Anion directed cation templated synthesis of three ternary copper(II) complexes with a monocondensed N2O donor Schiff base and different pseudohalides

Three copper(II) complexes, [Cu2(L)2(μ1,1-N3)2] (1), [Cu2(L)2(μ1,1-NCO)2] (2) and [Cu(L)(μ1,5-dca)]n (3), where HL is a tridentate mono-condensed Schiff base, 1-(2-aminoethyliminomethyl)naphthalen-2-ol, and dca is dicyanamide, have been prepared and characterized by elemental analysis, IR, UV–Vis and fluorescence spectroscopy and single crystal X-ray diffraction studies. The Schiff base ligand was prepared by a counter anion mediated copper(II) templated synthesis. The azide ligand in complex 1 and the cyanate ligand in complex 2 show μ-1,1 bridging modes, whereas the dca ligand shows the μ-1,5 bridging mode in complex 3. Three equatorial positions of copper(II) are occupied by the tridentate Schiff bases in all three complexes. The fourth equatorial sites are occupied by nitrogen atoms of azide in 1, cyanate in 2 and dca in 3. Another nitrogen atom from a symmetry related pseudohalide coordinates in the axial position of copper(II) to complete its square pyramidal geometry in each of the complexes. Significant supramolecular interactions are observed in all the complexes. Variable temperature magnetic measurements indicate antiferromagnetic interactions between the copper(II) centres in all three complexes

(S S,2S,3R)-2-(2-Methyl­propane-2-sulfin­amido)-3-phenyl­butyronitrile

The absolute configuration has been determined for the title compound, C14H20N2OS. Inter­molecular N—H⋯O hydrogen bonds are observed in the crystal packing, forming infinitive one-dimensional chains with the base vector [100]

End-on cyanate or end-to-end thiocyanate bridged dinuclear copper(II) complexes with a tridentate Schiff base blocking ligand: Synthesis, structure and magnetic studies

Two dinuclear copper(II) complexes, [Cu2(L)2(1,1-NCO)2] (1) and [Cu2(L)2(1,3-NCS)2]H2ODMF (2) have been synthesized using a tridentate N2O donor Schiff base ligand (HL) [1((2-(ethylamino)ethylimino)methyl)naphthalen-2-ol] and characterized by elemental analysis, spectral study and X-ray crystallography. Both complexes are centrosymmetric dimers in which square pyramidal copper(II) centres are connected by pseudo-halides; end-on cyanate in 1 and end-to-end (EE) thiocyanate in 2. Variable temperature (2–300 K) magnetic susceptibility measurements indicate the presence of ferromagnetic exchange coupling between copper(II) centres in complex 1 (J = 0.97 cm-1), and antiferromagnetic exchange coupling in 2 (J = - 0.6 cm–1)

rac-3-[(Anilino)(naphthalen-2-yl)­methyl]thian-4-one

In the title compound, C22H21NOS, the thio­pyran­one ring adopts a chair-like conformation with the substituent in the axial position. The relative configuration of the racemic compound is 3R,7S according to the numbering scheme used in this publication. In the crystal packing, centrosymmetric dimers are built up via N—H⋯O hydrogen bonds, with graph set R 2 2(8)

Testing for the fitness benefits of natural transformation during community-embedded evolution

Natural transformation is a process where bacteria actively take up DNA from the environment and recombine it into their genome or reconvert it into extra-chromosomal genetic elements. The evolutionary benefits of transformation are still under debate. One main explanation is that foreign allele and gene uptake facilitates natural selection by increasing genetic variation, analogous to meiotic sex. However, previous experimental evolution studies comparing fitness gains of evolved transforming- and isogenic non-transforming strains have yielded mixed support for the ‘sex hypothesis.’ Previous studies testing the sex hypothesis for natural transformation have largely ignored species interactions, which theory predicts provide conditions favourable to sex. To test for the adaptive benefits of bacterial transformation, the naturally transformable wild-type Acinetobacter baylyi and a transformation-deficient ∆comA mutant were evolved for 5weeks. To provide strong and potentially fluctuating selection, A. baylyi was embedded in a community of five other bacterial species. DNA from a pool of different Acinetobacter strains was provided as a substrate for transformation. No effect of transformation ability on the fitness of evolved populations was found, with fitness increasing non-significantly in most treatments. Populations showed fitness improvement in their respective environments, with no apparent costs of adaptation to competing species. Despite the absence of fitness effects of transformation, wild-type populations evolved variable transformation frequencies that were slightly greater than their ancestor which potentially could be caused by genetic drift

Antimicrobial resistance acquisition via natural transformation: context is everything

Natural transformation is a process where bacterial cells actively take up free DNA from the environment and recombine it into their genome or reconvert it into extra-chromosomal genetic elements. Although this mechanism is known to mediate the uptake of antibiotic resistance determinants in a range of human pathogens, its importance in the spread of antimicrobial resistance is not always appreciated. This review highlights the context in which transformation takes place: in diverse microbiomes, in interaction with other forms of horizontal gene transfer and in increasingly polluted environments. This examination of the abiotic and biotic drivers of transformation reveals that it could be more important in the dissemination of resistance genes than is often recognised

rac-3-[(3-Chloro­anilino)(4-chloro­phenyl)meth­yl]thian-4-one

In the title compound, C18H17Cl2NOS, the thio­pyran­one ring adopts a chair conformation, with the substituent in the axial position. The dihedral angle between the two benzene rings is 89.43 (1)°. In the crystal, mol­ecules form inversion dimers through inter­molecular N—H⋯O hydrogen bonds [graph set R 2 2(8)]

catena-Poly[[[diaqua­(di-2-pyridylamine-κ2 N,N′)nickel(II)]-μ-fumarato-κ2 O 1:O 4] tetra­hydrate]

In the crystal structure of the title compound, {[Ni(C4H2O4)(C10H9N3)(H2O)2]·4H2O}n, zigzag chains are built up from cis-[Ni(dpya)(H2O)2]2+ cations (dpya is di-2-pyridylamine) linked by bis-monodentate coordinated bridging fumarate ligands. The NiII atom is coordinated by one chelating dpya ligand, two aqua ligands in trans positions and two monodentate fumarate ligands in cis positions in the form of a deformed octa­hedron. The water mol­ecules, O atoms of the fumarate carboxyl­ate groups and the amine group of the dpya ligand are involved in an extended network of intra- and inter­molecular O—H⋯O hydrogen bonds. Moreover, π–π inter­actions between the pyridine rings of the dpya ligand contribute to the stability of the structure. Two of the five uncoordinated water molecules are half-occupied

Evolutionary Instability of Collateral Susceptibility Networks in Ciprofloxacin-Resistant Clinical Escherichia coli Strains

ABSTRACT Collateral sensitivity and resistance occur when resistance development toward one antimicrobial either potentiates or deteriorates the effect of others. Previous reports on collateral effects on susceptibility focus on newly acquired resistance determinants and propose that novel treatment guidelines informed by collateral networks may reduce the evolution, selection, and spread of antimicrobial resistance. In this study, we investigate the evolutionary stability of collateral networks in five ciprofloxacin-resistant, clinical Escherichia coli strains. After 300 generations of experimental evolution without antimicrobials, we show complete fitness restoration in four of five genetic backgrounds and demonstrate evolutionary instability in collateral networks of newly acquired resistance determinants. We show that compensatory mutations reducing efflux expression are the main drivers destabilizing initial collateral networks and identify rpoS as a putative target for compensatory evolution. Our results add another layer of complexity to future predictions and clinical application of collateral networks. IMPORTANCE Antimicrobial resistance occurs due to genetic alterations that affect different processes in bacteria. Thus, developing resistance toward one antimicrobial drug may also alter the response toward others (collateral effects). Understanding the mechanisms of such collateral effects may provide clinicians with a framework for informed antimicrobial treatment strategies, limiting the emergence of antimicrobial resistance. However, for clinical implementation, it is important that the collateral effects of resistance development are repeatable and temporarily stable. Here, we show that collateral effects caused by resistance development toward ciprofloxacin in clinical Escherichia coli strains are not temporarily stable because of compensatory mutations restoring the fitness burden of the initial resistance mutations. Consequently, this instability is complicating the general applicability and clinical implementation of collateral effects into treatment strategies