Does deletion of chpC cause a loss of swimming phenotype or is there a hidden secondary mutation?
Mentor 1
Sonia Bardy
Start Date
1-5-2020 12:00 AM
Description
Pseudomonas aeruginosa is an opportunistic pathogen that is able to live in a wide range of environments. The capacity to live in this breadth of habitats is aided by its swimming motility mediated by a single flagellum and its twitching motility mediated by Type IV pili (TFP). These motility structures are controlled by chemosensory systems that allow bacteria to respond to their outside environment. The Chp system is a the chemosensory system in P. aeruginosa that controls TFP mediated twitching motility and regulates intracellular levels of adenosine 3’, 5’-cyclic monophosphate (cAMP). This system allows response to the cell’s outside environment based on communication with methyl-accepting chemotaxis proteins (MCPs). ChpC is an adaptor protein involved in twitching motility environmental response. ChpC connects with the MCP and is a homolog of CheW protein (found in Escherichia coli’s flagella chemotaxis system). Deletion of chpC (ΔchpC) is known to reduce twitching motility responses to environmental signals, but was not expected to have an effect on swimming motility. However, recent studies in our lab have unexpectedly shown that ΔchpC might be affecting flagellum formation and function. I have verified this phenotype by testing a lineage of our strains to determine when this altered phenotype first occurred. I will generate a fresh chpC deletion to determine if this deletion is truly responsible for loss of flagellation biogenesis and/or function, resulting in swimming motility flaws. If ΔchpC is responsible, complementation of chpC should restore swimming motility. Understanding the relationship between chpC and swimming capability can either confirm or deny relations between twitching and swimming motility systems in P. aeruginosa, leading to better understanding of the Chp system and regulation of different motility systems.
Does deletion of chpC cause a loss of swimming phenotype or is there a hidden secondary mutation?
Pseudomonas aeruginosa is an opportunistic pathogen that is able to live in a wide range of environments. The capacity to live in this breadth of habitats is aided by its swimming motility mediated by a single flagellum and its twitching motility mediated by Type IV pili (TFP). These motility structures are controlled by chemosensory systems that allow bacteria to respond to their outside environment. The Chp system is a the chemosensory system in P. aeruginosa that controls TFP mediated twitching motility and regulates intracellular levels of adenosine 3’, 5’-cyclic monophosphate (cAMP). This system allows response to the cell’s outside environment based on communication with methyl-accepting chemotaxis proteins (MCPs). ChpC is an adaptor protein involved in twitching motility environmental response. ChpC connects with the MCP and is a homolog of CheW protein (found in Escherichia coli’s flagella chemotaxis system). Deletion of chpC (ΔchpC) is known to reduce twitching motility responses to environmental signals, but was not expected to have an effect on swimming motility. However, recent studies in our lab have unexpectedly shown that ΔchpC might be affecting flagellum formation and function. I have verified this phenotype by testing a lineage of our strains to determine when this altered phenotype first occurred. I will generate a fresh chpC deletion to determine if this deletion is truly responsible for loss of flagellation biogenesis and/or function, resulting in swimming motility flaws. If ΔchpC is responsible, complementation of chpC should restore swimming motility. Understanding the relationship between chpC and swimming capability can either confirm or deny relations between twitching and swimming motility systems in P. aeruginosa, leading to better understanding of the Chp system and regulation of different motility systems.
