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Data from: Experimental analysis of organ decay and pH gradients within a carcass and the implications for phosphatization of soft tissues

Citation

Clements, Thomas; Purnell, Mark; Gabbott, Sarah (2022), Data from: Experimental analysis of organ decay and pH gradients within a carcass and the implications for phosphatization of soft tissues, Dryad, Dataset, https://doi.org/10.5061/dryad.k6djh9w8n

Abstract

Replacement of soft-tissues by calcium phosphate yields spectacular fossils. Decay experiments have shown that pH is a major control on the precipitation of calcium phosphate and tissue replication: for this to occur pH must fall below the carbonic acid dissociation constant (pH 6.38). However, in the fossil record, phosphatisation is highly selective - some internal organs, such as muscles, stomachs, and intestines, appear to preferentially phosphatise while other organs seldomly phosphatise. The reasons for this are unclear but one hypothesis is that, during decay, organs create distinct chemical microenvironments and only some fall below the critical pH threshold for mineralization to occur. Here, we present a novel investigation using microelectrodes that records fluctuating dynamic spatial and temporal pH gradients inside of organs within a carcass in real time. Our experiments demonstrate that within a decaying carcass, organ-specific microenvironments are not generated. Rather, a pervasive pH environment forms within the body cavity (i.e. the coelom) which persists until integumentary failure. With no evidence to support the development of organ-specific microenvironments during decay other factors must control organ phosphatisation. We propose it is tissue histology that plays an important role in selective phosphatisation. Tissues with high phosphate content (and those rich in collagen) are most likely to phosphatise. Internal organs that have low tissue-bound phosphate, including the integuments of the stomach and intestine, only phosphatise when associated with ingested phosphate-rich organic matter. Identifying the driver behind selective phosphatisation may provide insights into other highly selective modes of soft-tissue preservation i.e. pyritization.

Methods

The experiment was recorded pH data using Lazar PHR-146XS-7C pH probes (accuracy: ±0.01pH) connected to independently to an electronic 'reader' (JENCO 6230N) and calibrated immediately prior to each experiment. The readers were plugged into a USB super-hub via RS232 cables and then connected to a computer. Data was logged every half hour automatically and transposed in MS Excel.  

Funding