Magnetic structures of RbCuCl_3 in a transverse field

A recent high-field magnetization experiment found a phase transition of unknown character in the layered, frustrated antiferromagnet RbCuCl_3, in a transverse field (in the layers). Motivated by these results, we have examined the magnetic structures predicted by a model of RbCuCl_3, using the classical approximation. At small fields, we obtain the structure already known to be optimal, an incommensurate (IC) spiral with wave vector q in the layers. At higher fields, we find a staircase of long-period commensurate (C) phases (separated initially by the low-field IC phase), then two narrow IC phases, then a fourth IC phase (also with intermediate C phases), and finally the ferromagnetically aligned phase at the saturation field H_S. The three-sublattice C states familiar from the theory of the triangular antiferromagnet are never optimal. The C phases and the two intermediate IC phases were previously unknown in this context. The magnetization is discontinuous at a field \approx 0.4H_S, in qualitative agreement with experiment, though we find much fine structure not reported.Comment: 9 pages, 8 figure

Oblique triangular antiferromagnetic phase in CsCu1−x_{1-x}Cox_xCl3_3

The spin-1/2 stacked triangular antiferromagnet CsCu$_{1-x}$Co$_x$Cl$_3$ with $0.015<x<0.032$ undergoes two phase transitions at zero field. The low-temperature phase is produced by the small amount of Co$^{2+}$ doping. In order to investigate the magnetic structures of the two ordered phases, the neutron elastic scattering experiments have been carried out for the sample with $x\approx 0.03$. It is found that the intermediate phase is identical to the ordered phase of CsCuCl$_3$, and that the low-temperature phase is an oblique triangular antiferromagnetic phase in which the spins form a triangular structure in a plane tilted from the basal plane. The tilting angle which is 42$^{\circ}$ at $T=1.6$ K decreases with increasing temperature, and becomes zero at $T_{\rm N2} =7.2$ K. An off-diagonal exchange term is proposed as the origin of the oblique phase.Comment: 6 pages, 7 figure

Fluctuation-induced phase in CsCuCl3 in transverse magnetic field: Theory

CsCuCl3 is a quantum triangular antiferromagnet, ferromagnetically stacked, with an incommensurate (IC) structure due to a Dzyaloshinskii-Moriya interaction. Because of the classical degeneracy caused by the frustration, fluctuations in CsCuCl3 have extraordinarily large effects, such as the phase transition in longitudinal magnetic field (normal to the planes, parallel to the IC wavenumber q) and the plateau in q in transverse field (perpendicular to q). We argue that fluctuations are responsible also for the new IC phase discovered in transverse field near the Neel temperature T_N, by T. Werner et al. [Solid State Commun. 102, p.609 (1997)]. We develop and analyse the corresponding minimal Landau theory; the effects of fluctuations on the frustration are included phenomenologically, by means of a biquadratic term. The Landau theory gives two IC phases, one familiar from previous studies; properties of the new IC phase, which occupies a pocket of the temperature-field phase diagram near T_N, agree qualitatively with those of the new phase found experimentally.Comment: 12 pages, revtex, 4 postscript figures, submitted to J. Phys: Condens. Matte

Electronic structure of Co_xTiSe_2 and Cr_xTiSe_2

The results of investigations of intercalated compounds Cr_xTiSe_2 and Co_xTiSe_2 by X-ray photoelectron spectroscopy (XPS) and X-ray emission spectroscopy (XES) are presented. The data obtained are compared with theoretical results of spin-polarized band structure calculations. A good agreement between theoretical and experimental data for the electronic structure of the investigated materials has been observed. The interplay between the M3d--Ti3d hybridization (M=Cr, Co) and the magnetic moment at the M site is discussed. A 0.9 eV large splitting of the core Cr2p{3/2} level was observed, which reveals a strong exchange magnetic interaction of 3d-2p electrons of Cr. In the case of a strong localization of the Cr3d electrons (for x<0.25), the broadening of the CrL spectra into the region of the states above the nominal Fermi level was observed and attributed to X-ray re-emission. The measured kinetic properties are in good accordance with spectral investigations and band calculation results.Comment: 14 pages, 11 figures, submitted to Phys.Rev.

Hypoxia Impairs Primordial Germ Cell Migration in Zebrafish (Danio rerio) Embryos

Background: As a global environmental concern, hypoxia is known to be associated with many biological and physiological impairments in aquatic ecosystems. Previous studies have mainly focused on the effect of hypoxia in adult animals. However, the effect of hypoxia and the underlying mechanism of how hypoxia affects embryonic development of aquatic animals remain unclear. Methodology/Principal Findings: In the current study, the effect of hypoxia on primordial germ cell (PGC) migration in zebrafish embryos was investigated. Hypoxic embryos showed PGC migration defect as indicated by the presence of mis-migrated ectopic PGCs. Insulin-like growth factor (IGF) signaling is required for embryonic germ line development. Using real-time PCR, we found that the mRNA expression levels of insulin-like growth factor binding protein (IGFBP-1), an inhibitor of IGF bioactivity, were significantly increased in hypoxic embryos. Morpholino knockdown of IGFBP-1 rescued the PGC migration defect phenotype in hypoxic embryos, suggesting the role of IGFBP-1 in inducing PGC mis-migration. Conclusions/Significance: This study provides novel evidence that hypoxia disrupts PGC migration during embryonic development in fish. IGF signaling is shown to be one of the possible mechanisms for the causal link between hypoxia and PGC migration. We propose that hypoxia causes PGC migration defect by inhibiting IGF signaling through the induction of IGFBP-1

Evidence for a lack of a direct transcriptional suppression of the iron regulatory peptide hepcidin by hypoxia-inducible factors.

BACKGROUND: Hepcidin is a major regulator of iron metabolism and plays a key role in anemia of chronic disease, reducing intestinal iron uptake and release from body iron stores. Hypoxia and chemical stabilizers of the hypoxia-inducible transcription factor (HIF) have been shown to suppress hepcidin expression. We therefore investigated the role of HIF in hepcidin regulation. METHODOLOGY/PRINCIPAL FINDINGS: Hepcidin mRNA was down-regulated in hepatoma cells by chemical HIF stabilizers and iron chelators, respectively. In contrast, the response to hypoxia was variable. The decrease in hepcidin mRNA was not reversed by HIF-1alpha or HIF-2alpha knock-down or by depletion of the HIF and iron regulatory protein (IRP) target transferrin receptor 1 (TfR1). However, the response of hepcidin to hypoxia and chemical HIF inducers paralleled the regulation of transferrin receptor 2 (TfR2), one of the genes critical to hepcidin expression. Hepcidin expression was also markedly and rapidly decreased by serum deprivation, independent of transferrin-bound iron, and by the phosphatidylinositol 3 (PI3) kinase inhibitor LY294002, indicating that growth factors are required for hepcidin expression in vitro. Hepcidin promoter constructs mirrored the response of mRNA levels to interleukin-6 and bone morphogenetic proteins, but not consistently to hypoxia or HIF stabilizers, and deletion of the putative HIF binding motifs did not alter the response to different hypoxic stimuli. In mice exposed to carbon monoxide, hypoxia or the chemical HIF inducer N-oxalylglycine, liver hepcidin 1 mRNA was elevated rather than decreased. CONCLUSIONS/SIGNIFICANCE: Taken together, these data indicate that hepcidin is neither a direct target of HIF, nor indirectly regulated by HIF through induction of TfR1 expression. Hepcidin mRNA expression in vitro is highly sensitive to the presence of serum factors and PI3 kinase inhibition and parallels TfR2 expression

Transcription Regulation of Sex-Biased Genes during Ontogeny in the Malaria Vector Anopheles gambiae

In Anopheles gambiae, sex-regulated genes are responsible for controlling gender dimorphism and are therefore crucial in determining the ability of female mosquitoes to transmit human malaria. The identification and functional characterization of these genes will shed light on the sexual development and maturation of mosquitoes and provide useful targets for genetic control measures aimed at reducing mosquito fertility and/or distorting the sex ratio

Duplication and Diversification of the Hypoxia-Inducible IGFBP-1 Gene in Zebrafish

Gene duplication is the primary force of new gene evolution. Deciphering whether a pair of duplicated genes has evolved divergent functions is often challenging. The zebrafish is uniquely positioned to provide insight into the process of functional gene evolution due to its amenability to genetic and experimental manipulation and because it possess a large number of duplicated genes.We report the identification and characterization of two hypoxia-inducible genes in zebrafish that are co-ortholgs of human IGF binding protein-1 (IGFBP-1). IGFBP-1 is a secreted protein that binds to IGF and modulates IGF actions in somatic growth, development, and aging. Like their human and mouse counterparts, in adult zebrafish igfbp-1a and igfbp-1b are exclusively expressed in the liver. During embryogenesis, the two genes are expressed in overlapping spatial domains but with distinct temporal patterns. While zebrafish IGFBP-1a mRNA was easily detected throughout embryogenesis, IGFBP-1b mRNA was detectable only in advanced stages. Hypoxia induces igfbp-1a expression in early embryogenesis, but induces the igfbp-1b expression later in embryogenesis. Both IGFBP-1a and -b are capable of IGF binding, but IGFBP-1b has much lower affinities for IGF-I and -II because of greater dissociation rates. Overexpression of IGFBP-1a and -1b in zebrafish embryos caused significant decreases in growth and developmental rates. When tested in cultured zebrafish embryonic cells, IGFBP-1a and -1b both inhibited IGF-1-induced cell proliferation but the activity of IGFBP-1b was significantly weaker.These results indicate subfunction partitioning of the duplicated IGFBP-1 genes at the levels of gene expression, physiological regulation, protein structure, and biological actions. The duplicated IGFBP-1 may provide additional flexibility in fine-tuning IGF signaling activities under hypoxia and other catabolic conditions

Infectious Speciation Revisited: Impact of Symbiont-Depletion on Female Fitness and Mating Behavior of Drosophila paulistorum

The neotropical Drosophila paulistorum superspecies, consisting of at least six geographically overlapping but reproductively isolated semispecies, has been the object of extensive research since at least 1955, when it was initially trapped mid-evolution in flagrant statu nascendi. In this classic system females express strong premating isolation patterns against mates belonging to any other semispecies, and yet uncharacterized microbial reproductive tract symbionts were described triggering hybrid inviability and male sterility. Based on theoretical models and limited experimental data, prime candidates fostering symbiont-driven speciation in arthropods are intracellular bacteria belonging to the genus Wolbachia. They are maternally inherited symbionts of many arthropods capable of manipulating host reproductive biology for their own benefits. However, it is an ongoing debate as to whether or not reproductive symbionts are capable of driving host speciation in nature and if so, to what extent. Here we have reevaluated this classic case of infectious speciation by means of present day molecular approaches and artificial symbiont depletion experiments. We have isolated the α-proteobacteria Wolbachia as the maternally transmitted core endosymbionts of all D. paulistorum semispecies that have coevolved towards obligate mutualism with their respective native hosts. In hybrids, however, these mutualists transform into pathogens by overreplication causing embryonic inviability and male sterility. We show that experimental reduction in native Wolbachia titer causes alterations in sex ratio, fecundity, and mate discrimination. Our results indicate that formerly designated Mycoplasma-like organisms are most likely Wolbachia that have evolved by becoming essential mutualistic symbionts in their respective natural hosts; they have the potential to trigger pre- and postmating isolation. Furthermore, in light of our new findings, we revisit the concept of infectious speciation and discuss potential mechanisms that can restrict or promote symbiont-induced speciation at post- and prezygotic levels in nature and under artificial laboratory conditions