The mechanisms and timing of mineralization of fossil phosphatized soft tissues

Wilby, Philip Richard (1993). The mechanisms and timing of mineralization of fossil phosphatized soft tissues. PhD thesis The Open University.



Fossil phosphatized soft tissues offer palaeontologists a unique opportunity to examine the biology and physiology of extinct organisms at the cellular and even macromolecular level. All phosphatized soft tissues are preserved by one or more of three preservational styles. These are: 1) phosphatized microbial infestations, 2) non-microbial (i. e. inorganic) phosphatic coatings, and 3) inorganic replacements. This suggests that three different (but related) processes are involved in the phosphatization of soft tissues. Each of these processes preserves the tissues at a predictable resolution; the most detailed preservation being afforded by inorganic replacements. In general, the soft tissues of closely related organisms have similar preservational styles. This reflects similarities in the biochemistry and taphonomy of closely related taxa.

In the majority of cases of soft tissue phosphatization, the most important source of phosphorus appears to have been external to the organism undergoing mineralization. An accessible source of phosphorus is, however, not the only variable dictating mineralization; phosphatization is extremely taxon-, tissue-, and biomolecule-specific. Of particular importance is: a) the concentration of phosphorus in the organism's soft tissues; b) the tissue's proximity to the source of phosphorus; c) the rate of tissue decay relative to the onset of mineralization; and, d) the pH and chemical composition of the decay-induced microenvironment surrounding the carcass. Certain groups of organisms (e. g. crustaceans, squid, and fish) appear to be somewhat 'preconditioned' for phosphatization.

All fossil phosphatized soft tissues exhibit evidence of decay. Taphonomic experiments suggest the period between death and phosphatization to have been as little as 55 hours. In the case of microbial infestation, decay would have permitted the microbes to gain access to the carcass, and to release organically-bound phosphorus from its tissues. In inorganic phosphatization, decay stimulates mineralization by: a) degrading membranes and thus accelerating the rate at which dissolved phosphorus and calcium may invade the tissues; b) creating new "reactive" organic substrates on which apatite may precipitate; c) destroying intracellular nucleation inhibitors; and, d) creating a favourable chemical microenvironment for the precipitation of apatite. Inorganic postmortem phosphatization may therefore be considered to be an "end-member" of pathological biomineralization.

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