In this issue of The EMBO Journal, Wilson et al (2012) elegantly discovered an important new axis for intestinal homeostasis and cancer, using an RNAi screen to enhance the RAS-induced multivulva (MUV) phenotype in Caenorhabditis elegans.
Recently reporting in Science, Nakagawa et al. describe an unexpected role for Dicer in chromosome fragmentation during apoptosis in C. elegans. They find that cleavage of DCR-1 by the caspase CED-3 redirects its regulatory activity, by destroying its dsRNase activity while activating an intrinsic DNase activity.
An article by Polley and Fay in this issue of GENETICS provides an excellent opportunity to introduce or reinforce concepts of reverse genetics and RNA interference, suppressor screens, synthetic phenotypes, and phenocopy. Necessary background, explanations of these concepts, and a sample approach to classroom use of the original article, including discussion questions, are provided.
A landmark study has revealed that an interleukin-17-like signaling system modulates a neural circuit that controls the aggregation behavior of nematodes.
CED-3, a protein that is essential for programmed cell death, also has an unexpected role in the regulation of non-apoptotic genes during normal development.
Why are proteins glycosylated? On the basis of new studies, I propose two models to clarify the specific functions of glycosylation in worms. The first explains how intra- and inter-cellular trafficking of an N-glycosylated disintegrin-metalloprotease guides somatic gonadal cells through their migratory route, determining the shape of an organ. The second explains how rigid coats of secreted chondroitin proteoglycans bend membranes to drive cytokinesis and epithelial invagination.