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Regulation of apoptosis in the Caeno...

Nehme, Ralda.

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Regulation of apoptosis in the Caenorhabditis elegans nervous system.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Regulation of apoptosis in the Caenorhabditis elegans nervous system./
作者:	Nehme, Ralda.
面頁冊數:	161 p.
附註:	Source: Dissertation Abstracts International, Volume: 71-05, Section: B, page: 2807.
Contained By:	Dissertation Abstracts International71-05B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3398937
ISBN:	9781109733846

Regulation of apoptosis in the Caenorhabditis elegans nervous system.
Nehme, Ralda.

Regulation of apoptosis in the Caenorhabditis elegans nervous system. - 161 p.

Source: Dissertation Abstracts International, Volume: 71-05, Section: B, page: 2807.

Thesis (Ph.D.)--Dartmouth College, 2010.

Most of the cells that die during the development of a C. elegans hermaphrodite do so within 30 min after being generated. In these cells, the pro-caspase proCED-3 is inherited from progenitors and the transcriptional upregulation of the BH3-only gene egl-1 is thought to be sufficient for apoptosis induction. For instance, the NSM sister cells die &sim;20 min after being generated, while their sisters, the NSMs, survive and differentiate into serotonergic neurons. Using forward and reverse genetic approaches, I characterized factors previously not implicated in the NSM sister cell death that regulate egl-1 activity to specify the cell-death fate of the NSM sister cells.

ISBN: 9781109733846Subjects--Topical Terms:

1017730
Biology, Genetics.

Regulation of apoptosis in the Caenorhabditis elegans nervous system.
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245 1 0 $a Regulation of apoptosis in the Caenorhabditis elegans nervous system.
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500 $a Source: Dissertation Abstracts International, Volume: 71-05, Section: B, page: 2807.
500 $a Adviser: Barbara Conradt.
502 $a Thesis (Ph.D.)--Dartmouth College, 2010.
520 $a Most of the cells that die during the development of a C. elegans hermaphrodite do so within 30 min after being generated. In these cells, the pro-caspase proCED-3 is inherited from progenitors and the transcriptional upregulation of the BH3-only gene egl-1 is thought to be sufficient for apoptosis induction. For instance, the NSM sister cells die &sim;20 min after being generated, while their sisters, the NSMs, survive and differentiate into serotonergic neurons. Using forward and reverse genetic approaches, I characterized factors previously not implicated in the NSM sister cell death that regulate egl-1 activity to specify the cell-death fate of the NSM sister cells.
520 $a A few cells that die during C. elegans development, however, survive for more than 30 min before they die. For example, the four CEM neurons die only &sim;150 min after being generated. Furthermore, the CEMs die in hermaphrodites but not males or masculinized hermaphrodites. I found that in the CEMs, the transcriptional activation of both the egl-1 and ced-3 gene is necessary for apoptosis induction. In addition, the Bar homeodomain transcription factor CEH-30 represses egl-1 and ced-3 transcription in the CEMs, thereby causing their survival. I also identified three genes, unc-86, lrs-1 and unc-132, which encode a POU homeodomain transcription factor, a leucyl-tRNA synthetase and a protein with similarity to the mammalian proto-oncoprotein PIM-1, respectively, that promote the expression of the ceh-30 gene in the CEMs. I propose that egl-1 and ced-3 transcription are co-regulated in the CEMs to compensate for limiting proCED-3 levels, caused by proCED-3 turn over. Finally, I present evidence that the life-versus-death decision of the CEMs is also affected by cell migration and cell attachment. Specifically, the inactivation of genes encoding components of the focal adhesion complex results in the inappropriate death of the CEMs in masculinized hermaphrodites, and in the repression of ceh-30 expression. This provides the first evidence that cell non-autonomous, extra-cellular signals control the apoptotic death of neurons in C. elegans.
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790 1 0 $a Saito, Richard $e committee member
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