The Experts below are selected from a list of 36 Experts worldwide ranked by ideXlab platform
Cb Whitchurch - One of the best experts on this subject based on the ideXlab platform.
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ChpC controls twitching motility-mediated expansion of Pseudomonas aeruginosa biofilms in response to serum albumin, mucin and oligopeptides
'Microbiology Society', 2020Co-Authors: Lm Nolan, Lc Mccaughey, Merjane J, Turnbull L, Cb WhitchurchAbstract:Twitching motility-mediated biofilm expansion occurs via coordinated, multi-cellular collective behaviour to allow bacteria to actively expand across Surfaces. Type-IV pili (T4P) are cell-associated virulence factors which mediate twitching motility via rounds of Extension, Surface attachment and retraction. The Chp chemosensory system is thought to respond to environmental signals to regulate the biogenesis, assembly and twitching motility function of T4P. In other well characterised chemosensory systems, methyl-accepting chemotaxis proteins (MCPs) feed environmental signals through a CheW adapter protein to the histidine kinase CheA to modulate motility. The Pseudomonas aeruginosa Chp system has an MCP PilJ and two CheW adapter proteins, PilI and ChpC, that likely interact with the histidine kinase ChpA to feed environmental signals into the system. In the current study we show that ChpC is involved in the response to host-derived signals serum albumin, mucin and oligopeptides. We demonstrate that these signals stimulate an increase in twitching motility, as well as in levels of 3′−5′-cyclic adenosine monophosphate (cAMP) and Surface-assembled T4P. Interestingly, our data shows that changes in cAMP and Surface piliation levels are independent of ChpC but that the twitching motility response to these environmental signals requires ChpC. Furthermore, we show that protease activity is required for the twitching motility response of P. aeruginosa to environmental signals. Based upon our data we propose a model whereby ChpC feeds these environmental signals into the Chp system, potentially via PilJ or another MCP, to control twitching motility. PilJ and PilI then modulate T4P Surface levels to allow the cell to continue to undergo twitching motility. Our study is the first to link environmental signals to the Chp chemosensory system and refines our understanding of how this system controls twitching motility-mediated biofilm expansion in P. aeruginosa
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chpc controls twitching motility mediated expansion of pseudomonas aeruginosa biofilms in response to serum albumin mucin and oligopeptides
bioRxiv, 2019Co-Authors: Cb Whitchurch, Laura M Nolan, Laura C Mccaughey, Jessica Merjane, Lynne TurnbullAbstract:Abstract Twitching motility-mediated biofilm expansion occurs via coordinated, multi-cellular collective behaviour to allow bacteria to actively expand across Surfaces. Type-IV pili (T4P) are cell-associated virulence factors which mediate this expansion via rounds of Extension, Surface attachment and retraction. The Chp chemosensory system is thought to respond to environmental signals to regulate the biogenesis, assembly and twitching motility function of T4P. In other well characterised chemosensory systems, methyl-accepting chemotaxis proteins (MCPs) feed environmental signals through a CheW adapter protein to the histidine kinase CheA to modulate motility. The Pseudomonas aeruginosa Chp system has two CheW adapter proteins, PilI and ChpC, and an MCP PilJ that likely interacts via PilI with the histidine kinase ChpA. It is thought that ChpC associates with other MCPs to feed environmental signals into the system, however no such signals have been identified. In the current study we show that ChpC is involved in the response to host-derived signals serum albumin, mucin and oligopeptides. We demonstrate that these signals stimulate an increase in twitching motility, as well as in levels of 3’-5’-cyclic adenosine monophosphate (cAMP) and Surface-assembled T4P. Interestingly, our data shows that changes in cAMP and Surface piliation levels are independent of ChpC but that the twitching motility response to these environmental signals requires ChpC. Based upon our data we propose a model whereby ChpC associates with an MCP other than PilJ to feed these environmental signals through the Chp system to control twitching motility. The MCP PilJ and the CheW adapter PilI then modulate T4P Surface levels to allow the cell to continue to undergo twitching motility. Our study is the first to link environmental signals to the Chp chemosensory system and refines our understanding of how this system controls twitching motility-mediated biofilm expansion in P. aeruginosa.
Laura M Nolan - One of the best experts on this subject based on the ideXlab platform.
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chpc controls twitching motility mediated expansion of pseudomonas aeruginosa biofilms in response to serum albumin mucin and oligopeptides
bioRxiv, 2019Co-Authors: Cb Whitchurch, Laura M Nolan, Laura C Mccaughey, Jessica Merjane, Lynne TurnbullAbstract:Abstract Twitching motility-mediated biofilm expansion occurs via coordinated, multi-cellular collective behaviour to allow bacteria to actively expand across Surfaces. Type-IV pili (T4P) are cell-associated virulence factors which mediate this expansion via rounds of Extension, Surface attachment and retraction. The Chp chemosensory system is thought to respond to environmental signals to regulate the biogenesis, assembly and twitching motility function of T4P. In other well characterised chemosensory systems, methyl-accepting chemotaxis proteins (MCPs) feed environmental signals through a CheW adapter protein to the histidine kinase CheA to modulate motility. The Pseudomonas aeruginosa Chp system has two CheW adapter proteins, PilI and ChpC, and an MCP PilJ that likely interacts via PilI with the histidine kinase ChpA. It is thought that ChpC associates with other MCPs to feed environmental signals into the system, however no such signals have been identified. In the current study we show that ChpC is involved in the response to host-derived signals serum albumin, mucin and oligopeptides. We demonstrate that these signals stimulate an increase in twitching motility, as well as in levels of 3’-5’-cyclic adenosine monophosphate (cAMP) and Surface-assembled T4P. Interestingly, our data shows that changes in cAMP and Surface piliation levels are independent of ChpC but that the twitching motility response to these environmental signals requires ChpC. Based upon our data we propose a model whereby ChpC associates with an MCP other than PilJ to feed these environmental signals through the Chp system to control twitching motility. The MCP PilJ and the CheW adapter PilI then modulate T4P Surface levels to allow the cell to continue to undergo twitching motility. Our study is the first to link environmental signals to the Chp chemosensory system and refines our understanding of how this system controls twitching motility-mediated biofilm expansion in P. aeruginosa.
Laura C Mccaughey - One of the best experts on this subject based on the ideXlab platform.
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chpc controls twitching motility mediated expansion of pseudomonas aeruginosa biofilms in response to serum albumin mucin and oligopeptides
bioRxiv, 2019Co-Authors: Cb Whitchurch, Laura M Nolan, Laura C Mccaughey, Jessica Merjane, Lynne TurnbullAbstract:Abstract Twitching motility-mediated biofilm expansion occurs via coordinated, multi-cellular collective behaviour to allow bacteria to actively expand across Surfaces. Type-IV pili (T4P) are cell-associated virulence factors which mediate this expansion via rounds of Extension, Surface attachment and retraction. The Chp chemosensory system is thought to respond to environmental signals to regulate the biogenesis, assembly and twitching motility function of T4P. In other well characterised chemosensory systems, methyl-accepting chemotaxis proteins (MCPs) feed environmental signals through a CheW adapter protein to the histidine kinase CheA to modulate motility. The Pseudomonas aeruginosa Chp system has two CheW adapter proteins, PilI and ChpC, and an MCP PilJ that likely interacts via PilI with the histidine kinase ChpA. It is thought that ChpC associates with other MCPs to feed environmental signals into the system, however no such signals have been identified. In the current study we show that ChpC is involved in the response to host-derived signals serum albumin, mucin and oligopeptides. We demonstrate that these signals stimulate an increase in twitching motility, as well as in levels of 3’-5’-cyclic adenosine monophosphate (cAMP) and Surface-assembled T4P. Interestingly, our data shows that changes in cAMP and Surface piliation levels are independent of ChpC but that the twitching motility response to these environmental signals requires ChpC. Based upon our data we propose a model whereby ChpC associates with an MCP other than PilJ to feed these environmental signals through the Chp system to control twitching motility. The MCP PilJ and the CheW adapter PilI then modulate T4P Surface levels to allow the cell to continue to undergo twitching motility. Our study is the first to link environmental signals to the Chp chemosensory system and refines our understanding of how this system controls twitching motility-mediated biofilm expansion in P. aeruginosa.
Il Hyung Park - One of the best experts on this subject based on the ideXlab platform.
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Articular Surface Area of the Coronoid Process and Radial Head in Elbow Extension: Surface Ratio in Cadavers and a Computed Tomography Study In Vivo
Journal of Hand Surgery (European Volume), 2010Co-Authors: Seong Ho Shin, Matthew B. A. Mccullough, Jae Hyuck Yi, In-ho Jeon, Il Hyung ParkAbstract:Purpose To quantify the articular Surface area ratio of the radial head to the coronoid process to gain a better understanding of the stress distribution across these articulations and possibly to explain the patterns of osteoarthritis that are commonly seen in the elbow. Methods Thirty cadaveric elbows were harvested and dissected to allow measurement of the radial head and coronoid process articular Surfaces. The articular Surface areas were measured using the Image J program (National Institutes of Health, Chicago, IL). Twelve men were recruited for this study, and all received a computed tomography (CT) scan of the elbow. A 3-dimensional image of the proximal radioulnar articular Surface was created using volume rendering. All specimens were measured 3 times by 2 observers. Results In the cadaveric measurements, the mean area of the radial head articular fossa was 247.3 ± 52.6 mm 2 (mean ± SD). The mean area of the medial facet of the coronoid process was 232.29 ± 36.5 mm 2 , and the mean area of the lateral facet was 141.9 ± 33.3 mm 2 . The articular Surface area ratio of radial head to coronoid process was 1:1.5. In the CT measurement, the mean area of the radial head articular fossa was 258.9 ± 26.3 mm 2 . The mean area of the coronoid process articular Surface was 376.9 ± 37.0 mm 2 . The articular Surface area ratio of radial head to coronoid process was 1:1.46. Conclusions The ratio of articular Surface area of radial head to coronoid process is 1:1.51 in cadavers and 1:1.46 using a CT in vivo , which is the reverse of the reported force transmission ratio across the elbow joint.
Lm Nolan - One of the best experts on this subject based on the ideXlab platform.
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ChpC controls twitching motility-mediated expansion of Pseudomonas aeruginosa biofilms in response to serum albumin, mucin and oligopeptides
'Microbiology Society', 2020Co-Authors: Lm Nolan, Lc Mccaughey, Merjane J, Turnbull L, Cb WhitchurchAbstract:Twitching motility-mediated biofilm expansion occurs via coordinated, multi-cellular collective behaviour to allow bacteria to actively expand across Surfaces. Type-IV pili (T4P) are cell-associated virulence factors which mediate twitching motility via rounds of Extension, Surface attachment and retraction. The Chp chemosensory system is thought to respond to environmental signals to regulate the biogenesis, assembly and twitching motility function of T4P. In other well characterised chemosensory systems, methyl-accepting chemotaxis proteins (MCPs) feed environmental signals through a CheW adapter protein to the histidine kinase CheA to modulate motility. The Pseudomonas aeruginosa Chp system has an MCP PilJ and two CheW adapter proteins, PilI and ChpC, that likely interact with the histidine kinase ChpA to feed environmental signals into the system. In the current study we show that ChpC is involved in the response to host-derived signals serum albumin, mucin and oligopeptides. We demonstrate that these signals stimulate an increase in twitching motility, as well as in levels of 3′−5′-cyclic adenosine monophosphate (cAMP) and Surface-assembled T4P. Interestingly, our data shows that changes in cAMP and Surface piliation levels are independent of ChpC but that the twitching motility response to these environmental signals requires ChpC. Furthermore, we show that protease activity is required for the twitching motility response of P. aeruginosa to environmental signals. Based upon our data we propose a model whereby ChpC feeds these environmental signals into the Chp system, potentially via PilJ or another MCP, to control twitching motility. PilJ and PilI then modulate T4P Surface levels to allow the cell to continue to undergo twitching motility. Our study is the first to link environmental signals to the Chp chemosensory system and refines our understanding of how this system controls twitching motility-mediated biofilm expansion in P. aeruginosa
