202 research outputs found

    On the Milnor formula in arbitrary characteristic

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    The Milnor formula μ=2δr+1\mu=2\delta-r+1 relates the Milnor number μ\mu, the double point number δ\delta and the number rr of branches of a plane curve singularity. It holds over the fields of characteristic zero. Melle and Wall based on a result by Deligne proved the inequality μ2δr+1\mu\geq 2\delta-r+1 in arbitrary characteristic and showed that the equality μ=2δr+1\mu=2\delta-r+1 characterizes the singularities with no wild vanishing cycles. In this note we give an account of results on the Milnor formula in characteristic pp. It holds if the plane singularity is Newton non-degenerate (Boubakri et al. Rev. Mat. Complut. (2010) 25) or if pp is greater than the intersection number of the singularity with its generic polar (Nguyen H.D., Annales de l'Institut Fourier, Tome 66 (5) (2016)). Then we improve our result on the Milnor number of irreducible singularities (Bull. London Math. Soc. 48 (2016)). Our considerations are based on the properties of polars of plane singularities in characteristic pp.Comment: 18 page

    The conserved C-terminus of the PcrA/UvrD helicase interacts directly with RNA polymerase

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    Copyright: © 2013 Gwynn et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: This work was supported by a Wellcome Trust project grant to MD (Reference: 077368), an ERC starting grant to MD (Acronym: SM-DNA-REPAIR) and a BBSRC project grant to PM, NS and MD (Reference: BB/I003142/1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewedPublisher PD

    Political connections and corporate financial decision making

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    This paper investigates whether and how political connections influence managerial financial decisions. Our study reveals that those firms that have a politician on its board of directors are highly leveraged, use more long-term debt, hold large excess cash and are associated with low quality financial reporting compared to their non-connected counterparts. These effects escalate with the strength of the connected politician and whether he or his party is in power. The winning party effect is observed to be stronger than victory by the politician himself. Overall, our paper provides strong evidence that political connection is a two-edged sword. It is indeed a valuable resource for connected firms, but it comes at a cost of higher agency problems

    Co-directional replication-transcription conflicts lead to replication restart

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    August 24, 2011Head-on encounters between the replication and transcription machineries on the lagging DNA strand can lead to replication fork arrest and genomic instability1, 2. To avoid head-on encounters, most genes, especially essential and highly transcribed genes, are encoded on the leading strand such that transcription and replication are co-directional. Virtually all bacteria have the highly expressed ribosomal RNA genes co-directional with replication3. In bacteria, co-directional encounters seem inevitable because the rate of replication is about 10–20-fold greater than the rate of transcription. However, these encounters are generally thought to be benign2, 4, 5, 6, 7, 8, 9. Biochemical analyses indicate that head-on encounters10 are more deleterious than co-directional encounters8 and that in both situations, replication resumes without the need for any auxiliary restart proteins, at least in vitro. Here we show that in vivo, co-directional transcription can disrupt replication, leading to the involvement of replication restart proteins. We found that highly transcribed rRNA genes are hotspots for co-directional conflicts between replication and transcription in rapidly growing Bacillus subtilis cells. We observed a transcription-dependent increase in association of the replicative helicase and replication restart proteins where head-on and co-directional conflicts occur. Our results indicate that there are co-directional conflicts between replication and transcription in vivo. Furthermore, in contrast to the findings in vitro, the replication restart machinery is involved in vivo in resolving potentially deleterious encounters due to head-on and co-directional conflicts. These conflicts probably occur in many organisms and at many chromosomal locations and help to explain the presence of important auxiliary proteins involved in replication restart and in helping to clear a path along the DNA for the replisome.Biotechnology and Biological Sciences Research Council (Great Britain) (Grant BB/E006450/1)Wellcome Trust (London, England) (Grant 091968/Z/10/Z)National Institutes of Health (U.S.) (Grant GM41934)National Institutes of Health (U.S.) (Postdoctoral Fellowship GM093408)Biotechnology and Biological Sciences Research Council (Great Britain) (Sabbatical Visit

    DNA helicase and helicase–nuclease enzymes with a conserved iron–sulfur cluster

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    Conserved Iron–Sulfur (Fe–S) clusters are found in a growing family of metalloproteins that are implicated in prokaryotic and eukaryotic DNA replication and repair. Among these are DNA helicase and helicase–nuclease enzymes that preserve chromosomal stability and are genetically linked to diseases characterized by DNA repair defects and/or a poor response to replication stress. Insight to the structural and functional importance of the conserved Fe–S domain in DNA helicases has been gleaned from structural studies of the purified proteins and characterization of Fe–S cluster site-directed mutants. In this review, we will provide a current perspective of what is known about the Fe–S cluster helicases, with an emphasis on how the conserved redox active domain may facilitate mechanistic aspects of helicase function. We will discuss testable models for how the conserved Fe–S cluster might operate in helicase and helicase–nuclease enzymes to conduct their specialized functions that help to preserve the integrity of the genome
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