The outer membrane of Gram-negative bacteria is composed of lipopolysaccharide, a large glycolipid that prevents drugs from entering the cells. Disrupting lipopolysaccharide assembly hypersensitizes bacteria to antibiotics. Sherman et al. used biochemical tools to observe lipopolysaccharide transport. Seven proteins, which are conserved in all Gram-negative bacteria, appear to form a protein bridge that uses adenosine triphosphate to power transport of lipopolysaccharide from one membrane to another. The ability to monitor intermembrane transport of lipopolysaccharide will help in efforts to develop and characterize inhibitors.Science, this issue p. 798Gram-negative bacteria have an outer membrane that serves as a barrier to noxious agents in the environment. This protective function is dependent on lipopolysaccharide, a large glycolipid located in the outer leaflet of the outer membrane. Lipopolysaccharide is synthesized at the cytoplasmic membrane and must be transported to the cell surface. To understand this transport process, we reconstituted membrane-to-membrane movement of lipopolysaccharide by incorporating purified inner and outer membrane transport complexes into separate proteoliposomes. Transport involved stable association between the inner and outer membrane proteoliposomes. Our results support a model in which lipopolysaccharide molecules are pushed one after the other in a PEZ dispenser–like manner across a protein bridge that connects the inner and outer membranes.
Different types of phenotypic traits consistently exhibit different levels of genetic variation in natural populations. There are two potential explanations: either mutation produces genetic variation at different rates, or natural selection removes or promotes genetic variation at different rates. Whether mutation or selection is of greater general importance is a longstanding unresolved question in evolutionary genetics. We report mutational variances (VM) for 19 traits related to the first mitotic cell division in C. elegans, and compare them to the standing genetic variances (VG) for the same suite of traits in a worldwide collection C. elegans. Two robust conclusions emerge. First, the mutational process is highly repeatable: the correlation between VM in two independent sets of mutation accumulation lines is 0.9. Second, VM for a trait is a good predictor of VG for that trait: the correlation between VM and VG is 0.9. This result is predicted for a population at mutation-selection balance; it is not predicted if balancing selection plays a primary role in maintaining genetic variation.