Selective clusters

find that interactions between proteins, not lipids, drive the formation of plasma membrane microdomains in signaling T cells. In active T cells, signal transduction proteins cluster within the plasma membrane , probably to enhance signaling by concentrating the interacting proteins. Popular model mechanisms for clustering involve either lipid rafts or actin. But Doug-lass and Vale found that the signaling proteins themselves hold clusters together. In their system, T cell clusters included the LAT adaptor protein, the Lck tyrosine kinase, and the CD2 costimulatory transmembrane protein. LAT and Lck are thought to be raft-localized proteins. But mutation of their raft-localizing regions did not alter LAT or Lck diffusion or clustering. By contrast, mutating A GFP-tagged LAT molecules become trapped (blue) at CD2 clusters (light gray). LAT residues that are essential for protein–protein interactions prevented LAT clustering. Clusters were also maintained in the absence of actin polymerization, although actin was needed for cluster formation. Douglass and Vale think that actin or actomyosin may be needed for the initial movement of proteins into clusters, but not for anchoring them together. When tracking single molecules, the authors noticed that LAT and Lck diffused rapidly outside of clusters but became temporarily trapped, probably via protein–protein interactions, when encountering cluster sites. Nonclustering proteins were rarely trapped and were forced to navigate between clusters. Vale notes that their findings do not rule out the existence of lipid rafts. Rather, the findings support the idea that " protein–protein interactions may be a more common mechanism for creating signaling micro-domains, " he says. He hopes eventually to understand why microdomains need to be formed during T cell signaling. " Many people in the signaling field think about which molecules interact with one another, " he says, " but the issue of how the molecules are organized spatially and how this affects their function is often not addressed. " openings and clos-ings of ion channels that cause membrane potential fluctuations. When the noise becomes too great, a spontaneous action potential ensues, which can disrupt communication between axons. As the rate of this spontaneous firing increases exponentially as axon diameter decreases, Faisal wondered whether channel noise limits axon size. To test this question, the team developed a mathematical model that tracks axon dynamics when single ion channels " behave badly, " or open and close at the maximum threshold observed experimentally. Using data from well-studied biological systems, such as specialized cortical …