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Genetics, Vol. 167, 673-685, June 2004, Copyright © 2004
doi:10.1534/genetics.103.020503
The Caenorhabditis elegans pvl-5 Gene Protects Hypodermal Cells From ced-3-Dependent, ced-4-Independent Cell Death
Pradeep Joshi and David M. Eisenmann1
Department of Biological Sciences, University of Maryland, Baltimore County, Baltimore, Maryland 21250
1 Corresponding author: University of Maryland, Baltimore County, Department of Biological Sciences, 1000 Hilltop Circle, Baltimore, MD 21250.
E-mail: eisenman{at}umbc.edu
Programmed cell death (PCD) is regulated by multiple evolutionarily conserved mechanisms to ensure the survival of the cell. Here we describe pvl-5, a gene that likely regulates PCD in Caenorhabditis elegans. In wild-type hermaphrodites at the L2 stage there are 11 Pn.p hypodermal cells in the ventral midline arrayed along the anterior-posterior axis and 6 of these cells become the vulval precursor cells. In pvl-5(ga87) animals there are fewer Pn.p cells (average of 7.0) present at this time. Lineage analysis reveals that the missing Pn.p cells die around the time of the L1 molt in a manner that often resembles the programmed cell deaths that occur normally in C. elegans development. This Pn.p cell death is suppressed by mutations in the caspase gene ced-3 and in the bcl-2 homolog ced-9, suggesting that the Pn.p cells are dying by PCD in pvl-5 mutants. Surprisingly, the Pn.p cell death is not suppressed by loss of ced-4 function. ced-4 (Apaf-1) is required for all previously known apoptotic cell deaths in C. elegans. This suggests that loss of pvl-5 function leads to the activation of a ced-3-dependent, ced-4-independent form of PCD and that pvl-5 may normally function to protect cells from inappropriate activation of the apoptotic pathway.
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