A conserved but plant-specific CDK-mediated regulation of DNA replication protein A2 in the precise control of stomatal terminal division

The R2R3-MYB transcription factor FOUR LIPS (FLP) controls the stomatal terminal division through transcriptional repression of the cell cycle genes CYCLIN-DEPENDENT KINASE (CDK) B1s (CDKB1s), CDKA; 1, and CYCLIN A2s (CYCA2s). We mutagenized the weak mutant allele flp-1 seeds with ethylmethane sulfonate and screened out a flp-1 suppressor 1 (fsp1) that suppressed the flp-1 stomatal cluster phenotype. FSP1 encodes RPA2a subunit of Replication Protein A (RPA) complexes that play important roles in DNA replication, recombination, and repair. Here, we show that FSP1/RPA2a functions together with CDKB1s and CYCA2s in restricting stomatal precursor proliferation, ensuring the stomatal terminal division and maintaining a normal guard-cell size and DNA content. Furthermore, we provide direct evidence for the existence of an evolutionarily conserved, but plant-specific, CDK-mediated RPA regulatory pathway. Serine-11 and Serine-21 at the N terminus of RPA2a are CDK phosphorylation target residues. The expression of the phosphorylation-mimic variant RPA2a(S11,21/D) partially complemented the defective cell division and DNA damage hypersensitivity in cdkb1;1 1;2 mutants. Thus, our study provides a mechanistic understanding of the CDK-mediated phosphorylation of RPA in the precise control of cell cycle and DNA repair in plants

The extended BLMSSM with a 125 GeV Higgs boson and dark matter

To extend the BLMSSM, we not only add exotic Higgs superfields $(\Phi_{NL},\varphi_{NL})$ to make the exotic lepton heavy, but also introduce the superfields($Y$,$Y^\prime$) having couplings with lepton and exotic lepton at tree level. The obtained model is called as EBLMSSM, which has difference from BLMSSM especially for the exotic slepton(lepton) and exotic sneutrino(neutrino). We deduce the mass matrices and the needed couplings in this model. To confine the parameter space, the Higgs boson mass $m_{h^0}$ and the processes $h^0\rightarrow \gamma\gamma$, $h^0\rightarrow VV, V=(Z,W)$ are studied in the EBLMSSM. With the assumed parameter space, we obtain reasonable numerical results according to data on Higgs from ATLAS and CMS. As a cold dark mater candidate, the relic density for the lightest mass eigenstate of $Y$ and $Y'$ mixing is also studied

μ-Biphenyl-3,3′,4,4′-tetra­carboxyl­ato-κ2 O 3:O 3′-bis­[triaqua­(2,2′-bipyridyl-κ2 N,N′)nickel(II)] hexa­hydrate

The asymmetric unit of the title complex, [Ni2(C16H6O8)(C10H8N2)2(H2O)6]·6H2O, contains one NiII atom, one 2,2′-bipyridine ligand, three coordinated water mol­ecules, one-half of a fully deprotonated biphenyl-3,3′,4,4′-tetra­carboxyl­ate anion and three lattice water mol­ecules. The NiII atom displays a distorted NiN2O4 octa­hedral coordination formed by one carboxyl­ate O atom, three water O atoms and two N atoms of the chelating ligand. The complete biphenyl-3,3′,4,4′-tetra­carboxyl­ate ligand displays inversion symmetry and links two symmetry-related NiII atoms into a binuclear complex. Neighbouring complex mol­ecules are linked through O—H⋯O hydrogen bonds into a three-dimensional structure. Additional O—H⋯O hydrogen bonds between the lattice water mol­ecules help to consolidate the crystal packing

RNA-Seq analysis uncovers non-coding small RNA system of Mycobacterium neoaurum in the metabolism of sterols to accumulate steroid intermediates

Additional file 6: Figure S2. Negative networks of differentially expressed sRNA candidates and their target genes. (a): Mn-CC/C; (b): Mn-9OHAD/CC; (c) Mn-ADD/CC; and (d): Mn-BNA/CC. Squares represent the upregulated (amaranth) or downregulated sRNA candidates (blue); circles represent the putative upregulated (red) or downregulated (green) target genes; links represent the regulation of sRNAs on their target genes

Prognostic significance of hemoglobin A1c level in patients hospitalized with coronary artery disease. A systematic review and meta-analysis

<p>Abstract</p> <p>Background</p> <p>The prognostic value of hemoglobin A1c (HbA1c) in coronary artery disease (CAD) remains controversial. Herein, we conducted a systematic review to quantify the association between elevated HbA1c levels and all-cause mortality among patients hospitalized with CAD.</p> <p>Methods</p> <p>A systematic search of electronic databases (PubMed, EMBASE, OVID, Web of Science, The Cochrane Library) for studies published from 1970 to May 2011 was performed. Cohort, case-control studies, and randomized controlled trials that examined the effect of HbA1c on all-cause mortality were included.</p> <p>Results</p> <p>Twenty studies met final inclusion criteria (total n = 13, 224). From the pooled analyses, elevated HbA1c level was significantly associated with increased short-term (OR 2.32, 95% CI, 1.61 to 3.35) and long-term (OR 1.54, 95% CI, 1.23 to 1.94) mortality risk. Subgroup analyses suggested elevated HbA1c level predicted higher mortality risk in patients without diabetes (OR 1.84, 95% CI, 1.51 to 2.24). In contrast, in patients with diabetes, elevated HbA1c level was not associated with increased risk of mortality (OR 0.95, 95% CI, 0.70 to 1.28). In a risk-adjusted sensitivity analyses, elevated HbA1c was also associated with a significantly high risk of adjusted mortality in patients without diabetes (adjusted OR 1.49, 95% CI, 1.24 to 1.79), but had a borderline effect in patients with diabetes (adjusted OR 1.05, 95% CI, 1.00 to 1.11).</p> <p>Conclusions</p> <p>Our findings demonstrate that elevated HbA1c level is an independent risk factor for mortality in CAD patients without diabetes, but not in patients with established diabetes. Prospective studies should further investigate whether glycemic control might improve outcomes in CAD patients without previously diagnosed diabetes.</p