The mechanisms and timing of mineralization of fossil phosphatized soft tissues.
Fossil phosphatizeds oft tissueso ffer palaeontologistsa uniqueo pportunity 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.