Cloning and expression of first gene for biodegrading microcystins by Sphingopyxis sp. USTB-05

Harmful cyanobacterial blooms (HCBs) in natural waters are a growing environmental problem worldwide because microcystins (MCs) produced by cyanobacteria are potent hepatotoxins and tumor promoters. MCs are resistant against physical and chemical factors. Thus, biodegradation is the most efficient method for removing MCs, and a number of bacterial strains, especially genus _Sphingomonas_, have been isolated for biodegrading MCs. Although the pathway, enzyme, and gene for biodegrading MCs by _Sphingomonas sp._ have been widely identified recently, no gene concerned with the biodegradation of MCs has been successfully cloned and expressed. In this study, we show that the first and most important gene of mlrA, containing 1,008 bp nucleotides in length, in the biodegradation pathway of MCs by _Sphingopyxis sp._ USTB-05, which encodes an enzyme MlrA containing 336 amino acid residues, is firstly cloned and expressed in _E. coli_ DH5α, with a cloning vector of pGEM-T easy and an expression vector of pGEX-4T-1. The encoded and expressed enzyme MlrA is responsible for cleaving the target peptide bond between 3-amino-9-methoxy-2,6,8-trimethyl-10-phenyl-deca-4,6-dienoic acid (Adda) and Arg in the cyclic structure of microcystin-RR （MC-RR）and microcystin-LR（MC-LR), two typical and toxic types of MCs. Linear MC-RR and MC-LR are produced as the first products. These findings are important in constructing a new genetic bacterial strain for the efficient removal of MCs from the important water supplies and resolving the controversy on the biodegradation pathway of different types of MCs by genus _Sphingomonas_

Loop-corrected belief propagation for lattice spin models

Belief propagation (BP) is a message-passing method for solving probabilistic graphical models. It is very successful in treating disordered models (such as spin glasses) on random graphs. On the other hand, finite-dimensional lattice models have an abundant number of short loops, and the BP method is still far from being satisfactory in treating the complicated loop-induced correlations in these systems. Here we propose a loop-corrected BP method to take into account the effect of short loops in lattice spin models. We demonstrate, through an application to the square-lattice Ising model, that loop-corrected BP improves over the naive BP method significantly. We also implement loop-corrected BP at the coarse-grained region graph level to further boost its performance.Comment: 11 pages, minor changes with new references added. Final version as published in EPJ

pig-1 MELK and ced-3 Caspase cooperate to control cell polarity in the C. elegans NSM neuroblast

Snail-like genes encode zinc-finger transcription factors that play essential roles in development, and one of their well-known functions is the epithelial-mesenchymal transition (EMT) induction. Many studies performed in organisms ranging from Drosophila melanogaster to mammals have reported that Snail transcription factors regulate various aspects of stem cell development, such as cell polarity and cell cycle progression. However, the mechanisms through which Snail-like genes regulate these developmental processes are not completely understood. To uncover these mechanisms, I studied the neurosecretory motor neuron neuroblast (NSMnb) lineage during C. elegans embryogenesis. In the NSMnb lineage, we have previously found that CES-1 Snail controls cell cycle progression by regulating expression of the gene cdc-25.2 CDC25. However, the mechanism by which ces-1 controls the asymmetric division of the NSMnb is unknown. By analyzing CES-1 ChIP-seq data acquired from the modENCODE Project, we identified more than 3,000 potential targets of CES-1 Snail. From the potential candidates that are involved in regulating asymmetric cell division, pig-1 was found to play an essential role in asymmetric NSMnb division. pig-1 encodes the sole C. elegans ortholog of Maternal Embryonic Leucine-zipper kinase (MELK) kinase. Through genetic studies, I confirmed that pig-1 acts downstream of ces-1 to control the asymmetric positioning of the NSMnb cleavage plane. Furthermore, by using a single-copy transcriptional reporter of pig-1, I observed that loss of ces-1 increases the transcriptional level of pig-1, while gain of ces-1 activity decreases the level of pig-1. Therefore, I conclude that CES-1 Snail regulates asymmetric positioning of the NSMnb cleavage plane by repressing expression of the gene pig-1. In the NSMnb, CES-1 Snail coordinates the cell cycle through cdc-25.2 and asymmetric positioning of the cleavage plane through pig-1 to ensure asymmetric cell division and the generation of two daughter cells of different sizes and fates: the larger NSM, which survives, and the smaller NSM sister cell (NSMsc), which dies. Apart from influencing the positioning of the cleavage plane, ces-1 and pig-1 also play roles in controlling the orientation of the NSMnb cleavage plane and in specifying the fate of the daughter cell, NSMsc. On the other hand, I show that ced-3, which encodes a Caspase and which usually executes cell death in C. elegans, also plays a role in regulating the asymmetric positioning of the NSMnb cleavage plane. Loss of ced-3 alone did not affect the asymmetric positioning of the NSMnb cleavage plane at lateral-dorsal side, but loss of both ced-3 and pig-1 reversed the cleavage plane to the medial-ventral side and generated a small NSM and a large NSMsc. This indicates that in the NSMnb lineage, ced-3 may have other functions in addition to executing cell death in the smaller daughter (NSMsc). Furthermore, I confirmed that this function is dependent on the Caspase activity of CED-3 protein. Taken together, ces-1 Snail and pig-1 MELK are two key factors that coordinate cell polarity and cell fate in the NSMnb lineage during C. elegans embryogenesis. In addition, ced-3 Caspase acts in parallel to pig-1 and ces-1 to promote the correct positioning of the cleavage plane in the NSMnb

Branching fractions of semileptonic DD and DsD_s decays from the covariant light-front quark model

Based on the predictions of the relevant form factors from the covariant light-front quark model, we show the branching fractions for the $D (D_s) \to (P,\,S,\,V,\,A)\,\ell\nu_\ell$ ($\ell=e$ or $\mu$) decays, where $P$ denotes the pseudoscalar meson, $S$ the scalar meson with a mass above 1 GeV, $V$ the vector meson and $A$ the axial-vector one. Comparison with the available experimental results are made, and we find an excellent agreement. The predictions for other decay modes can be tested in a charm factory, e.g., the BESIII detector. The future measurements will definitely further enrich our knowledge on the hadronic transition form factor as well as the inner structure of the even-parity mesons ($S$ and $A$).Comment: Predictions on D-> K1(1270), K1(1400) l nu rates correcte

The semileptonic baryonic decay Ds+→ppˉe+νeD_s^+\to p\bar p e^+ \nu_e

The decay $D_s^+\to p \bar p e^+\nu_e$ with a proton-antiproton pair in the final state is unique in the sense that it is the only semileptonic baryonic decay which is physically allowed in the charmed meson sector. Its measurement will test our basic knowledge on semileptonic $D_s^+$ decays and the low-energy $p\bar p$ interactions. Taking into account the major intermediate state contributions from $\eta, \eta', f_0(980)$ and $X(1835)$, we find that its branching fraction is at the level of $10^{-9} \sim 10^{-8}$. The location and the nature of $X(1835)$ state are crucial for the precise determination of the branching fraction. We wish to trigger a new round of a careful study with the upcoming more data in BESIII as well as the future super tau-charm factory.Comment: final version, accepted for publication in Phys. Lett.