A 0535+26 in the August/September 2005 outburst observed by RXTE and INTEGRAL

In this Letter we present results from INTEGRAL and RXTE observations of the spectral and timing behavior of the High Mass X-ray Binary A 0535+26 during its August/September 2005 normal (type I) outburst with an average flux F(5-100keV)~400mCrab. The search for cyclotron resonance scattering features (fundamental and harmonic) is one major focus of the paper. Our analysis is based on data from INTEGRAL and RXTE Target of Opportunity Observations performed during the outburst. The pulse period is determined. X-ray pulse profiles in different energy ranges are analyzed. The broad band INTEGRAL and RXTE pulse phase averaged X-ray spectra are studied. The evolution of the fundamental cyclotron line at different luminosities is analyzed. The pulse period P is measured to be 103.39315(5)s at MJD 53614.5137. Two absorption features are detected in the phase averaged spectra at E_1~45keV and E_2~100keV. These can be interpreted as the fundamental cyclotron resonance scattering feature and its first harmonic and therefore the magnetic field can be estimated to be B~4x10^12G.Comment: 4 pages, 5 figures, accepted for publication in A&A Letter

Resonant Spin Excitation in an Overdoped High Temperature Superconductor

An inelastic neutron scattering study of overdoped Bi_2Sr_2CaCu_2O_{8+\delta} $ (T_c = 83 K) has revealed a resonant spin excitation in the superconducting state. The mode energy is E_res=38 meV, significantly lower than in optimally doped Bi_2Sr_2CaCu_2O_{8+\delta} (T_c = 91 K, E_ res =43 meV). This observation, which indicates a constant ratio E_res /k_B T_c \sim 5.4, helps resolve a long-standing controversy about the origin of the resonant spin excitation in high-temperature superconductors.Comment: final version: PRL 86, 1610 (2001

Calmodulin Interaction with hEAG1 Visualized by FRET Microscopy

BACKGROUND: Ca(2+)-mediated regulation of ion channels provides a link between intracellular signaling pathways and membrane electrical activity. Intracellular Ca(2+) inhibits the voltage-gated potassium channel EAG1 through the direct binding of calmodulin (CaM). Three CaM binding sites (BD-C1: 674-683, BD-C2: 711-721, BD-N: 151-165) have been identified in a peptide screen and were proposed to mediate binding. The participation of the three sites in CaM binding to the native channel, however, remains unclear. METHODOLOGY/PRINCIPAL FINDINGS: Here we studied the binding of Ca(2+)/CaM to the EAG channel by visualizing the interaction between YFP-labeled CaM and Cerulean-labeled hEAG1 in mammalian cells by FRET. The results of our cellular approach substantiate that two CaM binding sites are predominantly involved; the high-affinity 1-8-14 based CaM binding domain in the N-terminus and the second C-terminal binding domain BD-C2. Mutations at these sites completely abolished CaM binding to hEAG1. CONCLUSIONS/SIGNIFICANCE: We demonstrated that the BD-N and BD-C2 binding domains are sufficient for CaM binding to the native channel, and, therefore, that BD-C1 is unable to bind CaM independently

Allele-specific demethylation at an imprinted mammalian promoter

A screen for imprinted genes on mouse Chromosome 7 recently identified Inpp5f_v2, a paternally expressed retrogene lying within an intron of Inpp5f. Here, we identify a novel paternally expressed variant of the Inpp5f gene (Inpp5f_v3) that shows a number of unusual features. Inpp5f_v3 initiates from a CpG-rich repeat region adjoining two B1 elements, despite previous reports that SINEs are generally excluded from imprinted promoters. Accordingly, we find that the Inpp5f_v3 promoter acquires methylation around the time of implantation, when many repeat families undergo de novo epigenetic silencing. Methylation is then lost specifically on the paternally derived allele during the latter stages of embryonic development, resulting in imprinted transcriptional activation on the demethylated allele. Methylation analyses in embryos lacking maternal methylation imprints suggest that the primary imprinting mark resides within an intronic CpG island ∼1 kb downstream of the Inpp5f_v3 transcriptional start site. These data support the hypothesis that SINEs can influence gene expression by attracting de novo methylation during development, a property likely to explain their exclusion from other imprinted promoters

Self‐pollination in island and mainland populations of the introduced hummingbird‐pollinated plant, Nicotiana glauca (Solanaceae)

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142032/1/ajb20672.pd

Population regulation in lake whitefish, Coregonus clupeaformis (Mitchill)

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73745/1/j.1095-8649.1981.tb03822.x.pd

Rest-Mediated Regulation of Extracellular Matrix Is Crucial for Neural Development

Neural development from blastocysts is strictly controlled by intricate transcriptional programmes that initiate the down-regulation of pluripotent genes, Oct4, Nanog and Rex1 in blastocysts followed by up-regulation of lineage-specific genes as neural development proceeds. Here, we demonstrate that the expression pattern of the transcription factor Rest mirrors those of pluripotent genes during neural development from embryonic stem (ES) cells and an early abrogation of Rest in ES cells using a combination of gene targeting and RNAi approaches causes defects in this process. Specifically, Rest ablation does not alter ES cell pluripotency, but impedes the production of Nestin+ neural stem cells, neural progenitor cells and neurons, and results in defective adhesion, decrease in cell proliferation, increase in cell death and neuronal phenotypic defects typified by a reduction in migration and neurite elaboration. We also show that these Rest-null phenotypes are due to the dysregulation of its direct or indirect target genes, Lama1, Lamb1, Lamc1 and Lama2 and that these aberrant phenotypes can be rescued by laminins

The Drosophila homolog of the mammalian imprint regulator, CTCF, maintains the maternal genomic imprint in Drosophila melanogaster

<p>Abstract</p> <p>Background</p> <p>CTCF is a versatile zinc finger DNA-binding protein that functions as a highly conserved epigenetic transcriptional regulator. CTCF is known to act as a chromosomal insulator, bind promoter regions, and facilitate long-range chromatin interactions. In mammals, CTCF is active in the regulatory regions of some genes that exhibit genomic imprinting, acting as insulator on only one parental allele to facilitate parent-specific expression. In <it>Drosophila</it>, CTCF acts as a chromatin insulator and is thought to be actively involved in the global organization of the genome.</p> <p>Results</p> <p>To determine whether CTCF regulates imprinting in <it>Drosophila</it>, we generated <it>CTCF </it>mutant alleles and assayed gene expression from the imprinted <it>Dp(1;f)LJ9 </it>mini-X chromosome in the presence of reduced <it>CTCF </it>expression. We observed disruption of the maternal imprint when <it>CTCF </it>levels were reduced, but no effect was observed on the paternal imprint. The effect was restricted to maintenance of the imprint and was specific for the <it>Dp(1;f)LJ9 </it>mini-X chromosome.</p> <p>Conclusions</p> <p>CTCF in <it>Drosophila </it>functions in maintaining parent-specific expression from an imprinted domain as it does in mammals. We propose that <it>Drosophila </it>CTCF maintains an insulator boundary on the maternal X chromosome, shielding genes from the imprint-induced silencing that occurs on the paternally inherited X chromosome.</p> <p>See commentary: <url>http://www.biomedcentral.com/1741-7007/8/104</url></p