This study has an initial insight into the way bacterial colonies wage war. We know that the initial antibiotics came from fungi, but bacteria use them also to protect their colony:-http://phys.org/news/2015-12-bacteria-resist.html-"For this study, Stubbendieck put together two species of non-pathogenic, soil-borne bacteria, Streptomyces and Bacillus subtilis, in different ways in the laboratory. He monitored the bacteria for different patterns in growth, motility and other factors when the organisms were together as opposed to when they were separate.-"Stubbendieck noticed that the two bacteria would grow as expected in each colony initially, but over time one of the bacteria colonies would start to destroy the other one.-***-"The molecule turned out to be very strange. It doesn't look like any of the familiar antibiotics," Straight said. "We find it interesting, because its chemical structure suggests it's probably functioning in a way that is very different from the common antibiotics that are used."-***-"'With two pieces of the puzzle—the molecule itself identified plus a way in which the resistance to that molecule would arise, including the identity of the genes that are responsible for resistance—Reed was able to dissect the pathway of resistance," Straight said. "And it turns out that in a B. subtilis membrane, proteins work as signaling systems for lots of different things. They can receive signals from the external environment, signals from other bacteria, signals telling them about the status of their cell in a fluctuating environment.

"'If something damages a membrane, bacteria have a way of sensing that and then turning on the response," Straight said. (my bold)-***-"All of the mutations Stubbendieck identified were in the same gene that encodes for a protein in the membrane that functions like a signaling protein, or it has a partner that it talks to, and all mutations turned on the signaling system. And, because the mutants had proteins that were turned on all the time, the drug that previously would have been effective could no longer kill the bacteria.-"Additionally, not only did the researchers see that resistance could emerge that way but also the population of the B. subtilis, the one that's typically killed by the drug, changed in appearance.-"'It had morphological shapes and structures to it, which suggested that this organism had undergone a really profound change. That allowed it not only to be resistant to this drug, which causes lysis, but also to move as a population of bacteria across the agar surface in a petri dish," Straight said.-"'This shows a way that organisms can interact with each other in a competitive, dynamic environment that's very different from the way we typically think about antibiotics," he added. "It is not just a simple, one-way street of a molecule that's produced and causes growth inhibition of the pathogen, and the pathogen can become resistant and that might be a problem for health reasons. What we're seeing here are molecules that can function like an antibiotic and cause something like lysis, or cell death. And the organisms can use not just one resistance function but a combination of responses as a way of circumventing a competitive crisis.'"-Comment: Once again, protein reactions acting as signal agents. This can all be epigenetic cell-controlled events, per Shapiro, as described in his book, and in my view the instructions exist to direct this.