Forced to bond

he bonds between leukocytes and endothelial cells last longer when under some strain, as shown by Yago et al. (page 913). The results explain why these white blood cells attach to and roll along the vasculature only when blood flow is strong enough. Most explanations of this flow-enhanced adhesion suggest that flow increases the number of bonds that form between L-selectin on leukocytes and PSGL-1 or other ligands on vascular cells, possibly by rotating or deforming the blood cell. But some scientists believe that force generated from flow might also increase the lifetime of existing bonds. The new results show that catch bonds—those whose lifetimes are lengthened by force—between L-selectin and PSGL-1 control leukocyte rolling. The authors correlated the lasting power of individual bonds with the rolling stability of the cells. As the force imposed on bonds increased, their lifetimes increased. The blood cells thus rolled more slowly on PSGL-1 substrates. Slow rolling allows leukocytes to respond to chemokines and traverse the endo-thelium. The force requirement probably prevents inflammation and leukocyte clumping at vascular blockages. Above optimum shear, when blood cells roll most slowly, catch bonds became slip bonds, whose lifetimes are shortened by force. Rolling velocities thus increased, and the cells detached from the substrate. The transition to slip bonds may explain why leukocytes usually do not adhere in arteries, where blood flow is very strong. ᭿ T L-selectin bonds hold longer as force increases up to an optimum shear. o understand how chromosomes condense for mitosis, most researchers pick apart DNA's most compact form: metaphase chromosomes. On page 775, Kireeva et al. work from the other end and watch condensation as it occurs. From this perspective, condensation looks like a folding continuum with intermediates that do not fit the favored radial loop model. The authors used serial section micros-copy to examine chromosomes at stages of prophase, when most condensation occurs. At even the earliest stages, 10-and 30-nm chromatin fibers are folded into larger ‫ف‬ 100-nm fibers. In middle prophase, chromatids of 200–250 nm are present that appear to form from the folding of the 100-nm fibers. A further doubling in T Hitched genes still independent ranscribed genes move away from heterochromatin even if their silent neighbors do not, as shown by Zink et al. (page 815). Transcriptional status is closely related to nuclear positioning. Silenced genes, for example, are often associated with hetero-chromatin at the nuclear periphery, whereas …