Chopping and storing in one

Tmod points the way hen it comes to actin dynamics, the pointed end of the actin filament is the forgotten cousin. The barbed end is in a state of constant flux in motile cells, pushing out the front of the cell, whereas the pointed end rarely rates a mention. But now, Mardahl-Dumesnil and Fowler report that in the actin-containing thin filaments of developing fly muscles, which grow at a more leisurely pace, the action is at the pointed end (page 1043). The authors target the pointed end by transiently overexpressing the fly version of Tropomodulin (Tmod) in indirect flight muscles (IFM). If the Tmod is overexpressed during pupation when myofibrils are assembled, a central core of thin filaments is shorter than normal, which in the most serious cases results in adults that are unable to fly. The short filaments are permanently arrested— they do not resume their growth once Tmod levels decline to near normal—and a fraction of the overexpressed form of Tmod stays as a permanent cap on the pointed end. Fowler believes that the excess Tmod overwhelms a factor that normally makes Tmod capping of pointed ends dynamic. By the time the Tmod levels decline again, this factor may be far away in the central M line, conveyed from the foreshortened thin filaments by the continued elongation of the thick filaments of myosin. The outer thin filaments are not affected by the over-expression only because they are born later, after Tmod levels have returned to normal. ᭿ W Tmod overexpression (red, bottom) arrests filament extension before it reaches the M line. he cell may not be as lazy as we first thought. With an organelle that comes in multiple copies, there is always the option of leaving segregation of that organelle to random chance—in most cases each daughter cell will get at least one copy of the organelle. But budding yeast is not prepared to take that risk, especially when growing daughter cells are so much smaller than mature mothers. On page 979, Hoepfner et al. find that yeast cells actively segregate their T peroxisomes. The segregation machinery includes actin cables and a specific motor, Myo2p, and the substrate for the segregation is provided by the dynamin Vps1p, which cleaves the peroxisomes into manageable pieces. Hoepfner et al. came to these conclusions after observing the movement of individual GFP-labeled peroxisomes along the cell cortex to the bud neck, …