Transcriptional control of non-apoptotic developmental cell death in C. elegans.

Programmed cell death is an essential aspect of animal development. Mutations in vertebrate genes that mediate apoptosis only mildly perturb development, suggesting that other cell death modes likely have important roles. Linker cell-type death (LCD) is a morphologically conserved cell death form operating during the development of Caenorhabditis elegans and vertebrates.

HSF-1 activates the ubiquitin proteasome system to promote non-apoptotic developmental cell death in C. elegans.

Apoptosis is a prominent metazoan cell death form. Yet, mutations in apoptosis regulators cause only minor defects in vertebrate development, suggesting that another developmental cell death mechanism exists. While some non-apoptotic programs have been molecularly characterized, none appear to control developmental cell culling.

Natural variation identifies multiple loci controlling petal shape and size in Arabidopsis thaliana.

Natural variation in organ morphologies can have adaptive significance and contribute to speciation. However, the underlying allelic differences responsible for variation in organ size and shape remain poorly understood. We have utilized natural phenotypic variation in three Arabidopsis thaliana ecotypes to examine the genetic basis for quantitative variation in petal length, width, area, and shape.

Control 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.

Necrosis and the serpin under't.

Caspase proteases play essential roles in apoptotic cell death, while other proteases are active in necrotic cell death. In a recent paper in Cell, Luke et al. (2007) present findings demonstrating that a gene believed to be a natural protease inhibitor may have a role in preventing necrosis.

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.

Death without caspases, caspases without death.

Apoptosis is a conserved cell-death process displaying characteristic morphological and molecular changes including activation of caspase proteases. Recent work challenges the accepted roles of these proteases. New investigations in mice and the nematode Caenorhabditis elegans suggest that there could be caspase-independent pathways leading to cell death.