We demonstrate experimentally that a photonic crystal made of Al_{2}O_{3} cylinders exhibits topological time-reversal symmetric electromagnetic propagation, similar to the quantum spin Hall effect in electronic systems. A pseudospin degree of freedom in the electromagnetic system representing different states of orbital angular momentum arises due to a deformation of the photonic crystal from the ideal honeycomb lattice. It serves as the photonic analogue to the electronic Kramers pair. We visualized qualitatively and measured quantitatively that microwaves of a specific pseudospin propagate only in one direction along the interface between a topological photonic crystal and a trivial one. As only a conventional dielectric material is used and only local real-space manipulations are required, our scheme can be extended to visible light to inspire many future applications in the field of photonics and beyond.
BackgroundLyme disease is caused by spirochete bacteria from the Borrelia burgdorferi sensu lato (B. burgdorferi s.l.) species complex. To reconstruct the evolution of B. burgdorferi s.l. and identify the genomic basis of its human virulence, we compared the genomes of 23 B. burgdorferi s.l. isolates from Europe and the United States, including B. burgdorferi sensu stricto (B. burgdorferi s.s., 14 isolates), B. afzelii (2), B. garinii (2), B. “bavariensis” (1), B. spielmanii (1), B. valaisiana (1), B. bissettii (1), and B. “finlandensis” (1).ResultsRobust B. burgdorferi s.s. and B. burgdorferi s.l. phylogenies were obtained using genome-wide single-nucleotide polymorphisms, despite recombination. Phylogeny-based pan-genome analysis showed that the rate of gene acquisition was higher between species than within species, suggesting adaptive speciation. Strong positive natural selection drives the sequence evolution of lipoproteins, including chromosomally-encoded genes 0102 and 0404, cp26-encoded ospC and b08, and lp54-encoded dbpA, a07, a22, a33, a53, a65. Computer simulations predicted rapid adaptive radiation of genomic groups as population size increases.ConclusionsIntra- and inter-specific pan-genome sizes of B. burgdorferi s.l. expand linearly with phylogenetic diversity. Yet gene-acquisition rates in B. burgdorferi s.l. are among the lowest in bacterial pathogens, resulting in high genome stability and few lineage-specific genes. Genome adaptation of B. burgdorferi s.l. is driven predominantly by copy-number and sequence variations of lipoprotein genes. New genomic groups are likely to emerge if the current trend of B. burgdorferi s.l. population expansion continues.
Comparative genomics of closely related bacterial isolates is a powerful method for uncovering virulence and other important genome elements. We determined draft sequences (8-fold coverage) of the genomes of strains JD1 and N40 of Borrelia burgdorferi sensu stricto, the causative agent of Lyme disease, and we compared the predicted genes from the two genomes with those from the previously sequenced B31 genome. The three genomes are closely related and are evolutionarily approximately equidistant (Ϸ0.5% pairwise nucleotide differences on the main chromosome). We used a Poisson model of nucleotide substitution to screen for genes with elevated levels of nucleotide polymorphisms. The three-way genome comparison allowed distinction between polymorphisms introduced by mutations and those introduced by recombination using the method of phylogenetic partitioning. Tests for recombination suggested that patches of high-density nucleotide polymorphisms on the chromosome and plasmids arise by DNA exchange. The role of recombination as the main mechanism driving B. burgdorferi diversification was confirmed by multilocus sequence typing of 18 clinical isolates at 18 polymorphic loci. A strong linkage between the multilocus sequence genotypes and the major alleles of outer-surface protein C (ospC) suggested that balancing selection at ospC is a dominant force maintaining B. burgdorferi diversity in local populations. We conclude that B. burgdorferi undergoes genome-wide genetic exchange, including plasmid transfers, and previous reports of its clonality are artifacts from the use of geographically and ecological isolated samples. Frequent recombination implies a potential for rapid adaptive evolution and a possible polygenic basis of B. burgdorferi pathogenicity.omparative genomics of closely related species is a powerful method for tracking microbial epidemics (1, 2), uncovering microbial virulence factors (3-5), and annotating genes and other conserved elements in genomes (6, 7). A powerful method of bacterial genotyping is multilocus sequence typing (MLST), which is the comparative sequencing of selected genes (5,(8)(9)(10). (Note that in this article by MLST we refer to the comparative sequencing of multiple loci at large, not necessarily housekeeping genes.) We have taken a comparative genomics approach to identify polymorphic ORFs in the genomes of Borrelia burgdorferi sensu stricto, which is the predominant bacterial species causing Lyme disease in North America (11). Measuring rates of sequence evolution and selective constraints (12, 13) is a means of uncovering virulence factors and candidates for vaccine, diagnostics, and therapeutics.Early population studies of B. burgdorferi using multilocus enzyme electrophoresis (MLEE) (14) and DNA sequences (15) found little evidence for genetic exchange among different isolates. In fact, one report (16) concluded that B. burgdorferi was among the most clonal of bacterial species. However, these studies were based on archival strains isolated from several worldwide locations, ...
The PCR and conventional library screening were used to clone the brain-specific somatostatin receptor rSSTR-4 from a rat genomic library. The deduced amino add sequence encodes a protein of 384 amino acids and displays structural and sequence homologies with members of the G protein-receptor superfamily. The , a cyclic tetradecapeptide, was originally isolated from ovine hypothalamus and found to have potent inhibitory effects on growth hormone and thyroidstimulating hormone secretion from the anterior pituitary (1, 2). SS-14 was subsequently found to have a widespread distribution, occurring primarily in the central nervous system and gut, where it exerts inhibitory effects on secretion, both exocrine and endocrine, as well as on neural function (3). As with many small peptides, SS-14 is synthesized as part of a larger precursor molecule, from which the mature hormone is proteolytically processed. In mammals, a single gene encodes the 92-amino acid common precursor to both SS-14 and somatostatin 28 (SS-28), a second biologically active NH2-terminally extended form of the tetradecapeptide (4).The inhibitory actions of SS-14 and SS-28 are initiated after binding to high-affinity receptors that have been identified on target tissues (5-9). SS-14 and SS-28 appear to exert their inhibitory effects by a dual mechanism involving receptor activation of Gi, the inhibitory guanine nucleotide-binding protein (10). In part, their effects are mediated through inhibition of stimulated adenylyl cyclase activity and reduction of cAMP production (11, 12). In addition, both peptides cause membrane hyperpolarization through effects on a voltage-dependent plasma-membrane potassium channel, leading to a decrease in Ca2+ influx and a reduction of cytosolic Ca2+ concentration (13
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