differently. Closer examination of one of these regions identified <italic>thickveins</italic> (<italic>tkv</italic>) as a source of intergenic noncomplementation with <italic> brat</italic>. Because <italic>tkv </italic> is a Type I Transforming Growth Factor-β (TGF-β) receptor, these results link <italic>brat</italic> to signal transduction.
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<italic>decapentaplegic</italic> (<italic>dpp</italic>), a gene important to <italic>D. melanogaster</italic> development and a member of the TGF-β superfamily, regulates transcription of several genes in the wing imaginal disc. Reduced accumulation of proteins encoded by these genes in <italic> brat</italic> mutant larval tissues connects <italic>brat</italic> more specifically to <italic>dpp</italic> signaling. Because providing only a single copy of functional <italic>brat</italic> failed to suppress a phenotype caused by ectopic expression of a constitutively active TKV, <italic>brat</italic> appears to act upstream of the receptor in the <italic>dpp</italic> signaling pathway. I argue that these results implicate <italic>brat</italic> in TKV-DPP interactions. In this way, <italic>brain tumor</italic> acts as a positive regulator of <italic> dpp</italic> signaling.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3028272
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