Orbit(ing) the furrow

alcium just got a promotion. Findings by Caroppo et al. (page 111) reveal that in addition to its many roles inside the cell, Ca 2 ϩ has a distinct extracellular purpose: it acts via a Ca 2 ϩ receptor (CaR) to regulate the function of gastric epithelial cells. It has been known for some time that extracellular Ca 2 ϩ can be sensed by the CaR. The team noted that a Ca 2 ϩ gradient was generated outside gastric cells after cholinergic stimulation with carbachol, which mimics a signal received during digestion processes. Ca 2 ϩ levels increased on the apical side and decreased on the basolateral side, and prompted secretion of pepsino-gen. Proteolytic cleavage of pepsinogen yields the digestive enzyme pepsin. It is well known that carbachol boosts intracellular Ca 2 ϩ in gastric cells, and a resultant increase in extracellular Ca 2 ϩ is no surprise. But the authors found that extracellular Ca 2 ϩ was both necessary and sufficient for the induction of pepsinogen secretion. Perhaps cells economize by using a single messenger, calcium, both inside and outside of the cell. In this way, the authors speculate, cells can use the raised Ca 2 ϩ levels that are present outside cells during intracellular Ca 2 ϩ signaling events to control necessary functions. ᭿ C Pepsinogen stores (top) are excreted in response to an increase in extra-cellular Ca 2ϩ (bottom). ike the hard candy shell around an M&M, oligodendrocytes swathe axons with a sheath of myelin for protection. Now, Edgar et al. (page 121) show that the myelin casing may do more than just provide shelter and stability; it may also set up conditions necessary for fast axonal transport. The team noticed multiple organelles amassed within optic nerve ax-ons in mice with a null mutation of the Plp gene, which encodes two major proteins of the myelin sheath. These organelle traffic jams implied that there might be problems with transport in these cells. So Edgar et al. looked at movement of labeled tracers in fast antero-grade and retrograde transport. There were minor defects in fast forward transport that took some time to accumulate, and severe defects in fast backward transport. A closer look at motor proteins revealed that levels of the retrograde motor dynein and associated dynactin were elevated, possibly due to the accumulation of proteins on stalled vesicles. Anterograde motors were unaffected. The primary function of myelin …