Ready to replicate? So vesiculate!

ells that passively swell and contract with changes in osmolarity are the key to detecting those changes, say Most cells have at least two mechanisms for maintaining homeostasis in response to changes in salt concentrations. Without these mechanisms, osmotic forces take over: more water and thus less salt outside cells leads water to flood into a cell. But this swelling doesn't occur in most cells because they pump ions out. Even if there is some swelling, the cells prevent membrane Osmosensing neurons (ONs) swell to detect a decrease in salt concentration. stretching by adding extra membrane to compensate. The osmosensory neurons studied by Zhang and Bourque lack both of these responses, so they swell and contract with changes in salt concentration. " It's a behavior you expect from passive diffusion across a membrane, " says Bourque. The neurons have membrane reserves so that they do not pop as they swell. But channels in the membrane are affected: the ironing out of membrane folds, tension on underlying cytoskeleton, or both act to turn off the channels. The resultant hyperpolarization and lack of firing leads to less vasopressin release so that the kidney directs more water to be excreted. ᭿ N ␤-COP (green) moves to help nuclear pore proteins (red) break down nuclear envelopes (right). Salt Lake City, UT). Vesicles have previously been isolated from cells in which nuclear envelope breakdown has occurred, but it was always possible that the vesicles were formed as part of extract isolation rather than normal physiology. Now, the Utah team has found that the nuclear pore protein Nup153, COP1 coatomer proteins, and ARF GTPase are needed for nuclear envelope breakdown in frog egg extracts. COP1 components, which are better known for driving vesicle formation during intra-Golgi and Golgi-to-ER traffic, were also found to associate with Nup153 and to move from the Golgi to the nuclear periphery at the start of mitosis. Initiation of nuclear envelope breakdown may be controlled by regulating COP1 access to Nup153, which is primarily exposed in the nucleoplasm. This may occur by the micro-tubule-mediated ripping of the nuclear envelope or nuclear pore reconfiguration noted by others. The relative contributions of ripping and vesiculation in different cell types remain to be determined. Vesicles are not necessarily seen as an endpoint in nuclear envelope breakdown, but Ullman notes that they may be an intermediate before nuclear membranes fuse with the ER. ᭿ Prions by …