261 research outputs found

    A Survey of Genomic Traces Reveals a Common Sequencing Error, RNA Editing, and DNA Editing

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    While it is widely held that an organism's genomic information should remain constant, several protein families are known to modify it. Members of the AID/APOBEC protein family can deaminate DNA. Similarly, members of the ADAR family can deaminate RNA. Characterizing the scope of these events is challenging. Here we use large genomic data sets, such as the two billion sequences in the NCBI Trace Archive, to look for clusters of mismatches of the same type, which are a hallmark of editing events caused by APOBEC3 and ADAR. We align 603,249,815 traces from the NCBI trace archive to their reference genomes. In clusters of mismatches of increasing size, at least one systematic sequencing error dominates the results (G-to-A). It is still present in mismatches with 99% accuracy and only vanishes in mismatches at 99.99% accuracy or higher. The error appears to have entered into about 1% of the HapMap, possibly affecting other users that rely on this resource. Further investigation, using stringent quality thresholds, uncovers thousands of mismatch clusters with no apparent defects in their chromatograms. These traces provide the first reported candidates of endogenous DNA editing in human, further elucidating RNA editing in human and mouse and also revealing, for the first time, extensive RNA editing in Xenopus tropicalis. We show that the NCBI Trace Archive provides a valuable resource for the investigation of the phenomena of DNA and RNA editing, as well as setting the stage for a comprehensive mapping of editing events in large-scale genomic datasets

    Higher-order multipole amplitudes in charmonium radiative transitions

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    Using 24 million ψ′≡ψ(2S)\psi' \equiv \psi(2S) decays in CLEO-c, we have searched for higher multipole admixtures in electric-dipole-dominated radiative transitions in charmonia. We find good agreement between our data and theoretical predictions for magnetic quadrupole (M2) amplitudes in the transitions ψ′→γχc1,2\psi' \to \gamma \chi_{c1,2} and χc1,2→γJ/ψ\chi_{c1,2} \to \gamma J/\psi, in striking contrast to some previous measurements. Let b2Jb_2^J and a2Ja_2^J denote the normalized M2 amplitudes in the respective aforementioned decays, where the superscript JJ refers to the angular momentum of the χcJ\chi_{cJ}. By performing unbinned maximum likelihood fits to full five-parameter angular distributions, we determine the ratios a2J=1/a2J=2=0.67−0.13+0.19a_2^{J=1}/a_2^{J=2} = 0.67^{+0.19}_{-0.13} and a2J=1/b2J=1=−2.27−0.99+0.57a_2^{J=1}/b_2^{J=1} = -2.27^{+0.57}_{-0.99}, where the theoretical predictions are independent of the charmed quark magnetic moment and are a2J=1/a2J=2=0.676±0.071a_2^{J=1}/a_2^{J=2} = 0.676 \pm 0.071 and a2J=1/b2J=1=−2.27±0.16a_2^{J=1}/b_2^{J=1} = -2.27 \pm 0.16.Comment: 32 pages, 7 figures, acceptance updat

    Charmonium decays to gamma pi0, gamma eta, and gamma eta'

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    Using data acquired with the CLEO-c detector at the CESR e+e- collider, we measure branching fractions for J/psi, psi(2S), and psi(3770) decays to gamma pi0, gamma eta, and gamma eta'. Defining R_n = B[ psi(nS)-->gamma eta ]/B[ psi(nS)-->gamma eta' ], we obtain R_1 = (21.1 +- 0.9)% and, unexpectedly, an order of magnitude smaller limit, R_2 < 1.8% at 90% C.L. We also use J/psi-->gamma eta' events to determine branching fractions of improved precision for the five most copious eta' decay modes.Comment: 14 pages, available through http://www.lns.cornell.edu/public/CLNS/, published in Physical Review

    Precision Measurement of B(D+ -> mu+ nu) and the Pseudoscalar Decay Constant fD+

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    We measure the branching ratio of the purely leptonic decay of the D+ meson with unprecedented precision as B(D+ -> mu+ nu) = (3.82 +/- 0.32 +/- 0.09)x10^(-4), using 818/pb of data taken on the psi(3770) resonance with the CLEO-c detector at the CESR collider. We use this determination to derive a value for the pseudoscalar decay constant fD+, combining with measurements of the D+ lifetime and assuming |Vcd| = |Vus|. We find fD+ = (205.8 +/- 8.5 +/- 2.5) MeV. The decay rate asymmetry [B(D+ -> mu+ nu)-B(D- -> mu- nu)]/[B(D+ -> mu+ nu)+B(D- -> mu- nu)] = 0.08 +/- 0.08, consistent with no CP violation. We also set 90% confidence level upper limits on B(D+ -> tau+ nu) < 1.2x10^(-3) and B(D+ -> e+ nu) < 8.8x10^(-6).Comment: 24 pages, 11 figures and 6 tables, v2 replaced some figure vertical axis scales, v3 corrections from PRD revie

    Precision Measurement of the Mass of the h_c(1P1) State of Charmonium

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    A precision measurement of the mass of the h_c(1P1) state of charmonium has been made using a sample of 24.5 million psi(2S) events produced in e+e- annihilation at CESR. The reaction used was psi(2S) -> pi0 h_c, pi0 -> gamma gamma, h_c -> gamma eta_c, and the reaction products were detected in the CLEO-c detector. Data have been analyzed both for the inclusive reaction and for the exclusive reactions in which eta_c decays are reconstructed in fifteen hadronic decay channels. Consistent results are obtained in the two analyses. The averaged results of the present measurements are M(h_c)=3525.28+-0.19 (stat)+-0.12(syst) MeV, and B(psi(2S) -> pi0 h_c)xB(h_c -> gamma eta_c)= (4.19+-0.32+-0.45)x10^-4. Using the 3PJ centroid mass, Delta M_hf(1P)= - M(h_c) = +0.02+-0.19+-0.13 MeV.Comment: 9 pages, available through http://www.lns.cornell.edu/public/CLNS/, submitted to PR

    J/psi and psi(2S) Radiative Transitions to eta_c

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    Using 24.5 million psi(2S) decays collected with the CLEO-c detector at CESR we present the most precise measurements of magnetic dipole transitions in the charmonium system. We measure B(psi(2S)->gamma eta_c) = (4.32+/-0.16+/-0.60)x10^-3, B(J/psi->gamma eta_c)/B(psi(2S)->gamma eta_c) = 4.59+/-0.23+/-0.64, and B(J/psi->gamma eta_c) = (1.98+/-0.09+/-0.30)%. We observe a distortion in the eta_c line shape due to the photon-energy dependence of the magnetic dipole transition rate. We find that measurements of the eta_c mass are sensitive to the line shape, suggesting an explanation for the discrepancy between measurements of the eta_c mass in radiative transitions and other production mechanisms.Comment: 11 pages, 3 figure

    Inclusive chi_bJ(nP) Decays to D0 X

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    Using Upsilon(2S) and Upsilon(3S) data collected with the CLEO III detector we have searched for decays of chi_bJ to final states with open charm. We fully reconstruct D0 mesons with p_D0 > 2.5 GeV/c in three decay modes (K-pi+, K-pi+pi0, and K-pi-pi+pi+) in coincidence with radiative transition photons that tag the production of one of the chi_bJ(nP) states. We obtain significant signals for the two J=1 states. Recent NRQCD calculations of chi_{bJ}(nP) --> c cbar X depend on one non-perturbative parameter per chi_bJ triplet. The extrapolation from the observed D0 X rate over a limited momentum range to a full c cbar X rate also depends on these same parameters. Using our data to fit for these parameters, we extract results which agree well with NRQCD predictions, confirming the expectation that charm production is largest for the J=1 states. In particular, for J=1, our results are consistent with c cbar g accounting for about one-quarter of all hadronic decays.Comment: Version 2 updates include corrections to important errors in Table V and VII column headers which summarize results, and additional minor edits. 17 pages, available through http://www.lns.cornell.edu/public/CLNS

    DNA deaminases: AIDing hormones in immunity and cancer

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    It is well established that hormones can cause cancer, much less known is how they induce this change in our somatic cells. This review highlights the recent finding that estrogen can exert its DNA-damaging potential by directly activating DNA deaminases. This recently discovered class of proteins deaminate cytosine to uracil in DNA, and are essential enzymes in the immune system. The enhanced production of a given DNA deaminase, induced by estrogen, can lead not only to a more active immune response, but also to an increase in mutations and oncogenic translocations. Identifying the direct molecular link between estrogen and a mutation event provides us with new targets for studying and possibly inhibiting the pathological side-effects of estrogen
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