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Review
. 2008 Aug 15;7(16):2479-84.
doi: 10.4161/cc.7.16.6479. Epub 2008 Aug 19.

Cell death specification in C. elegans

Erin Peden  1 , Darrell J Killian, Ding Xue
Affiliations
Review

Cell death specification in C. elegans

Erin Peden et al. Cell Cycle. .

Abstract

Years of research have identified a highly conserved mechanism required for apoptotic cell killing. How certain cells are specified to die is not well understood. With a rich history in programmed cell death research, the nematode C. elegans offers an excellent animal model with which to study cell death specification events. Developing hermaphrodites have 131 invariant cell death events that can be studied with single cell resolution. Recent genetic studies have begun to identify diverse sets of factors required for the proper specification of individual cell death events. The limited findings thus far suggest that cell death specification is controlled through transcriptional regulation of at least two members of the core cell death pathway, egl-1 and ced-3. However, it remains unclear if additional modes of cell death specification exist. Here we briefly summarize current findings in the field of C. elegans cell death specification and consider those questions that remain to be answered.

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Figures

Figure 1
Figure 1. C. elegans programmed cell death specification
(A) The core cell death pathway in C. elegans where X activates egl-1. X may be any number of known and unknown cell-specific factors that regulate cell death fate. (B) The NSM sister cell is specified for death by HLH-2/HLH-3 activation of egl-1. Four separate E-boxes, bHLH binding sites, were identified in egl-1; Box: I 3947–3952, Box II: 3788–3793, Box III: 3713–3718, Box IV: 3667–3672. (C) In the NSMs, CES-1 inhibits cell death by competing with HLH-2/HLH-3 in binding to the Snail elements that coincide with the E-boxes in egl-1. (D) The P11.aaap cell is specified for cell death by CEH-20/MAB-5 activation of egl-1. (E) The tail-spike cell is specified for cell death by PAL-1 transcriptional activation of ced-3 via binding to 3 regions of the ced-3 promoter (Region A: -1203-1178, Region B: -1162-1137, and Region C: -1131-1107). (F) The HSN is protected from cell death in hermaphrodites by TRA-1A binding to egl-1 and repressing egl-1 transcription. (G) The male CEM is protected from cell death due to transcriptional upregulation of ceh-30 by UNC-86 in the absence of TRA-1A (denoted by dashed lines), which antagonizes the activity of UNC-86. The direct target(s) of the CEH-30/UNC-37 repressosome remain to be identified.
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