The Experts below are selected from a list of 4071 Experts worldwide ranked by ideXlab platform
Zeynep Baharoglu - One of the best experts on this subject based on the ideXlab platform.
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RadD Contributes to R-Loop Avoidance in Sub-MIC Tobramycin
mBio, 2019Co-Authors: Veronica Negro, Evelyne Krin, Sebastian Aguilar Pierlé, Thibault Chaze, Quentin Giai Gianetto, Sean Kennedy, Mariette Matondo, Didier Mazel, Zeynep BaharogluAbstract:We have previously identified Vibrio cholerae mutants in which the stress response to subinhibitory concentrations of aminoglycoside is altered. One gene identified, VC1636, encodes a putative DNA/RNA helicase, recently named RadD in Escherichia coli. Here we combined extensive genetic characterization and high-throughput approaches in order to identify partners and molecular mechanisms involving RadD. We show that double-strand DNA breaks (DSBs) are formed upon subinhibitory tobramycin treatment in the absence of radD and recBCD and that formation of these DSBs can be overcome by RNase H1 overexpression. Loss of RNase H1, or of the transcription-translation coupling factor EF-P, is lethal in the radD deletion mutant. We propose that R-Loops are formed upon sublethal aminoglycoside treatment, leading to the formation of DSBs that can be repaired by the RecBCD ho-mologous recombination pathway, and that RadD counteracts such R-Loop accumulation. We discuss how R-Loops that can occur upon translation-transcription uncou-pling could be the link between tobramycin treatment and DNA break formation. IMPORTANCE Bacteria frequently encounter low concentrations of antibiotics. Active antibiotics are commonly detected in soil and water at concentrations much below lethal concentration. Although sub-MICs of antibiotics do not kill bacteria, they can have a major impact on bacterial populations by contributing to the development of antibiotic resistance through mutations in originally sensitive bacteria or acquisition of DNA from resistant bacteria. It was shown that concentrations as low as 100-fold below the MIC can actually lead to the selection of antibiotic-resistant cells. We seek to understand how bacterial cells react to such antibiotic concentrations using E. coli, the Gram-negative bacterial paradigm, and V. cholerae, the causative agent of cholera. Our findings shed light on the processes triggered at the DNA level by antibiotics targeting translation, how damage occurs, and what the bacterial strategies are to respond to such DNA damage.
Veronica Negro - One of the best experts on this subject based on the ideXlab platform.
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RadD Contributes to R-Loop Avoidance in Sub-MIC Tobramycin
mBio, 2019Co-Authors: Veronica Negro, Evelyne Krin, Sebastian Aguilar Pierlé, Thibault Chaze, Quentin Giai Gianetto, Sean Kennedy, Mariette Matondo, Didier Mazel, Zeynep BaharogluAbstract:We have previously identified Vibrio cholerae mutants in which the stress response to subinhibitory concentrations of aminoglycoside is altered. One gene identified, VC1636, encodes a putative DNA/RNA helicase, recently named RadD in Escherichia coli. Here we combined extensive genetic characterization and high-throughput approaches in order to identify partners and molecular mechanisms involving RadD. We show that double-strand DNA breaks (DSBs) are formed upon subinhibitory tobramycin treatment in the absence of radD and recBCD and that formation of these DSBs can be overcome by RNase H1 overexpression. Loss of RNase H1, or of the transcription-translation coupling factor EF-P, is lethal in the radD deletion mutant. We propose that R-Loops are formed upon sublethal aminoglycoside treatment, leading to the formation of DSBs that can be repaired by the RecBCD ho-mologous recombination pathway, and that RadD counteracts such R-Loop accumulation. We discuss how R-Loops that can occur upon translation-transcription uncou-pling could be the link between tobramycin treatment and DNA break formation. IMPORTANCE Bacteria frequently encounter low concentrations of antibiotics. Active antibiotics are commonly detected in soil and water at concentrations much below lethal concentration. Although sub-MICs of antibiotics do not kill bacteria, they can have a major impact on bacterial populations by contributing to the development of antibiotic resistance through mutations in originally sensitive bacteria or acquisition of DNA from resistant bacteria. It was shown that concentrations as low as 100-fold below the MIC can actually lead to the selection of antibiotic-resistant cells. We seek to understand how bacterial cells react to such antibiotic concentrations using E. coli, the Gram-negative bacterial paradigm, and V. cholerae, the causative agent of cholera. Our findings shed light on the processes triggered at the DNA level by antibiotics targeting translation, how damage occurs, and what the bacterial strategies are to respond to such DNA damage.
Hussein T Mouftah - One of the best experts on this subject based on the ideXlab platform.
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a hop by hop delay constrained routing algorithm with explicit Loop Avoidance and backup routing information
International Journal of Communication Systems, 2004Co-Authors: Baoxian Zhang, Changjia Chen, Hussein T MouftahAbstract:QoS Routing is crucial for QoS provisioning in high-speed networks. In general, QoS routing can be classified into two paradigms: source routing and hop-by-hop routing. In source routing, the entire path to the destination node of a communication request is locally computed at the source node based on the global state that it maintains, which does not scale well to large networks. In hop-by-hop routing, a path-selecting process is shared among intermediate nodes between the source node and the destination node, which can largely improve the protocol scalability. In this paper, we present the design of hop-by-hop routing with backup route information such that each intermediate node can recursively update the best known feasible path, if possible, by collectively utilizing the routing information gathered thus far and the information that it locally stores. Such a route is kept as a backup route and its path cost is used as a reference to guide the subsequent routing process to search for a lower-cost constrained path and avoid performance degradation. In this way, the information gathered is maximally utilized for improved performance. We prove the correctness of our presented algorithm and deduce its worst message complexity to be O(∣V∣2), where ∣V∣ is the number of network nodes. Simulation results indicate that, however, the designed algorithm requires much fewer messages on average. Therefore it scales well with respect to the network size. Moreover, simulation results demonstrate that the cost performance of our algorithm is near-optimal. Copyright © 2004 John Wiley & Sons, Ltd.
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a hop by hop delay constrained routing algorithm with explicit Loop Avoidance and backup routing information research articles
International Journal of Communication Systems, 2004Co-Authors: Baoxian Zhang, Changjia Chen, Hussein T MouftahAbstract:QoS Routing is crucial for QoS provisioning in high-speed networks. In general, QoS routing can be classified into two paradigms: source routing and hop-by-hop routing. In source routing, the entire path to the destination node of a communication request is locally computed at the source node based on the global state that it maintains, which does not scale well to large networks. In hop-by-hop routing, a path-selecting process is shared among intermediate nodes between the source node and the destination node, which can largely improve the protocol scalability.In this paper, we present the design of hop-by-hop routing with backup route information such that each intermediate node can recursively update the best known feasible path, if possible, by collectively utilizing the routing information gathered thus far and the information that it locally stores. Such a route is kept as a backup route and its path cost is used as a reference to guide the subsequent routing process to search for a lower-cost constrained path and avoid performance degradation. In this way, the information gathered is maximally utilized for improved performance. We prove the correctness of our presented algorithm and deduce its worst message complexity to be O(mVm2), where mVm is the number of network nodes. Simulation results indicate that, however, the designed algorithm requires much fewer messages on average. Therefore it scales well with respect to the network size. Moreover, simulation results demonstrate that the cost performance of our algorithm is near-optimal. Copyright © 2004 John Wiley & Sons, Ltd.
Didier Mazel - One of the best experts on this subject based on the ideXlab platform.
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RadD Contributes to R-Loop Avoidance in Sub-MIC Tobramycin
mBio, 2019Co-Authors: Veronica Negro, Evelyne Krin, Sebastian Aguilar Pierlé, Thibault Chaze, Quentin Giai Gianetto, Sean Kennedy, Mariette Matondo, Didier Mazel, Zeynep BaharogluAbstract:We have previously identified Vibrio cholerae mutants in which the stress response to subinhibitory concentrations of aminoglycoside is altered. One gene identified, VC1636, encodes a putative DNA/RNA helicase, recently named RadD in Escherichia coli. Here we combined extensive genetic characterization and high-throughput approaches in order to identify partners and molecular mechanisms involving RadD. We show that double-strand DNA breaks (DSBs) are formed upon subinhibitory tobramycin treatment in the absence of radD and recBCD and that formation of these DSBs can be overcome by RNase H1 overexpression. Loss of RNase H1, or of the transcription-translation coupling factor EF-P, is lethal in the radD deletion mutant. We propose that R-Loops are formed upon sublethal aminoglycoside treatment, leading to the formation of DSBs that can be repaired by the RecBCD ho-mologous recombination pathway, and that RadD counteracts such R-Loop accumulation. We discuss how R-Loops that can occur upon translation-transcription uncou-pling could be the link between tobramycin treatment and DNA break formation. IMPORTANCE Bacteria frequently encounter low concentrations of antibiotics. Active antibiotics are commonly detected in soil and water at concentrations much below lethal concentration. Although sub-MICs of antibiotics do not kill bacteria, they can have a major impact on bacterial populations by contributing to the development of antibiotic resistance through mutations in originally sensitive bacteria or acquisition of DNA from resistant bacteria. It was shown that concentrations as low as 100-fold below the MIC can actually lead to the selection of antibiotic-resistant cells. We seek to understand how bacterial cells react to such antibiotic concentrations using E. coli, the Gram-negative bacterial paradigm, and V. cholerae, the causative agent of cholera. Our findings shed light on the processes triggered at the DNA level by antibiotics targeting translation, how damage occurs, and what the bacterial strategies are to respond to such DNA damage.
Evelyne Krin - One of the best experts on this subject based on the ideXlab platform.
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RadD Contributes to R-Loop Avoidance in Sub-MIC Tobramycin
mBio, 2019Co-Authors: Veronica Negro, Evelyne Krin, Sebastian Aguilar Pierlé, Thibault Chaze, Quentin Giai Gianetto, Sean Kennedy, Mariette Matondo, Didier Mazel, Zeynep BaharogluAbstract:We have previously identified Vibrio cholerae mutants in which the stress response to subinhibitory concentrations of aminoglycoside is altered. One gene identified, VC1636, encodes a putative DNA/RNA helicase, recently named RadD in Escherichia coli. Here we combined extensive genetic characterization and high-throughput approaches in order to identify partners and molecular mechanisms involving RadD. We show that double-strand DNA breaks (DSBs) are formed upon subinhibitory tobramycin treatment in the absence of radD and recBCD and that formation of these DSBs can be overcome by RNase H1 overexpression. Loss of RNase H1, or of the transcription-translation coupling factor EF-P, is lethal in the radD deletion mutant. We propose that R-Loops are formed upon sublethal aminoglycoside treatment, leading to the formation of DSBs that can be repaired by the RecBCD ho-mologous recombination pathway, and that RadD counteracts such R-Loop accumulation. We discuss how R-Loops that can occur upon translation-transcription uncou-pling could be the link between tobramycin treatment and DNA break formation. IMPORTANCE Bacteria frequently encounter low concentrations of antibiotics. Active antibiotics are commonly detected in soil and water at concentrations much below lethal concentration. Although sub-MICs of antibiotics do not kill bacteria, they can have a major impact on bacterial populations by contributing to the development of antibiotic resistance through mutations in originally sensitive bacteria or acquisition of DNA from resistant bacteria. It was shown that concentrations as low as 100-fold below the MIC can actually lead to the selection of antibiotic-resistant cells. We seek to understand how bacterial cells react to such antibiotic concentrations using E. coli, the Gram-negative bacterial paradigm, and V. cholerae, the causative agent of cholera. Our findings shed light on the processes triggered at the DNA level by antibiotics targeting translation, how damage occurs, and what the bacterial strategies are to respond to such DNA damage.
