Cooperative T4 Phage Resistance in E. coli

Studies by Delbruck and Luria of the resistance of the common bacteria E. coli to bacteriophages ushered in the age of quantitive molecular biology. The sophisticated analysis using colony number fluctuation ``jackpots’’ was used to support the assumption of the authors that resistance to phage occurred in previous generations of bacteria by random chance, and not by exposure to the phage. This presumably put a stake in heart of the Lamarckian hypothesis of acquired phenotypes, and so it is taught in countless introductory biology courses.

But in the years following this work we have learned that Lamarck is not so easily dismissed, and we now know that there are many ways for organisms from bacteria to man to acquire heritable phenotype changes upon transient exposure to stress. We have show in a previous publication that stress gradients imposed over a metapopulation of weakly interacting communities can greatly increase the rate at which de novo evolved resistance the mutagenic antibiotic ciproflaxen. This begs the question: can a similar application of fundamental theories of evolution in small interconnected populations also be used to accelerate the {em de novo} emergence of phage resistance in E. coli? We do not aim to disprove the classic experiments of Delbruck and Luria of course, they are correct as implemented. But we do wish to show those experiments were incomplete and we show that indeed rapid de novo emergence to phage can occur upon exposure to phage.