Bacteriophages (phages) are the most abundant entities in nature, yet little is known about their capacity to acquire new hosts and invade new niches. By exploiting the Gram-positive soil bacterium Bacillus subtilis (B. subtilis) and its lytic phage SPO1 as a model, we followed the coevolution of bacteria and phages. After infection, phage-resistant bacteria were readily isolated. These bacteria were defective in production of glycosylated wall teichoic acid (WTA) polymers that served as SPO1 receptor. Subsequently, a SPO1 mutant phage that could infect the resistant bacteria evolved. The emerging phage contained mutations in two genes, encoding the baseplate and fibers required for host attachment. Remarkably, the mutant phage gained the capacity to infect non-host Bacillus species that are not infected by the wild-type phage. We provide evidence that the evolved phage lost its dependency on the species-specific glycosylation pattern of WTA polymers. Instead, the mutant phage gained the capacity to directly adhere to the WTA backbone, conserved among different species, thereby crossing the species barrier.

Colonies are an abundant form of bacterial multicellularity; however, relatively little is known about the initial stages of their construction. We have previously described that colony development of the soil bacterium Bacillus subtilis is a highly ordered process, typically initiating with the formation of extending cell chains arranged in a Y shape structure. Furthermore, we demonstrated that Y arm extension is a key for defining the size of the future colony. Here we conducted a genetic screen surveying for mutants deficient in these early developmental stages, and revealed LtaS, the major lipoteichoic acid (LTA) synthase, to be crucial for execution of these events. We found that the ltaS mutant fails to produce proper Y shape structures, forming extremely elongated chains of cells with no evidence of chain breakage, necessary for Y shape formation. Furthermore, we show that frequent cell death at the tips of the cell chains is a major cause in limiting arm extension. Collectively, these perturbations lead to the production of a small sized colony by the mutant. Thus, deficiency in LTA synthesis causes a mechanical failure in executing the colony developmental program.