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Genetic and cellular analysis of the...
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Bany, Irene Amelia.
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Genetic and cellular analysis of the inhibition of egg laying in Caenorhabditis elegans.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Genetic and cellular analysis of the inhibition of egg laying in Caenorhabditis elegans./
作者:
Bany, Irene Amelia.
面頁冊數:
171 p.
附註:
Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1106.
Contained By:
Dissertation Abstracts International65-03B.
標題:
Biology, Cell. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3125154
ISBN:
049672444X
Genetic and cellular analysis of the inhibition of egg laying in Caenorhabditis elegans.
Bany, Irene Amelia.
Genetic and cellular analysis of the inhibition of egg laying in Caenorhabditis elegans.
- 171 p.
Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1106.
Thesis (Ph.D.)--Yale University, 2004.
Egg-laying behavior in Caenorhabditis elegans is activated by signaling through the G protein Galphaq and inhibited by signaling through a second G protein, Galphao. Activation of egg laying depends on the serotonergic HSN neurons, but the neurotransmitter(s) and cell(s) that signal to inhibit egg laying are not known. Mutants for G protein signaling genes have well-characterized defects in egg laying. Here I present an analysis of hyperactive egg-laying mutants.
ISBN: 049672444XSubjects--Topical Terms:
1017686
Biology, Cell.
Genetic and cellular analysis of the inhibition of egg laying in Caenorhabditis elegans.
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Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1106.
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Egg-laying behavior in Caenorhabditis elegans is activated by signaling through the G protein Galphaq and inhibited by signaling through a second G protein, Galphao. Activation of egg laying depends on the serotonergic HSN neurons, but the neurotransmitter(s) and cell(s) that signal to inhibit egg laying are not known. Mutants for G protein signaling genes have well-characterized defects in egg laying. Here I present an analysis of hyperactive egg-laying mutants.
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I analyzed a panel of previously characterized uncoordinated (Unc) mutants for defects in the inhibition of egg laying. Of the nine strongest hyperactive egg-laying mutants, six have morphological defects in the VC neurons, which synapse onto both the HSNs and the egg-laying muscles and are thus the third cell type comprising the egg-laying system. Laser-ablating VC neurons could also disrupt the inhibition of egg laying. The remaining three mutants ( unc-4, cha-1, unc-17) are defective for synthesis and/or packaging of acetylcholine in the VCs. The egg-laying defects of unc-4, cha-1 , and unc-17 were rescued by VC-specific expression of the corresponding cDNAs. In addition, increasing synaptic acetylcholine by reducing acetylcholinesterase activity, either with mutations or the inhibitor aldicarb, decreased egg laying. Finally, we found that a knockout for the HSN-expressed receptor GAR-2 (G&barbelow; protein coupled a&barbelow;cetylcholine r&barbelow;eceptor 2) shows a partial defect in the inhibition of egg laying and fails to respond to aldicarb. Our results show that acetylcholine released from the VC neurons inhibits egg-laying behavior. This inhibition may be due, in part, to acetylcholine signaling onto the HSN presynaptic termini, via GAR-2, to inhibit neurotransmitter release.
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I screened 39,000 mutagenized haploid C. elegans genomes for hyperactive egg-laying mutants that might represent new components of the signaling pathway that inhibits egg laying. Seventeen mutants were strong enough to pursue, and represent mutations in two known G protein signaling genes, two previously characterized genes not known to regulate egg laying, and ten genes that remain to be identified. Studying the genes identified by these mutations should help us gain a more complete cellular and molecular understanding of how neurotransmitters, acting through G proteins, regulate behavior.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3125154
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