A model for the effects of germanium on silica biomineralization in choanoflagellates

Silica biomineralization is a widespread phenomenon of major biotechnological interest. Modifying biosilica with substances like germanium (Ge) can confer useful new properties, although exposure to high levels of Ge disrupts normal biosilicification. No clear mechanism explains why this disruption occurs. Here, we study the effect of Ge on loricate choanoflagellates, a group of protists that construct a species-specific extracellular lorica from multiple siliceous costal strips. High Ge exposures were toxic, whereas lower Ge exposures produced cells with incomplete or absent loricae. These effects can be ameliorated by restoring the germanium : silicon ratio, as observed in other biosilicifying organisms. We developed simulations of how Ge interacts with polymerizing silica. In our models, Ge is readily incorporated at the ends of silica forming from silicic acid condensation, but this prevents further silica polymerization. Our ‘Ge-capping’ model is supported by observations from loricate choanoflagellates. Ge exposure terminates costal strip synthesis and lorica formation, resulting in disruption to cytokinesis and fatal build-up of silicic acid. Applying the Ge-capping model to other siliceous organisms explains the general toxicity of Ge and identifies potential protective responses in metalloid uptake and sensing. This can improve the design of new silica biomaterials, and further our understanding of silicon metabolism.

Calcofluor white and Congo red inhibit chitin microfibril assembly of Poterioochromonas: evidence for a gap between polymerization and microfibril formation.

The influence of the light microscopical stains, Calcofluor white and Congo red, on the process of chitin microfibril formation of the chrysoflagellate alga Poterioochromonas stipitata was studied with light and electron microscopy. There is a concentration-dependent inhibition of lorica formation with both dyes. In the presence of the inhibitors malformed loricae are made, which do not show the usual ultrastructure and arrangement of the chitin microfibrils. Instead of long, laterally associated microfibrils, short rods or irregular networks of subelementary (15-25 A) fibrils are found. Microfibril assembly obviously takes place on the accessible outside of the plasma membrane. There must be a gap between the polymerization and microfibril formation reactions, allowing the stains to bind to the polymerized subunits. Thus, later association of these units to form microfibrils is disturbed. The microfibril-orienting mechanism also depends on normal microfibril formation. A model summarizing these hypotheses is suggested.