biostudies-literature00610Blum ESNICHD NIH HHSNINDS NIH HHSNCI NIH HHS970-3https://www.ebi.ac.uk/biostudies/studies/S-EPMC3858082biostudies-literatureUnknown335(6071)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.Science (New York, N.Y.)Control of nonapoptotic developmental cell death in Caenorhabditis elegans by a polyglutamine-repeat protein.PMC3858082CA09673R01HD042680R01 HD042680R01 NS081490T32 CA009673Blum ESLu YAbraham MCShaham SYoshimura S61falseControl of nonapoptotic developmental cell death in Caenorhabditis elegans by a polyglutamine-repeat protein.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.2012-01-01T00:00:00Z2012 Feb2020-10-29T13:51:09Z2019-03-27T01:18:16ZS-EPMC38580822236300810.1126/science.1215156