For instance, it is interesting to speculate that the four conserved interferonstimulated bottlenecks may jointly control the regulation of different overlapping aspects of the interferon response, similar to the complex regulation seen in some pathogens. Further, the topological properties of the bottleneck genes indicate that they may drive downstream processes either directly or indirectly, and that the downstream processes should be reGSK2118436 presented in their network neighborhood. Thus abrogating the expression of a bottleneck gene should have an impact on the expression of some or all of its neighbors. We showed this to be true in the case of Ifit1. When the expression of Ifit1 is suppressed using siRNA in macrophage cells, the expression of downstream genes Usp18 and M61 were also suppressed in response to LPS. This supports the relationship between Ifit1 and its predicted first-order network, implicating Ifit1 as a functional bottleneck that affects downstream processes. The data presented here indicate that the bio-surfactant serratamolide can act as a novel S. marcescens hemolysin, and that the non-ribosomal peptide synthetase SwrW is necessary for hemolysis in some clinical and laboratory strains. Elevated in crp and hexS mutants that over-express swrW. Biochemical data indicate that purified serratamolide is sufficient to lyse red blood cells and damage epithelial cells in vitro. Genetic data suggests that serratamolide production is regulated by cAMP-CRP in strain CMS376, namely that surfactant zones are increased in a crp mutant and hemolysis is increased in mutant strains with altered ability to respond to or make cAMP. Since the cAMP-CRP pathway is well known to regulate genes in response to the nutritional environment of the cell, this may indicate that serratamolide plays a role in a bacterium’s ability to acquire or compete for nutrients. Consistent with the role of serratamolide in competition, it has been shown that serratamolide has antimicrobial activity against both prokaryotes and fungi, and that swarming motility, which requires biosurfactants such as serratamolide, confers resistance to antibiotics. Another role for serratamolide was suggested by BarrNess and colleagues. They showed that mutant strains deficient in serratamolide had reduced surface hydrophobicity, and the authors suggested that the highly hydrophobic surface of S. marcescencs contributes to its dispersal in the environment and virulence. Lipopeptide surfactants, such as surfactin from Bacillus species and syringomycins from Pseudomonas species can act as hemolysins. Serramic acid, another S. marcescens product was shown to be hemolytic to human and horse red blood cells, but only poorly hemolytic to bovine and sheep red blood cells. This same study tested serratamolide for hemolytic activity against human red blood cells, and the result was negative. The differences between this current study and the previously described study, in which serratamolide was tested for hemolysis, may be due to experimental differences, in that the previous authors delivered serratamolide using liposomes composed of several phospholipids, rather than serratamolide alone. Furthermore, the previous study tested serratamolide against human red blood cells but not sheep or murine red blood cells; it is possible that differences in membrane phospholipid composition or surface proteins may result in differential hemolytic activity.