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Control of Nonapoptotic Developmental Cell Death in Caenorhabditis elegans by a Polyglutamine-Repeat Protein

Death for Development Cell death is critical for animal development and for the promotion of gastrulation, as well as for sculpting tissues. Although cell death by apoptosis is essential in some invertebrates, genes promoting apoptosis in the mouse are not required for viability. This surprising observation prompted investigations by Blum et al. (p. 970; see the Perspective by Link and Saldi), who have discovered a nonapoptotic developmental cell death process mediated by a polyglutamine-repeat protein in the nematode worm Caenorhabditis elegans. This form of cell death is morphologically similar to cell death occurring during vertebrate development, particularly cell death accompanying polyglutamine-dependent neurodegeneration. A nematode protein containing runs of the amino acid glutamine, like some linked to neurodegeneration, causes cell death. Death is a vital developmental cell fate. In Caenorhabditis elegans, programmed death of the linker cell, which leads gonadal elongation, proceeds independently of caspases and apoptotic effectors. To identify genes promoting linker-cell death, we performed a genome-wide RNA interference screen. We show that linker-cell death requires the gene pqn-41, encoding an endogenous polyglutamine-repeat protein. pqn-41 functions cell-autonomously and is expressed at the onset of linker-cell death. pqn-41 expression is controlled by the mitogen-activated protein kinase kinase SEK-1, which functions in parallel to the zinc-finger protein LIN-29 to promote cellular demise. Linker-cell death is morphologically similar to cell death associated with normal vertebrate development and polyglutamine-induced neurodegeneration. Our results may therefore provide molecular inroads to understanding nonapoptotic cell death in metazoan development and disease.