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Mark J. Mcbride - One of the best experts on this subject based on the ideXlab platform.
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bacteroidetes Gliding Motility and the type ix secretion system
Microbiology spectrum, 2019Co-Authors: Mark J. McbrideAbstract:Members of the phylum Bacteroidetes have many unique features, including Gliding Motility and the type IX protein secretion system (T9SS). Bacteroidetes Gliding and T9SSs are common in, but apparently confined to, this phylum. Most, but not all, members of the phylum secrete proteins using the T9SS, and most also exhibit Gliding Motility. T9SSs secrete cell surface components of the Gliding Motility machinery and also secrete many extracellular or cell surface enzymes, adhesins, and virulence factors. The components of the T9SS are novel and are unrelated to those of other bacterial secretion systems. Proteins secreted by the T9SS rely on the Sec system to cross the cytoplasmic membrane, and they use the T9SS for delivery across the outer membrane. Secreted proteins typically have conserved C-terminal domains that target them to the T9SS. Some of the T9SS components were initially identified as proteins required for Gliding Motility. Gliding does not involve flagella or pili and instead relies on the rapid movement of Motility adhesins, such as SprB, along the cell surface by the Gliding motor. Contact of the adhesins with the substratum provides the traction that results in cell movement. SprB and other Motility adhesins are delivered to the cell surface by the T9SS. Gliding and the T9SS appear to be intertwined, and components of the T9SS that span the cytoplasmic membrane may energize both Gliding and protein secretion. The functions of the individual proteins in each process are the subject of ongoing investigations.
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Protein Secretion in Bacteria - Bacteroidetes Gliding Motility and the Type IX Secretion System.
Microbiology spectrum, 2019Co-Authors: Mark J. McbrideAbstract:Members of the phylum Bacteroidetes have many unique features, including Gliding Motility and the type IX protein secretion system (T9SS). Bacteroidetes Gliding and T9SSs are common in, but apparently confined to, this phylum. Most, but not all, members of the phylum secrete proteins using the T9SS, and most also exhibit Gliding Motility. T9SSs secrete cell surface components of the Gliding Motility machinery and also secrete many extracellular or cell surface enzymes, adhesins, and virulence factors. The components of the T9SS are novel and are unrelated to those of other bacterial secretion systems. Proteins secreted by the T9SS rely on the Sec system to cross the cytoplasmic membrane, and they use the T9SS for delivery across the outer membrane. Secreted proteins typically have conserved C-terminal domains that target them to the T9SS. Some of the T9SS components were initially identified as proteins required for Gliding Motility. Gliding does not involve flagella or pili and instead relies on the rapid movement of Motility adhesins, such as SprB, along the cell surface by the Gliding motor. Contact of the adhesins with the substratum provides the traction that results in cell movement. SprB and other Motility adhesins are delivered to the cell surface by the T9SS. Gliding and the T9SS appear to be intertwined, and components of the T9SS that span the cytoplasmic membrane may energize both Gliding and protein secretion. The functions of the individual proteins in each process are the subject of ongoing investigations.
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Untangling Flavobacterium johnsoniae Gliding Motility and Protein Secretion
Journal of bacteriology, 2017Co-Authors: Joseph J. Johnston, Abhishek Shrivastava, Mark J. McbrideAbstract:ABSTRACT Flavobacterium johnsoniae exhibits rapid Gliding Motility over surfaces. At least 20 genes are involved in this process. Seven of these, gldK , gldL , gldM , gldN , sprA , sprE , and sprT , encode proteins of the type IX protein secretion system (T9SS). The T9SS is required for surface localization of the Motility adhesins SprB and RemA, and for secretion of the soluble chitinase ChiA. Here, we demonstrate that the Gliding Motility proteins GldA, GldB, GldD, GldF, GldH, GldI, and GldJ are also essential for secretion. Cells with mutations in the genes encoding any of these seven proteins had normal levels of gldK mRNA but dramatically reduced levels of the GldK protein, which may explain the secretion defects of the Motility mutants. GldJ is necessary for stable accumulation of GldK, and each mutant lacked the GldJ protein. F. johnsoniae cells that produced truncated GldJ, lacking eight to 13 amino acids from the C terminus, accumulated GldK but were deficient in Gliding Motility. SprB was secreted by these cells but was not propelled along their surfaces. This C-terminal region of GldJ is thus required for Gliding Motility but not for secretion. The identification of mutants that are defective for Motility but competent for secretion begins to untangle the F. johnsoniae Gliding Motility machinery from the T9SS. IMPORTANCE Many members of the phylum Bacteroidetes secrete proteins using T9SSs. T9SSs appear to be confined to members of this phylum. Many of these bacteria also glide rapidly over surfaces using a Motility machine that is also confined to the Bacteroidetes and appears to be intertwined with the T9SS. This study identifies F. johnsoniae proteins that are required for both T9SS function and Gliding Motility. It also provides an explanation for the link between secretion and Gliding and identifies mutants with defects in Motility but not secretion.
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comparative analysis of cellulophaga algicola and flavobacterium johnsoniae Gliding Motility
Journal of Bacteriology, 2016Co-Authors: Yongtao Zhu, Mark J. McbrideAbstract:ABSTRACT Gliding Motility is common in members of the phylum Bacteroidetes, including Flavobacterium johnsoniae and Cellulophaga algicola.F. johnsoniae Gliding has been extensively studied and involves rapid movement of the cell surface adhesin SprB. Genetic analysis of C. algicola allowed a comparative analysis of Gliding. Sixty-three HimarEm1-induced mutants that formed nonspreading colonies were characterized. Each had an insertion in an ortholog of an F. johnsoniae Motility gene, highlighting similarities between the Motility systems. Differences were also observed. C. algicola lacks orthologs of the F. johnsoniae Motility genes gldA, gldF, and gldG that are thought to encode the components of an ATP-binding cassette (ABC) transporter. In addition, mutations in any of 12 F. johnsoniae gld genes result in complete loss of Motility, whereas all C. algicola gld mutants retained slight residual Motility. This may indicate that C. algicola has multiple Motility systems, that the Motility proteins exhibit partial redundancy of function, or that essential components of the Motility machinery of both C. algicola and F. johnsoniae remain to be discovered. IMPORTANCE The development of genetic tools for C. algicola and comparative analysis of F. johnsoniae and C. algicola Motility mutants identified similarities and differences between their Gliding Motility machineries. Gliding Motility is common in the phylum Bacteroidetes. Proteins that are important for Gliding in both C. algicola and F. johnsoniae are potential core components of the Bacteroidetes Gliding Motility machinery.
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Comparative Analysis of Cellulophaga algicola and Flavobacterium johnsoniae Gliding Motility
Journal of bacteriology, 2016Co-Authors: Yongtao Zhu, Mark J. McbrideAbstract:Gliding Motility is common in members of the phylum Bacteroidetes, including Flavobacterium johnsoniae and Cellulophaga algicola. F. johnsoniae Gliding has been extensively studied and involves rapid movement of the cell surface adhesin SprB. Genetic analysis of C. algicola allowed a comparative analysis of Gliding. Sixty-three HimarEm1-induced mutants that formed nonspreading colonies were characterized. Each had an insertion in an ortholog of an F. johnsoniae Motility gene, highlighting similarities between the Motility systems. Differences were also observed. C. algicola lacks orthologs of the F. johnsoniae Motility genes gldA, gldF, and gldG that are thought to encode the components of an ATP-binding cassette (ABC) transporter. In addition, mutations in any of 12 F. johnsoniae gld genes result in complete loss of Motility, whereas all C. algicola gld mutants retained slight residual Motility. This may indicate that C. algicola has multiple Motility systems, that the Motility proteins exhibit partial redundancy of function, or that essential components of the Motility machinery of both C. algicola and F. johnsoniae remain to be discovered. The development of genetic tools for C. algicola and comparative analysis of F. johnsoniae and C. algicola Motility mutants identified similarities and differences between their Gliding Motility machineries. Gliding Motility is common in the phylum Bacteroidetes Proteins that are important for Gliding in both C. algicola and F. johnsoniae are potential core components of the Bacteroidetes Gliding Motility machinery. Copyright © 2016, American Society for Microbiology. All Rights Reserved.
Hayley Cardamone - One of the best experts on this subject based on the ideXlab platform.
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plasmodium yoelii s4 celtos is important for sporozoite Gliding Motility and cell traversal
Cellular Microbiology, 2018Co-Authors: Ryan W J Steel, Ying Pei, Nelly Camargo, Alexis Kaushansky, Dorender Dankwa, Thomas Martinson, Thao Nguyen, Will Betz, Hayley CardamoneAbstract:Gliding Motility and cell traversal by the Plasmodium ookinete and sporozoite invasive stages allow penetration of cellular barriers to establish infection of the mosquito vector and mammalian host, respectively. Motility and traversal are not observed in red cell infectious merozoites, and we have previously classified genes that are expressed in sporozoites but not merozoites (S genes) in order to identify proteins involved in these processes. The S4 gene has been described as criticaly involved in Cell Traversal for Ookinetes and Sporozoites (CelTOS), yet knockout parasites (s4/celtos¯) do not generate robust salivary gland sporozoite numbers, precluding a thorough analysis of S4/CelTOS function during host infection. We show here that a failure of oocysts to develop or survive in the midgut contributes to the poor mosquito infection by Plasmodium yoelii (Py) s4/celtos¯ rodent malaria parasites. We rescued this phenotype by expressing S4/CelTOS under the ookinete-specific circumsporozoite protein and thrombospondin-related anonymous protein-related protein (CTRP) promoter (S4/CelTOSCTRP ), generating robust numbers of salivary gland sporozoites lacking S4/CelTOS that were suitable for phenotypic analysis. Py S4/CelTOSCTRP sporozoites showed reduced infectivity in BALB/c mice when compared to wild-type sporozoites, although they appeared more infectious than sporozoites deficient in the related traversal protein PLP1/SPECT2 (Py plp1/spect2¯). Using in vitro assays, we substantiate the role of S4/CelTOS in sporozoite cell traversal, but also uncover a previously unappreciated role for this protein for sporozoite Gliding Motility.
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Plasmodium yoelii S4/CelTOS is important for sporozoite Gliding Motility and cell traversal.
Cellular microbiology, 2018Co-Authors: Ryan W J Steel, Ying Pei, Nelly Camargo, Alexis Kaushansky, Dorender Dankwa, Thomas Martinson, Thao Nguyen, Will Betz, Hayley Cardamone, Vladimir VigdorovichAbstract:Gliding Motility and cell traversal by the Plasmodium ookinete and sporozoite invasive stages allow penetration of cellular barriers to establish infection of the mosquito vector and mammalian host, respectively. Motility and traversal are not observed in red cell infectious merozoites, and we have previously classified genes that are expressed in sporozoites but not merozoites (S genes) in order to identify proteins involved in these processes. The S4 gene has been described as criticaly involved in Cell Traversal for Ookinetes and Sporozoites (CelTOS), yet knockout parasites (s4/celtos¯) do not generate robust salivary gland sporozoite numbers, precluding a thorough analysis of S4/CelTOS function during host infection. We show here that a failure of oocysts to develop or survive in the midgut contributes to the poor mosquito infection by Plasmodium yoelii (Py) s4/celtos¯ rodent malaria parasites. We rescued this phenotype by expressing S4/CelTOS under the ookinete-specific circumsporozoite protein and thrombospondin-related anonymous protein-related protein (CTRP) promoter (S4/CelTOSCTRP ), generating robust numbers of salivary gland sporozoites lacking S4/CelTOS that were suitable for phenotypic analysis. Py S4/CelTOSCTRP sporozoites showed reduced infectivity in BALB/c mice when compared to wild-type sporozoites, although they appeared more infectious than sporozoites deficient in the related traversal protein PLP1/SPECT2 (Py plp1/spect2¯). Using in vitro assays, we substantiate the role of S4/CelTOS in sporozoite cell traversal, but also uncover a previously unappreciated role for this protein for sporozoite Gliding Motility.
Alexis Kaushansky - One of the best experts on this subject based on the ideXlab platform.
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plasmodium yoelii s4 celtos is important for sporozoite Gliding Motility and cell traversal
Cellular Microbiology, 2018Co-Authors: Ryan W J Steel, Ying Pei, Nelly Camargo, Alexis Kaushansky, Dorender Dankwa, Thomas Martinson, Thao Nguyen, Will Betz, Hayley CardamoneAbstract:Gliding Motility and cell traversal by the Plasmodium ookinete and sporozoite invasive stages allow penetration of cellular barriers to establish infection of the mosquito vector and mammalian host, respectively. Motility and traversal are not observed in red cell infectious merozoites, and we have previously classified genes that are expressed in sporozoites but not merozoites (S genes) in order to identify proteins involved in these processes. The S4 gene has been described as criticaly involved in Cell Traversal for Ookinetes and Sporozoites (CelTOS), yet knockout parasites (s4/celtos¯) do not generate robust salivary gland sporozoite numbers, precluding a thorough analysis of S4/CelTOS function during host infection. We show here that a failure of oocysts to develop or survive in the midgut contributes to the poor mosquito infection by Plasmodium yoelii (Py) s4/celtos¯ rodent malaria parasites. We rescued this phenotype by expressing S4/CelTOS under the ookinete-specific circumsporozoite protein and thrombospondin-related anonymous protein-related protein (CTRP) promoter (S4/CelTOSCTRP ), generating robust numbers of salivary gland sporozoites lacking S4/CelTOS that were suitable for phenotypic analysis. Py S4/CelTOSCTRP sporozoites showed reduced infectivity in BALB/c mice when compared to wild-type sporozoites, although they appeared more infectious than sporozoites deficient in the related traversal protein PLP1/SPECT2 (Py plp1/spect2¯). Using in vitro assays, we substantiate the role of S4/CelTOS in sporozoite cell traversal, but also uncover a previously unappreciated role for this protein for sporozoite Gliding Motility.
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Plasmodium yoelii S4/CelTOS is important for sporozoite Gliding Motility and cell traversal.
Cellular microbiology, 2018Co-Authors: Ryan W J Steel, Ying Pei, Nelly Camargo, Alexis Kaushansky, Dorender Dankwa, Thomas Martinson, Thao Nguyen, Will Betz, Hayley Cardamone, Vladimir VigdorovichAbstract:Gliding Motility and cell traversal by the Plasmodium ookinete and sporozoite invasive stages allow penetration of cellular barriers to establish infection of the mosquito vector and mammalian host, respectively. Motility and traversal are not observed in red cell infectious merozoites, and we have previously classified genes that are expressed in sporozoites but not merozoites (S genes) in order to identify proteins involved in these processes. The S4 gene has been described as criticaly involved in Cell Traversal for Ookinetes and Sporozoites (CelTOS), yet knockout parasites (s4/celtos¯) do not generate robust salivary gland sporozoite numbers, precluding a thorough analysis of S4/CelTOS function during host infection. We show here that a failure of oocysts to develop or survive in the midgut contributes to the poor mosquito infection by Plasmodium yoelii (Py) s4/celtos¯ rodent malaria parasites. We rescued this phenotype by expressing S4/CelTOS under the ookinete-specific circumsporozoite protein and thrombospondin-related anonymous protein-related protein (CTRP) promoter (S4/CelTOSCTRP ), generating robust numbers of salivary gland sporozoites lacking S4/CelTOS that were suitable for phenotypic analysis. Py S4/CelTOSCTRP sporozoites showed reduced infectivity in BALB/c mice when compared to wild-type sporozoites, although they appeared more infectious than sporozoites deficient in the related traversal protein PLP1/SPECT2 (Py plp1/spect2¯). Using in vitro assays, we substantiate the role of S4/CelTOS in sporozoite cell traversal, but also uncover a previously unappreciated role for this protein for sporozoite Gliding Motility.
Ryan W J Steel - One of the best experts on this subject based on the ideXlab platform.
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plasmodium yoelii s4 celtos is important for sporozoite Gliding Motility and cell traversal
Cellular Microbiology, 2018Co-Authors: Ryan W J Steel, Ying Pei, Nelly Camargo, Alexis Kaushansky, Dorender Dankwa, Thomas Martinson, Thao Nguyen, Will Betz, Hayley CardamoneAbstract:Gliding Motility and cell traversal by the Plasmodium ookinete and sporozoite invasive stages allow penetration of cellular barriers to establish infection of the mosquito vector and mammalian host, respectively. Motility and traversal are not observed in red cell infectious merozoites, and we have previously classified genes that are expressed in sporozoites but not merozoites (S genes) in order to identify proteins involved in these processes. The S4 gene has been described as criticaly involved in Cell Traversal for Ookinetes and Sporozoites (CelTOS), yet knockout parasites (s4/celtos¯) do not generate robust salivary gland sporozoite numbers, precluding a thorough analysis of S4/CelTOS function during host infection. We show here that a failure of oocysts to develop or survive in the midgut contributes to the poor mosquito infection by Plasmodium yoelii (Py) s4/celtos¯ rodent malaria parasites. We rescued this phenotype by expressing S4/CelTOS under the ookinete-specific circumsporozoite protein and thrombospondin-related anonymous protein-related protein (CTRP) promoter (S4/CelTOSCTRP ), generating robust numbers of salivary gland sporozoites lacking S4/CelTOS that were suitable for phenotypic analysis. Py S4/CelTOSCTRP sporozoites showed reduced infectivity in BALB/c mice when compared to wild-type sporozoites, although they appeared more infectious than sporozoites deficient in the related traversal protein PLP1/SPECT2 (Py plp1/spect2¯). Using in vitro assays, we substantiate the role of S4/CelTOS in sporozoite cell traversal, but also uncover a previously unappreciated role for this protein for sporozoite Gliding Motility.
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Plasmodium yoelii S4/CelTOS is important for sporozoite Gliding Motility and cell traversal.
Cellular microbiology, 2018Co-Authors: Ryan W J Steel, Ying Pei, Nelly Camargo, Alexis Kaushansky, Dorender Dankwa, Thomas Martinson, Thao Nguyen, Will Betz, Hayley Cardamone, Vladimir VigdorovichAbstract:Gliding Motility and cell traversal by the Plasmodium ookinete and sporozoite invasive stages allow penetration of cellular barriers to establish infection of the mosquito vector and mammalian host, respectively. Motility and traversal are not observed in red cell infectious merozoites, and we have previously classified genes that are expressed in sporozoites but not merozoites (S genes) in order to identify proteins involved in these processes. The S4 gene has been described as criticaly involved in Cell Traversal for Ookinetes and Sporozoites (CelTOS), yet knockout parasites (s4/celtos¯) do not generate robust salivary gland sporozoite numbers, precluding a thorough analysis of S4/CelTOS function during host infection. We show here that a failure of oocysts to develop or survive in the midgut contributes to the poor mosquito infection by Plasmodium yoelii (Py) s4/celtos¯ rodent malaria parasites. We rescued this phenotype by expressing S4/CelTOS under the ookinete-specific circumsporozoite protein and thrombospondin-related anonymous protein-related protein (CTRP) promoter (S4/CelTOSCTRP ), generating robust numbers of salivary gland sporozoites lacking S4/CelTOS that were suitable for phenotypic analysis. Py S4/CelTOSCTRP sporozoites showed reduced infectivity in BALB/c mice when compared to wild-type sporozoites, although they appeared more infectious than sporozoites deficient in the related traversal protein PLP1/SPECT2 (Py plp1/spect2¯). Using in vitro assays, we substantiate the role of S4/CelTOS in sporozoite cell traversal, but also uncover a previously unappreciated role for this protein for sporozoite Gliding Motility.
Young Mok Park - One of the best experts on this subject based on the ideXlab platform.
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ctr1, a gene involved in a signal transduction pathway of the Gliding Motility in the cyanobacterium Synechocystis sp. PCC 6803.
FEBS letters, 2001Co-Authors: Y-h Chung, M-s Cho, Y-j Moon, J S Choi, Y C Yoo, Y I Park, K M Lee, K W Kang, Young Mok ParkAbstract:We generated random Tn5 mutations in Synechocystis sp. PCC 6803 in search for genes involved in the signal transduction cascade for the cyanobacterial Gliding Motility. One of the non-Gliding Tn5 mutants, S1-105, had an insertional inactivation in the slr1044 gene encoding a putative methyl-accepting chemotaxis protein. Interposon mutation on the slr1044 (named ctr1) in the bacterium also eliminated Gliding Motility. In the interposon mutant, the expression of pilA1 was 5-fold decreased compared with that of wild-type and thick pili, that are believed to be the motor for Gliding, could not be observed by an electron microscope. Therefore, we suggest that the Ctr1 protein functions as a transducer that regulates the expression of pilA1, and thus is required for the biogenesis of thick pili.
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The role of a methyl-accepting chemotaxis protein in Gliding Motility of the cyanobacterium Synechocystis sp. PCC 68,The role of a methyl-accepting chemotaxis protein in Gliding Motility of the cyanobacterium Synechocystis sp. PCC 68
Science Access, 2001Co-Authors: Y-h Chung, M-s Cho, Y-j Moon, Y-b Lee, Y-c Choo, Young Mok ParkAbstract:We found strong evidence that methyl-accepting chemotaxis protein influenced Gliding Motility of Synechocystis sp. PCC 6803. Random Tn5 mutagenesis was carried out to search for genes involved in phototactic Gliding movement. Among the pool of 4,500 Tn5 mutants, we initially isolated 35 nonGliding mutants on the agar surface. Using inverse PCR method, it was found that the slr1044 gene (Cyanobase, http://www.kazusa.or.jp/cyano/) encoding a putative methyl-accepting chemotaxis protein was disrupted in one of the nonGliding Tn5 mutant, S1-105. It was also confirmed by interposon mutagenesis that the slr1044 gene was responsible for the Gliding movement in Synechocystis. The slr1044 gene, renamed ctr1 (cyanobacterial transducer), was a part of gene cluster, which shows homology to pil gene cluster of P. aeruginosa , and was required for the normal expression of pilA1. In slr1044 inactivation mutant, the pilA1 gene expression was 4-fold decreased compared with that of wild-type. These data suggest that the ctr1 gene is a part of a signal transduction network involved in pili production and Gliding Motility of the cyanobacterium Synechocystis sp. PCC 6803.