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Elucidating pathways that modulate n...

Dybbs, Michael Philip.

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Elucidating pathways that modulate neurotransmission in Caenorhabditis elegans through genetics, RNA interference and computational approaches .

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Elucidating pathways that modulate neurotransmission in Caenorhabditis elegans through genetics, RNA interference and computational approaches ./
作者:	Dybbs, Michael Philip.
面頁冊數:	139 p.
附註:	Source: Dissertation Abstracts International, Volume: 66-08, Section: B, page: 4072.
Contained By:	Dissertation Abstracts International66-08B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3187026
ISBN:	9780542293481

Elucidating pathways that modulate neurotransmission in Caenorhabditis elegans through genetics, RNA interference and computational approaches .
Dybbs, Michael Philip.

Elucidating pathways that modulate neurotransmission in Caenorhabditis elegans through genetics, RNA interference and computational approaches . - 139 p.

Source: Dissertation Abstracts International, Volume: 66-08, Section: B, page: 4072.

Thesis (Ph.D.)--University of California, Berkeley, 2005.

Synaptic transmission serves as the primary mode of communication within the nervous system. This complex cellular process involves a large cast of proteins and is regulated via multiple pathways. Using the C. elegans neuromuscular junction as a model system, we employed genetic, genomic and computational approaches to identify novel genes and characterize their involvement in neurotransmitter release.

ISBN: 9780542293481Subjects--Topical Terms:

1017734
Biology, Microbiology.

Elucidating pathways that modulate neurotransmission in Caenorhabditis elegans through genetics, RNA interference and computational approaches .
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245 1 0 $a Elucidating pathways that modulate neurotransmission in Caenorhabditis elegans through genetics, RNA interference and computational approaches .
300 $a 139 p.
500 $a Source: Dissertation Abstracts International, Volume: 66-08, Section: B, page: 4072.
500 $a Chairs: Joshua Kaplan; John Ngai.
502 $a Thesis (Ph.D.)--University of California, Berkeley, 2005.
520 $a Synaptic transmission serves as the primary mode of communication within the nervous system. This complex cellular process involves a large cast of proteins and is regulated via multiple pathways. Using the C. elegans neuromuscular junction as a model system, we employed genetic, genomic and computational approaches to identify novel genes and characterize their involvement in neurotransmitter release.
520 $a Traditionally, the cloning and molecular characterization of mutants recovered in genetic screens has represented a significant bottleneck in gene discovery. This problem is particularly acute for neuronal phenotypes which are often subtle or must be assayed in populations of animals. We therefore developed a strategy using microarray hybridizations to facilitate positional cloning. This method relies on the fact that premature stop codons (i.e. nonsense mutations) constitute a frequent class of mutations isolated in screens and that nonsense mutant messenger RNAs are efficiently degraded by the conserved nonsense-mediated decay pathway. We validated this approach by identifying two previously uncharacterized mutations in C. elegans and applying it retrospectively to known mutants in C. elegans, Arabidopsis and mouse. Our results suggest that microarray hybridizations have the potential to significantly reduce the time and effort required for positional cloning.
520 $a Using microarray-based cloning, we identified tom-1, a mutation found in a forward genetic screen for enhanced acetylcholine secretion in C. elegans. Our characterization of tom-1 mutants suggests that TOM-1, the C. elegans ortholog of mammalian tomosyn, functions as an endogenous inhibitor of neurotransmitter release. Additionally, we uncovered a surprising connection between tomosyn and UNC-13/Munc13, an essential regulator of synaptic transmission. Our results, using both behavioral assays and in vivo measurements of synaptobrevin distribution suggest that the balance between UNC-13/Munc13 activation and tomosyn inhibition determines the availability of syntaxin and thus regulates neurotransmitter release.
520 $a Finally, we conducted systematic RNAi screens to identify genes required for the function and development of the C. elegans neuromuscular junction. These screens identified 185 genes that decreased acetylcholine secretion and 80 genes which potentiated cholinergic signaling. We constructed functional profiles for genes that decreased acetylcholine release by comparing secretion defects observed following RNAi under a variety of conditions. Hierarchical clustering of these profiles identified groups of functionally related genes, including those involved in the synaptic vesicle cycle, neuropeptide signaling, and responsiveness to phorbol esters. Additionally, we showed twenty-four of these genes encoded proteins that localized to presynaptic specializations.
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773 0 $t Dissertation Abstracts International $g 66-08B.
790 1 0 $a Kaplan, Joshua, $e advisor
790 1 0 $a Ngai, John, $e advisor
790 $a 0028
791 $a Ph.D.
792 $a 2005
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