21 research outputs found

    Observations of sustained phase shifted magnetic islands from externally imposed m/n = 1/1 RMP in LHD

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    New observations in the Large Helical Device (LHD) show that the magnetic islands externally imposed by m/n = 1/1 resonant magnetic perturbation (RMP) can be maintained in an intermediate state with a finite phase shift away from the value present in vacuum. Given the previous experimental observation that the saturated magnetic islands show either growth or healing, the intermediate states are realized in the “healing region” in the beta and collisionality space, which implies that a parameter other than beta and collisionality should exist in order to determine the island state. Theories based on the competition between electromagnetic torques and poloidal flow-induced viscous torques provide a prediction for the intermediate state. These two types of torques might be balanced to realize the steadily maintained intermediate state whereas the islands are placed in the growth state or healing state in the case in which the balance is broken. The experimental observation shows that there is a possibility for the magnetic island phase to deviate from its designed position. If the parameters are controlled properly, it is possible to control the phase of the magnetic island, which may permit continued utilization of the island divertor concept

    Effects of plasma turbulence on the nonlinear evolution of magnetic island in tokamak

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    Magnetic islands (MIs), resulting from a magnetic field reconnection, are ubiquitous structures in magnetized plasmas. In tokamak plasmas, recent researches suggested that the interaction between an MI and ambient turbulence can be important for the nonlinear MI evolution, but a lack of detailed experimental observations and analyses has prevented further understanding. Here, we provide comprehensive observations such as turbulence spreading into an MI and turbulence enhancement at the reconnection site, elucidating intricate effects of plasma turbulence on the nonlinear MI evolution

    CdgL is a degenerate nucleotide cyclase domain protein affecting flagellin synthesis and motility in Bacillus thuringiensis

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    In Bacillus subtilis, motility genes are expressed in a hierarchical pattern – governed by the σD transcription factor and other proteins such as the EpsE molecular clutch and SlrA/SlrR regulator proteins. In contrast, motile species in the Bacillus cereus group seem to express their motility genes in a non-hierarchical pattern, and less is known about their regulation, also given that no orthologs to σD, EpsE, SlrA or SlrR are found in B. cereus group genomes. Here we show that deletion of cdgL (BTB_RS26690/BTB_c54300) in Bacillus thuringiensis 407 (cry-) resulted in a six-to ten-fold downregulation of the entire motility locus, and loss of flagellar structures and swimming motility. cdgL is unique to the B. cereus group and is found in all phylogenetic clusters in the population except for group I, which comprises isolates of non-motile Bacillus pseudomycoides. Analysis of RNA-Seq data revealed cdgL to be expressed in a three-gene operon with a NupC like nucleoside transporter, and a putative glycosyl transferase for which transposon-based gene inactivation was previously shown to produce a similar phenotype to cdgL deletion. Interestingly, all three proteins were predicted to be membrane-bound and may provide a concerted function in the regulation of B. cereus group motility

    CdgL is a degenerate nucleotide cyclase domain protein affecting flagellin synthesis and motility in Bacillus thuringiensis

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    In Bacillus subtilis, motility genes are expressed in a hierarchical pattern – governed by the σD transcription factor and other proteins such as the EpsE molecular clutch and SlrA/SlrR regulator proteins. In contrast, motile species in the Bacillus cereus group seem to express their motility genes in a non-hierarchical pattern, and less is known about their regulation, also given that no orthologs to σD, EpsE, SlrA or SlrR are found in B. cereus group genomes. Here we show that deletion of cdgL (BTB_RS26690/BTB_c54300) in Bacillus thuringiensis 407 (cry-) resulted in a six-to ten-fold downregulation of the entire motility locus, and loss of flagellar structures and swimming motility. cdgL is unique to the B. cereus group and is found in all phylogenetic clusters in the population except for group I, which comprises isolates of non-motile Bacillus pseudomycoides. Analysis of RNA-Seq data revealed cdgL to be expressed in a three-gene operon with a NupC like nucleoside transporter, and a putative glycosyl transferase for which transposon-based gene inactivation was previously shown to produce a similar phenotype to cdgL deletion. Interestingly, all three proteins were predicted to be membrane-bound and may provide a concerted function in the regulation of B. cereus group motility

    SecDF as part of the Sec-Translocase facilitates efficient secretion of Bacillus cereus toxins and cell wall-associated proteins

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    The aim of this study was to explore the role of SecDF in protein secretion in Bacillus cereus ATCC 14579 by in-depth characterization of a markerless secDF knock out mutant. Deletion of secDF resulted in pleiotropic effects characterized by a moderately slower growth rate, aberrant cell morphology, enhanced susceptibility to xenobiotics, reduced virulence and motility. Most toxins, including food poisoning-associated enterotoxins Nhe, Hbl, and cytotoxin K, as well as phospholipase C were less abundant in the secretome of the ∆secDF mutant as determined by label-free mass spectrometry. Global transcriptome studies revealed profound transcriptional changes upon deletion of secDF indicating cell envelope stress. Interestingly, the addition of glucose enhanced the described phenotypes. This study shows that SecDF is an important part of the Sec-translocase mediating efficient secretion of virulence factors in the Gram-positive opportunistic pathogen B. cereus, and further supports the notion that B. cereus enterotoxins are secreted by the Sec-system.17 page(s
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