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Project Progress

We used vesicles of zwitterionic phospholipids, dipalmitoylphosphatidylcholine and ditridecanoylphosphatidycholine (DTPC), to represent prebiotic protocols (although we recognize that phospholipids are biologically produced, and that simpler lipids would have existed pre-biotically). We measured quantitative adsorption isotherms of both lipids on oxide particles (Figure 1) and imaged lipid bilayer formation on corresponding planar oxides using Atomic Force Microscopy (Figure 2). Results for both types of experiments at neutral pH revealed that adsorption is, indeed, oxide-dependent, with the affinity decreasing as corundum (α-Al₂O₃) > rutile (α-TiO₂) > quartz (α -SiO₂). This follows the sequence of decreasing points of zero charge of the oxides. We developed a model to explain the observed affinity sequence, which relies on a balance of electrostatic and van der Waals forces. The implication is that protocells would have had a greater affinity for adsorption on positively-charged surfaces than for negatively-charged surfaces.

We used whole bacterial cells to address the question of whether EPS provides armor against cell lysis. A newly developed EPS-lacking mutant strain of Pseudomonas aeruginosa (Figure 3), and the wild-type, which is a robust EPS producer (Figure 3), were used to conduct cell viability studies in suspensions of oxide particles with cells. Wild type cell viability was greater than that of the mutant type. Furthermore, viability was oxide-dependent, increasing as γ-Al₂O₃ < anatase (β-TiO₂) < amorphous silica. Thus, our results confirm our hypothesis that EPS acts as a shield against the toxicity of certain minerals. In ongoing experiments, we are examining which surface properties of the minerals control their toxicity and the mechanisms of toxicity.

We are currently planning to conduct silicification experiments for both wild and mutant type cells in order to examine differences in morphology for preservation differences.