Nervous chemokines

Nervous chemokines uidance molecules from the immune and nervous systems are getting mixed up in each others business. have found that a leukocyte attractant called stromal-derived factor 1 (SDF-1) is the main factor that entices embryonic cerebellar neurons to their correct location. SDF-1 is a chemokine—a peptide that attracts leukocytes by activating a G protein signaling cascade. In contrast, neuronal guidance molecules such as the netrins, ephrins, and Slit are proteins that bind single transmembrane receptors linked to a variety of downstream signaling pathways. The two worlds were bridged last year when Rao found that the neuronal repellant Slit could also inhibit leukocyte chemotaxis. Now, he has completed the loop by confirming SDF-1's function in the brain. This function was suspected when immunologists made mice lacking SDF-1 and noted a cerebellar defect, whereas others showed that SDF-1 affected either chemotaxis or the motility level of neurons. In Rao's experiments, collagen blocks embedded with SDF-1 attracted embryonic neuronal precursor cells, and the meninges (the outside lining of the brain) attracted the cells only if the gene encoding SDF-1 had not been knocked out. The meninges thus uses SDF-1 to attract the cells before they go on to form structures involved in motor control and other functions. The two worlds of chemokines and neuronal guidance may G olymerization of an actin-related protein may drive segregation of a bacterial plasmid, according to Jakob Denmark), and colleagues. Segregation in bacteria was thought to be a rather passive affair, with DNA attaching to the membrane and getting dragged along as cell growth led to membrane expansion. That model was challenged when DNA replication was found to be localized to one area at the cell center, followed by rapid movement of both plasmids and chromosomal DNA from midcell to more polar sites. In the meantime, Gerdes had been working on the segregation requirements for the R1 plasmid. He had found that ParR binds to the parC centromere-like site on the plasmid, and that ParM binds to ParR. Then, Møller-Jensen tried detecting native ParM directly, using immunofluorescence, and saw axial P have arisen, says Rao, because " if your assay is set up in a particular way, you get what you are looking for. " But now he thinks that factor participation in both immune and nervous systems will turn out to be " a common thing. " The next place to look may be in blood …