Running Time Analysis of MOEA/D on Pseudo-Boolean Functions.

Decomposition-based multiobjective evolutionary algorithms (MOEAs) are a class of popular methods for solving the multiobjective optimization problems (MOPs), and have been widely studied in numerical experiments and successfully applied in practice. However, we know little about these algorithms from the theoretical aspect. In this paper, we present running time analysis of a simple MOEA with mutation and crossover based on the MOEA/D framework (MOEA/D-C) on five pseudo-Boolean functions. Our rigorous theoretical analysis shows that by properly setting the number of subproblems, the upper bounds of expected running time of MOEA/D-C obtaining a set of solutions to cover the Pareto fronts (PFs) of these problems are apparently lower than those of the one with mutation-only (MOEA/D-M). Moreover, to effectively obtain a set of solutions to cover the PFs of these problem, MOEA/D-C only needs to decompose these MOPs into several subproblems with a set of simple weight vectors while MOEA/D-M needs to find Ω(n) optimally decomposed weight vectors. This result suggests that the use of crossover in decomposition-based MOEA can simplify the setting of weight vectors for different problems and make the algorithm more efficient. This paper provides some insights into the working principles of MOEA/D and explains why some existing decomposition-based MOEAs work well in computational experiments.

OxyR-activated expression of Dps is important for Vibrio cholerae oxidative stress resistance and pathogenesis.

Vibrio cholerae is the causative agent of cholera, a dehydrating diarrheal disease. This Gram-negative pathogen is able to modulate its gene expression in order to combat stresses encountered in both aquatic and host environments, including stress posed by reactive oxygen species (ROS). In order to further the understanding of V. cholerae's transcriptional response to ROS, we performed an RNA sequencing analysis to determine the transcriptional profile of V. cholerae when exposed to hydrogen hydroperoxide. Of 135 differentially expressed genes, VC0139 was amongst the genes with the largest induction. VC0139 encodes a protein homologous to the DPS (DNA-binding protein from starved cells) protein family, which are widely conserved and are implicated in ROS resistance in other bacteria. Using a promoter reporter assay, we show that during exponential growth, dps is induced by H2O2 in a manner dependent on the ROS-sensing transcriptional regulator, OxyR. Upon entry into stationary phase, the major stationary phase regulator RpoS is required to transcribe dps. Deletion of dps impaired V. cholerae resistance to both inorganic and organic hydroperoxides. Furthermore, we show that Dps is involved in resistance to multiple environmental stresses. Finally, we found that Dps is important for V. cholerae adult mouse colonization, but becomes dispensable in the presence of antioxidants. Taken together, our results suggest that Dps plays vital roles in both V. cholerae stress resistance and pathogenesis.

Structural and Functional Characterization of the FadR Regulatory Protein from Vibrio alginolyticus.

The structure of Vibrio cholerae FadR (VcFadR) complexed with the ligand oleoyl-CoA suggests an additional ligand-binding site. However, the fatty acid metabolism and its regulation is poorly addressed in Vibrio alginolyticus, a species closely-related to V. cholerae. Here, we show crystal structures of V. alginolyticus FadR (ValFadR) alone and its complex with the palmitoyl-CoA, a long-chain fatty acyl ligand different from the oleoyl-CoA occupied by VcFadR. Structural comparison indicates that both VcFadR and ValFadR consistently have an additional ligand-binding site (called site 2), which leads to more dramatic conformational-change of DNA-binding domain than that of the E. coli FadR (EcFadR). Isothermal titration calorimetry (ITC) analyses defines that the ligand-binding pattern of ValFadR (2:1) is distinct from that of EcFadR (1:1). Together with surface plasmon resonance (SPR), electrophoresis mobility shift assay (EMSA) demonstrates that ValFadR binds fabA, an important gene of unsaturated fatty acid (UFA) synthesis. The removal of fadR from V. cholerae attenuates fabA transcription and results in the unbalance of UFA/SFA incorporated into membrane phospholipids. Genetic complementation of the mutant version of fadR (Δ42, 136-177) lacking site 2 cannot restore the defective phenotypes of ΔfadR while the wild-type fadR gene and addition of exogenous oleate can restore them. Mice experiments reveals that VcFadR and its site 2 have roles in bacterial colonizing. Together, the results might represent an additional example that illustrates the Vibrio FadR-mediated lipid regulation and its role in pathogenesis.

Performance Analysis of Evolutionary Algorithms for Steiner Tree Problems.

The Steiner tree problem (STP) aims to determine some Steiner nodes such that the minimum spanning tree over these Steiner nodes and a given set of special nodes has the minimum weight, which is NP-hard. STP includes several important cases. The Steiner tree problem in graphs (GSTP) is one of them. Many heuristics have been proposed for STP, and some of them have proved to be performance guarantee approximation algorithms for this problem. Since evolutionary algorithms (EAs) are general and popular randomized heuristics, it is significant to investigate the performance of EAs for STP. Several empirical investigations have shown that EAs are efficient for STP. However, up to now, there is no theoretical work on the performance of EAs for STP. In this article, we reveal that the (1+1) EA achieves 3/2-approximation ratio for STP in a special class of quasi-bipartite graphs in expected runtime [Formula: see text], where [Formula: see text], [Formula: see text], and [Formula: see text] are, respectively, the number of Steiner nodes, the number of special nodes, and the largest weight among all edges in the input graph. We also show that the (1+1) EA is better than two other heuristics on two GSTP instances, and the (1+1) EA may be inefficient on a constructed GSTP instance.

Calcium Enhances Bile Salt-Dependent Virulence Activation in Vibrio cholerae.

Vibrio cholerae is the causative bacteria of the diarrheal disease cholera, but it also persists in aquatic environments, where it displays an expression profile that is distinct from that during infection. Upon entry into the host, a tightly regulated circuit coordinates the induction of two major virulence factors: cholera toxin and a toxin-coregulated pilus (TCP). It has been shown that a set of bile salts, including taurocholate, serve as host signals to activate V. cholerae virulence through inducing the activity of the transmembrane virulence regulator TcpP. In this study, we investigated the role of calcium, an abundant mental ion in the gut, in the regulation of virulence. We show that whereas Ca2+ alone does not affect virulence, Ca2+ enhances bile salt-dependent virulence activation for V. cholerae The induction of TCP by murine intestinal contents is counteracted when Ca2+ is depleted by the high-affinity calcium chelator EGTA, suggesting that the calcium present in the gut is a relevant signal for V. cholerae virulence induction in vivo We further show that Ca2+ enhances virulence by promoting bile salt-induced TcpP-TcpP interaction. Moreover, fluorescence recovery after photobleaching (FRAP) analysis demonstrated that exposure to bile salts and Ca2+ together decreases the recovery rate for fluorescently labeled TcpP, but not for another inner membrane protein (TatA). Together, these data support a model in which physiological levels of Ca2+ may result in altered bile salt-induced TcpP protein movement and activity, ultimately leading to an increased expression of virulence.