Trade-offs constrain adaptive pathways to type VI secretion system survival
Kathryn A. MacGillivray,
Siu Lung Ng,
Sophia Wiesenfeld,
Randi L. Guest,
Tahrima Jubery,
Thomas J. Silhavy,
William C. Ratcliff,
Brian K. Hammer
Affiliations
Kathryn A. MacGillivray
School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA, USA; Parker H. Petit Institute for Bioengineering & Bioscience, Georgia Institute of Technology, Atlanta, GA, USA; Center for Microbial Dynamics and Infection, Georgia Institute of Technology, Atlanta, GA, USA
Siu Lung Ng
School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA, USA; Parker H. Petit Institute for Bioengineering & Bioscience, Georgia Institute of Technology, Atlanta, GA, USA; Center for Microbial Dynamics and Infection, Georgia Institute of Technology, Atlanta, GA, USA
Sophia Wiesenfeld
School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA, USA; Parker H. Petit Institute for Bioengineering & Bioscience, Georgia Institute of Technology, Atlanta, GA, USA; Center for Microbial Dynamics and Infection, Georgia Institute of Technology, Atlanta, GA, USA
Randi L. Guest
Department of Molecular Biology, Princeton University, Princeton, NJ, USA
Tahrima Jubery
School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA, USA; Parker H. Petit Institute for Bioengineering & Bioscience, Georgia Institute of Technology, Atlanta, GA, USA; Center for Microbial Dynamics and Infection, Georgia Institute of Technology, Atlanta, GA, USA
Thomas J. Silhavy
Department of Molecular Biology, Princeton University, Princeton, NJ, USA
William C. Ratcliff
School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA, USA; Parker H. Petit Institute for Bioengineering & Bioscience, Georgia Institute of Technology, Atlanta, GA, USA; Center for Microbial Dynamics and Infection, Georgia Institute of Technology, Atlanta, GA, USA; Corresponding author
Brian K. Hammer
School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA, USA; Parker H. Petit Institute for Bioengineering & Bioscience, Georgia Institute of Technology, Atlanta, GA, USA; Center for Microbial Dynamics and Infection, Georgia Institute of Technology, Atlanta, GA, USA; Corresponding author
Summary: The Type VI Secretion System (T6SS) is a nano-harpoon used by many bacteria to inject toxins into neighboring cells. While much is understood about mechanisms of T6SS-mediated toxicity, less is known about the ways that competitors can defend themselves against this attack, especially in the absence of their own T6SS. Here we subjected eight replicate populations of Escherichia coli to T6SS attack by Vibrio cholerae. Over ∼500 generations of competition, isolates of the E. coli populations evolved to survive T6SS attack an average of 27-fold better, through two convergently evolved pathways: apaH was mutated in six of the eight replicate populations, while the other two populations each had mutations in both yejM and yjeP. However, the mutations we identified are pleiotropic, reducing cellular growth rates, and increasing susceptibility to antibiotics and elevated pH. These trade-offs help us understand how the T6SS shapes the evolution of bacterial interactions.
