sults provide further support for how network structure can be impacted by the environment, suggesting that a wide metabolic breadth requires larger numbers of nodes, in the form of unique assemblages of specialized enzymes. Such networks will also be more expansive since most carbon sources are not funneled through a single pathway. These two factors suggest that metabolic networks change as a result of variation in metabolic breadth. The recent emphasis on molecular networks has received few rigorous tests about the impact of network structures on evolutionary processes. Our results indicate that metabolic 25833960 network topology may not impose severe constraints on the evolution of carbon utilization phenotypes. Instead, our observation that traits are gained and lost independently of known metabolic network structure suggests that the networks themselves vary and evolve. Acknowledgments We thank Walter Eanes, Dan Dykhuizen, Omar Warsi, and Julius 
Fisher for helpful comments on the manuscript. T-killer cells of the immune system form conjugates with cells infected by viruses, as well as with tumor cells, and eliminate them via directed discharge of toxic compounds. The directionality is ZM-447439 supplier essential for the effectiveness of killing the intended target as well as for sparing healthy bystander cells, i.e. for specificity of cellular immune response. The killing apparatus is structurally associated with the Golgi apparatus and with the centrosome at the center of convergence of the microtubule fibers of the T-cell cytoskeleton. Polarization of this organelle complex in the T cell to the interface with the target cell is recognized as the cell-structural basis of the directionality of cellular immune response. Other types of cell-cell interactions in the immune system similarly involve centrosome polarization. The mechanism of centrosome positioning in T cells has not been established. It appears to be a form of rearrangement of the microtubule cytoskeleton. Other types of microtubule cytoskeleton rearrangements, for example during cell division, proceed to a large degree through disassembly and re-assembly of individual microtubules, which are termed microtubule 10980276 dynamics. Microtubule dynamics is therefore a foremost candidate for the driving force of the centrosome polarization in T cells, or at least for an essential facilitating mechanism. This view has its most direct support in two experimental studies, which uncovered signal transduction pathways in T cells that might lead to promoting, alternatively, microtubule assembly and disassembly. Earlier studies on primary cytotoxic T-lymphocytes, however, established that the centrosome polarization was insensitive to treatment with taxol, a drug used to suppress microtubule dynamics. Thus, the existing data on the role of microtubule dynamics in T cell polarization appear contradictory. In the present work, we have examined the sensitivity of polarization to inhibitors of microtubule dynamics in an experimental model that replaces the target cell surface with the optical glass surface coated with a stimulatory clone of antibodies to the T cell receptor. This experimental model has been widely used in cellular immunology because it permits reproducible stimulation of large numbers of T cells and facilitates microscopy data collection and analysis. Cultured T cells of the Jurkat line that are used in the present study have been previously shown to exhibit the same polarization response to this type