[
Nature,
2001]
The degredation of DNA is one of the hallmarks of programmed cell death (apoptosis). When forced to commit suicide, apoptotic cells - like good secret agents - grimly destroy their "instruction book," chewing up their genomic DNA into tiny morsels. Until now, only two DNA-destroying enzymes (nucleases) with a clear role in cell death were known, one in mammals and one in the nematode worm Caenorhabditis elegans. But, on pages 90-99 of this issue, Li and colleagues and Parrish and co-workers show that another nuclease, endonuclease G (endoG), also contributes to the carnage, and might even influence the likelihood that a cell will live or die.
[
Science,
2004]
The amazing precision with which different cell types find their correct locations in developing tissues has fascinated biologists for decades. Models of cell fate patterning during development emphasize the contrast between spatial gradients of developmental signals that act at long range and cell-to-cell signaling events that act locally. Development of the vulva in the nematode Caenorhabditis elegans provides an elegant model system for examining the patterning of cell fate in an animal. There is strong evidence that two different intercellular signals contribute to the relatively simple induction of cell fate among vulval precursor cells (VPCs): a long-range spatial gradient of epidermal growth factor (EGF) mediated by the EGF receptor (1, 2) and a cell-to-cell lateral signal mediated by the Notch-like receptor LIN-12 (35). It is well established that the combined action of the EGF receptor and LIN-12 receptor signaling pathways generate the pattern of VPCs in the developing vulva (6); however, the molecular details of this cooperative effect have remained elusive. On page 663 of this issue, Yoo et al. (7) provide the missing molecular connection. They report that VPCs activated by a low level of EGF are blocked from adopting a particular cell fate by a LIN-12 lateral signal from a neighboring cell.