## 3 Results
### Intraspecies Interactions  
To search for intraspecies bacteriocin/toxin effects we spotted 5 \(\upmu\)L of liquid cultures of various _Marinobacter_ species (Table S1) on low percentage agar plates that allow for colony expansion via swimming or swarming. When only a single aliquot of motile _M. algicola_ were spotted onto 0.25% agar plates (hereafter agar plates), the colony expanded evenly in a radial manner. However, when sibling colonies were spotted near each other (within a few cm), they also grew radially until the colony edges came close to one another (>1 cm apart) whereupon expansion ceased with formation of sharp inhibition zones at these interfacial areas (Figure 1). We initially hypothesized that colonies nearing each other were producing toxins such as the described \"sibling lethal factor\" [49; 50], which would result in the killing of cells at the interface. Figure 1: _M. algicola_ DG893 growth on low percentage marine agar (0.25%) plates. The left pane shows growth of a single colony expanding by swarming while the right pane shows the growth of two sibling colonies placed a few centimeters apart, showing a clear zone of inhibition where the two colonies approach one another. Scale bar: 1 cm. To assess whether the cells in the inhibition zone were dead, or viable and still metabolically active, we utilized various enzymatic tests, a vital dye incorporation assay, as well as grow-out experiments (Figure 2). Positive succinate dehydrogenase or peroxidase activities were visualized by TTC or DAB staining, respectively. The red color of cells adjacent to the inhibition zones resulting from formazan precipitation indicated an unperturbed Krebs cycle, while lack of staining of corresponding areas with DAB suggest a lack of peroxidase activity in cells adjacent to inhibition zones. Propidium iodide (PI) staining was observable only in the cells located in \"old\" areas close to the center of the colony, indicating a loss of cell viability in this region. Cells at the edges of the expanding colony remained unstained and were assumed to be viable. Cell viability was independent of the location around the colony periphery, and included those cells found at the edge of the inhibition zone. Thus, when bacteria picked from the edges of the inhibition zones or from areas far from it were cultured in marine broth, they reached similar optical density regardless of location. Finally, fluorescence microscopy of vital dye treated cells (SYBR Green and PI) positioned at the inhibition zone and at the edges of non-interacting zones confirmed that they were still viable with a constant ratio of live vs. dead cells at the interface between colonies and on the non-interacting edges of the colony, and dividing cells were still evident at the interface (Figure S1). Z-stack plots across a transect also revealed that at the edge of the colony opposite the interaction area, the colony spreading zone was only a few cells thick, while at the inhibition zone it appeared to be a biofilm hundreds of cells thick (Figure 3). This behavior is consistent with the hypothesis that the cells at the inhibition zone continue to divide but have lost motility. That the apparent motility inhibition was temporary was indicated by the fact that when cells from the inhibition zone were res  
Figure 2: Metabolic activity and viability of motile _M. aligicola_ DG893 cells. To assess whether the motile cells were metabolically active. Agar plates were overlaid with either triphenyltetrazolzolium chloride (**A**), or diaminobenzzidine and H\({}_{2}\)O\({}_{2}\) (**B**), to visualize succinate dehydrogenase or peroxidase enzymatic activity, respectively. Non-stained regions are considered as metabolically inactive. Propidium iodide (PI) is known to incorporate into dead or permeable cells, thus the lack of staining shows that the cells near the inhibition zone are still viable (**C**). To verify viability of cells from different zones (marked on section B), their growth after 24 h was measured by OD600.