A morphologically conserved nonapoptotic program promotes linker cell death in Caenorhabditis elegans.
Apoptosis, cell death characterized by stereotypical morphological features, requires caspase proteases. Nonapoptotic, caspase-independent cell death pathways have been postulated; however, little is known about their molecular constituents or in vivo functions. Here, we show that death of the Caenorhabditis elegans linker cell during development is independent of the ced-3 caspase and all known cell death genes. The linker cell employs a cell-autonomous death program, and a previously undescribed engulfment program is required for its clearance. Dying linker cells display nonapoptotic features, including nuclear crenellation, absence of chromatin condensation, organelle swelling, and accumulation of cytoplasmic membrane-bound structures. Similar features are seen during developmental death of neurons in the vertebrate spinal cord and ciliary ganglia. Linker cell death is controlled by the microRNA let-7 and Zn-finger protein LIN-29, components of the C. elegans developmental timing pathway. We propose that the program executing linker cell death is conserved and used during vertebrate development.
Abraham
Mary C
MC
Laboratory of Developmental Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.
Lu
Yun
Y
Shaham
Shai
S
D000818:Animals; D017173:Caenorhabditis elegans / Q000166:cytology* / Q000648:ultrastructure; D016923:Cell Death; D050437:Genes, Developmental; D008297:Male; D009154:Mutation / Q000235:genetics; D010587:Phagocytosis / Q000502:physiology; D014855:Wallerian Degeneration