Mutation of SLC35D3 causes metabolic syndrome by impairing dopamine signaling in striatal D1 neurons

We thank Dr. Ya-Qin Feng from Shanxi Medical University, Dr. Tian-Yun Gao from Nanjing University and Dr. Yan-Hong Xue from Institute of Biophysics (CAS) for technical assistance in this study. We are very thankful to Drs. Richard T. Swank and Xiao-Jiang Li for their critical reading of this manuscript and invaluable advice. Funding: This work was partially supported by grants from National Basic Research Program of China (2013CB530605; 2014CB942803), from National Natural Science Foundation of China 1230046; 31071252; 81101182) and from Chinese Academy of Sciences (KSCX2-EW-R-05, KJZD-EW-L08). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewedPublisher PD

The Zur of Xanthomonas campestris functions as a repressor and an activator of putative zinc homeostasis genes via recognizing two distinct sequences within its target promoters

It has been long considered that zinc homeostasis in bacteria is maintained by export systems and uptake systems, which are separately controlled by their own regulators and the uptake systems are negatively regulated by Zur which binds to an about 30-bp AT-rich sequence known as Zur-box present in its target promoters to block the entry of RNA polymerase. Here, we demonstrated in vivo and in vitro that in addition to act as a repressor of putative Zn2+-uptake systems, the Zur of the bacterial phytopathogen Xanthomonas campestris pathovar campestris (Xcc) acts as an activator of a Zn2+ efflux pump. The Xcc Zur binds to a similar Zur-box with ∼30-bp AT-rich sequence in the promoters of the genes encoding putative Zn2+-uptake systems but a 59-bp GC-rich sequence with a 20-bp inverted repeat overlapping the promoter's −35 to −10 sequence of the gene encoding a Zn2+-export system. Mutagenesis of the inverted repeat sequence resulted in abolishment of the in vitro binding and the in vivo and in vitro activation of the export gene's promoter by Zur. These results reveal that the Xcc Zur functions as a repressor and an activator of putative zinc homeostasis genes via recognizing two distinct sequences within its target promoters

Measurements of the Mass and Full-Width of the ηc\eta_c Meson

In a sample of 58 million $J/\psi$ events collected with the BES II detector, the process J/$\psi\to\gamma\eta_c$ is observed in five different decay channels: $\gamma K^+K^-\pi^+\pi^-$, $\gamma\pi^+\pi^-\pi^+\pi^-$, $\gamma K^\pm K^0_S \pi^\mp$ (with $K^0_S\to\pi^+\pi^-$), $\gamma \phi\phi$ (with $\phi\to K^+K^-$) and $\gamma p\bar{p}$. From a combined fit of all five channels, we determine the mass and full-width of $\eta_c$ to be $m_{\eta_c}=2977.5\pm1.0 ({stat.})\pm1.2 ({syst.})$ MeV/$c^2$ and $\Gamma_{\eta_c} = 17.0\pm3.7 ({stat.})\pm7.4 ({syst.})$ MeV/$c^2$.Comment: 9 pages, 2 figures and 4 table. Submitted to Phys. Lett.

Observation of a near-threshold enhancement in th p pbar mass spectrum from radiative J/psi-->gamma p pbar decays

We observe a narrow enhancement near 2mp in the invariant mass spectrum of ppbar pairs from radiative J/psi-->gamma ppbar decays. The enhancement can be fit with either an S- or P-wave Breit Wigner fuction. In the case of the S-wave fit, the peak mass is below the 2mp threshold and the full width is less than 30 MeV. These mass and width values are not consistent with the properties of any known meson resonance.Comment: 5 pages, 4 figures, submitted to Phys. Rev. Let