Myo6 gets choosy

Myo6 gets choosy timulated neurons that lack myo-sin VI (Myo6) fail to endocytose a subtype of glutamate receptors called AMPARs, report Osterweil et al. on page 329. However, the neurons do not have a general endocytosis defect, suggesting a role for Myo6 in specific endocytic events. Unlike other myosins, Myo6 moves toward the minus ends of actin filaments. Thus, in polarized cells or cell regions, such as the dendritic spines of neurons, Myo6 moves toward the inside of the cell. Dominant-negative mutants of Myo6 have a generalized defect in endocytosis, but this may be explained by Myo6's interaction with AP2, a clathrin adaptor protein, rather than Myo6's normal function. A GTP signal to the nucleolus ucleolar size and cell growth rate are positively correlated, perhaps based on ribosome biogenesis being localized to the nu-cleolus, but little is known about how nucleolar size is controlled. One possible mechanism is reversible localization of key regulators. On page 179, Tsai and McKay identify the mechanism controlling one such localization system. They find that nucleostemin, a nucleolar protein found preferentially in stem cell and cancer cells and required for them to remain in the cell cycle, localizes to the nucleolus when it is GTP bound. Based on mutants, three regions of nucleostemin affected nucleolar localization. An NH 2-terminal basic region conferred short-lived nucle-olar binding, whereas an internal domain appeared to inhibit entry into the nucleolus. However, this inhibitory function was turned off when GTP was bound to the third region, a GTP-binding domain. Furthermore, mutations that blocked GTP binding reduced nucleolar localization, as did the addition of an inhibitor of GTP biosynthesis. Together, the data suggest that the inhibitory domain and the GTP-binding domain work together as a gating mechanism to control nucleo-stemin's entry into the nucleolus, and that GTP is the switch that opens the gate. The use of GTP to control nucleolar localization enables the cell to transmit information regarding the surrounding environment to the nucleolus via cell-signaling pathways, and may provide a mechanism to link growth signals with the size and activity of the nucleolus. N Localization of nucleostemin to the nucleolus (top) is controlled by a GTP switch. he lipid phosphatase Sac1p inhibits transport out of the Golgi and, based on its expected target, should increase transport out of the ER. Now, Faulhammer et al. find that Sac1p switches from its ER role to the Golgi role in response to …