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The molecular mechanism of programmed cell death in C. elegans

Liu, Q A; Hengartner, M O (1999). The molecular mechanism of programmed cell death in C. elegans. Annals of the New York Academy of Sciences, 887:92-104.

Abstract

Programmed cell death or apoptosis plays a fundamental role during animal development, metamorphosis, and tissue homeostasis. It is a genetically controlled physiological process that comprises two distinct and sequential processes: the death of cells, and their subsequent removal by engulfing cells. In the nematode C. elegans, genetic studies led to the discovery of 15 genes that function in programmed cell death (FIG. 1). These 15 genes have been divided into four groups based on the order of their activity during the process of programmed cell death: (1) those involved in the decision making (ces-1 and ces-2); (2) in the process of execution (ced-3, ced-4, ced-9 and egl-1); (3) in the engulfment of dying cells by engulfing cells (ced-1, ced-2, ced-5, ced-6, ced-7, ced-10, ced-12); and (4) those in the degradation of cell corpses within engulfing cells (nuc-1). In the last five years, several genes in the genetic pathway of programmed cell death have been shown to be conserved across a wide range of species; all genes involved in the step of execution in C. elegans have their corresponding mammalian homologs (FIG. 2). Furthermore, emerging evidence from molecular studies of engulfment genes in several species suggests that the signaling process from apoptotic cells to engulfing cells and the subsequent engulfment process might be also conserved across species (TABLE 1).

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:07 Faculty of Science > Institute of Molecular Life Sciences
Dewey Decimal Classification:570 Life sciences; biology
Scopus Subject Areas:Life Sciences > General Neuroscience
Life Sciences > General Biochemistry, Genetics and Molecular Biology
Social Sciences & Humanities > History and Philosophy of Science
Language:English
Date:1999
Deposited On:11 Feb 2008 12:20
Last Modified:01 Jan 2025 04:37
Publisher:Wiley-Blackwell
ISSN:0077-8923
OA Status:Closed
Publisher DOI:https://doi.org/10.1111/j.1749-6632.1999.tb07925.x
PubMed ID:10668467
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