[
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,
1995]
When it comes to G proteins, cell biologists have amassed a great wealth of material. They have identified nearly 30 of these proteins, which serve as key relays in the pathways that transmit signals from hormones, neurotransmitters, and other cellular regulators from the cell membrane to the interior. And studies with cultured cells have enabled researchers to learn a great deal about the biochemistry of G proteins...
[
Worm,
2016]
Although several signaling pathways in oriented cell division have been well characterized such as delta/notch inductions or wnt/frizzled-based anterior-posterior polarity, there is strong evidence for additional signal pathways controlling early anterior-posterior polarity decisions. The homolog of the adhesion G protein-coupled receptor latrophilin, LAT-1 has been identified as a receptor essential for oriented cell division in an anterior-posterior direction of specific blastomeres in the early C. elegans embryo. We recently conducted a study aiming at clarifying the signals involved in LAT-1 function. We identified a Gs protein/adenylyl cyclase/cAMP pathway in vitro and demonstrated its physiological relevance in oriented cell division. By interaction with a Gs protein LAT-1 elevates cAMP levels. These data indicate that G-protein signaling in oriented cell division is not solely GPCR-independent. This commentary will discuss our findings in the context of the current knowledge of mechanisms controlling oriented cell division and anterior-posterior polarity. Further, we identify open questions which need to be addressed in the future.