Surface-enhanced Raman scattering (SERS) is commonly associated with noble metal substrates. However, over the years modest Raman enhancements (<104) have also been observed in semiconductor substrates. This enhancement stems predominantly from the excitonic resonance of the semiconductors. The use of two-dimensional semiconductors with large excitonic oscillator strength provides an attractive pathway to further enhance this effect. Here we report for the first time a >3 × 105 enhancement in SERS signal from an organic molecule (4-mercaptopyridine) placed in the near field of a two-dimensional semiconductor molybdenum disulfide (MoS2) monolayer. This large enhancement in the SERS signal is attributed to the charge transfer (CT) state formed at the interface of the 2D semiconductor and organic molecule and is found to occur when the excitation source is chosen to be in resonance with the CT state. This approach provides a new strategy for carrying out SERS experiments on molecules with very weak Raman signatures without the need for nanopatterning.

This paper presenfs the research and development of a daily imaging scheduling sysfem for a low-orbit, earth observation satellite. This satellite daily imaging schedulingproblem belongs lo a class of singlemachine scheduling problems wifh salient features of sequence-dependent setup effects, job-assembly characteristics, and time window constraints. If is NPhard in camputational camplexity. We adopt Loqangian relaxation and linear search techniques lo solve this problem. Numerical resulfs demonstrate that this approach is eficienf in applicotions to the real problems. It is .very effecfive to generafe a near-optimal, feasible schedule for the. imaging operations of the satellife.

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Bacteria and archaea acquire resistance to foreign genetic elements by integrating fragments of foreign DNA into CRISPR (clustered regularly interspaced short palindromic repeats) loci. In Escherichia coli, CRISPR-derived RNAs (crRNAs) assemble with Cas proteins into a multi-subunit surveillance complex called Cascade (CRISPR-associated complex for antiviral defense). Cascade recognizes DNA targets via protein-mediated recognition of a protospacer adjacent motif and complementary base pairing between the crRNA spacer and the DNA target. Previously determined structures of Cascade showed that the crRNA is stretched along an oligomeric protein assembly, leading us to ask how crRNA length impacts the assembly and function of this complex. We found that extending the spacer portion of the crRNA resulted in larger Cascade complexes with altered stoichiometry and preserved in vitro binding affinity for target DNA. Longer spacers also preserved the in vivo ability of Cascade to repress target gene expression and to recruit the Cas3 endonuclease for target degradation. Finally, longer spacers exhibited enhanced silencing at particular target locations and were sensitive to mismatches within the extended region. These findings demonstrate the flexibility of the Type I-E CRISPR machinery and suggest that spacer length can be modified to fine-tune Cascade activity.

b Polymyxins, which are increasingly being used to treat infections caused by multidrug-resistant bacteria, perform poorly against Serratia marcescens. To investigate the underlying mechanisms, Tn5 mutagenesis was performed and two mutants exhibiting increased polymyxin B (PB) susceptibility were isolated. The mutants were found to have Tn5 inserted into the arnB and arnC genes. In other bacteria, arnB and arnC belong to the seven-gene arn operon, which is involved in lipopolysaccharide (LPS) modification. LPSs of arn mutants had greater PB-binding abilities than that of wild-type LPS. Further, we identified PhoP, a bacterial two-component response regulator, as a regulator of PB susceptibility in S. marcescens. By the reporter assay, we found PB-and low-Mg 2؉ -induced expression of phoP and arn in the wild-type strain but not in the phoP mutant. Complementation of the phoP mutant with the full-length phoP gene restored the PB MIC and induction by PB and low Mg 2؉ levels, as in the wild type. An electrophoretic mobility shift assay (EMSA) further demonstrated that PhoP bound directly to the arn promoter. The PB challenge test confirmed that pretreatment with PB and low Mg 2؉ levels protected S. marcescens from a PB challenge in the wild-type strain but not in the phoP mutant. Real-time reverse transcriptase-PCR also indicated that PB serves as a signal to regulate expression of ugd, a gene required for LPS modification, in S. marcescens through a PhoP-dependent pathway. Finally, we found that PB-resistant clinical isolates displayed greater expression of arnA upon exposure to PB than did susceptible isolates. This is the first report to describe the role of S. marcescens arn in PB resistance and its modulation by PB and Mg 2؉ through the PhoP protein.