Hoarding bug

A bug that causes meningitis does not like to share. On page 627, Doulet et al. show that it hoards actin-binding proteins away from immune cells. The hoarding allows the bacterium to cross the blood–brain barrier and to prevent immune cells from responding. Many infl ammation-inducing leukocytes pass from the bloodstream to infected tissues through loosened endothelial cell–cell junctions. The endothelial cells form cup-like actin structures that help leukocytes adhere and migrate. But these cups did not form on endothelial cells where extracellular colonies of Neisseria meningitidis grew, the authors found. Leukocytes thus failed to migrate to cell junctions and were easily detached from the surface by fl ow. Cups were absent because the bug sequestered away host ezrin and moesin. These actin-binding proteins, which link adhesion molecules in the plasma membrane to the cytoskeleton, were required for cup formation and seem to be in limited quantities. Overexpression of either ezrin or moesin rescued leukocyte migration between infected cells. The bug uses ezrin, moesin, and cytoskeletal molecules to adhere tightly to host cells in large, stable colonies. The cytoskeletal changes also allow a few of the bacteria to cross the blood–brain barrier via in-ternalization at the apical surface and exocytosis out the other side, thus leading to meningitis. By usurping the same molecules that the immune cells use, N. meningitidis probably delays its pursuit by neutrophils, the host's fi rst line of defense. No animal model of meningitis exists, however, to test whether this putative delay is a selective advantage for the bacterium. This mechanism of immune interference may be specifi c to N. meningitidis. Most other human pathogenic bacteria, such as Listeria or Shigella, are quickly internalized, and thus have no lasting hold on ezrin or moesin. DNA recruits nuclear envelope D NA calls for the return of the nuclear envelope (NE) after mitosis, according to Ulbert et al. (page 469). The abundance of DNA may thus be one reason why the NE reforms so quickly. NE reformation occurs so quickly that breaking down the process in vivo has so far been impossible. Many scientists instead use in vitro reconstitution assays, which indicate that chromatin decondensation (as occurs at the end of mitosis) initiates the recruitment of vesicle populations to chromatin. In the new work, the authors aimed to identify membrane and chromatin components that mediate this recruitment and thus NE assembly. The main component of chromatin is, of …