How to Preserve a Dinosaur Cell

It seems that we’re not done with Schweitzer’s Bone paper. Dieter Britz was kind enough to send me a copy of the full paper, so I can tell you about the proposed preservation mechanism. And – by coincidence – Brian Thomas has written a second article on a different aspect of the same paper, called Did Scientists Find T. Rex DNA?

First, the “Molecular mechanism for preservation.” In the section just prior to the conclusion Schweitzer et al ask:

Cells are usually completely degraded soon after the death of the organism, so how could ‘cells’ and the molecules that comprise them persist in Mesozoic bone?

That’s not entirely unlike something Mr Thomas would say. But unlike the ICR’s “Science Writer” the authors go on to give a potential solution.

The answer may be that bones in particular offer an environment conducive to preservation. The argument from incredulity claiming that soft tissues simply could not survive millions of years is largely based on our own experiences with the meat on top of the bones – do these experiences translate so well to the stuff within bone? The paper says:

In the mineralized matrix of bone, many factors converge to alter the dynamics of cell death and degradation, ultimately contributing to disruption of the degradation pathway. For example, necrotic or apoptotic cells are rapidly destroyed by phagocytosis or by microbial attack post-mortem, but osteocytes are inaccessible to other live cells, which may, in part, explain their preservation in these ancient tissues. Second, osteocytes are inherently resistant to degradation because location within the bone matrix inhibits cell division, therefore cells may be required to last the lifetime of the organism. Osteocyte expression of apoptotic repressor proteins may also contribute to their persistence. The association of actin with alpha-actinin and fimbrin confers stability to actin over the lifetime of the cell and may also stabilize the protein after death. Finally, osteocytes have limited access to oxygen within the bone matrix, and may thus be protected from oxidative damage.

The authors believe that they have a large number of conceivable reasons why soft tissue could have survived so long – it remains to be seen how many of them are correct. The above would be most relevant, I think, to the first wee while after the organism dies – aside from a head start, as it were, in having as many cells to be potentially preserved as possible, I doubt they would be continuing to have such an effect tens of millions of years later. However it does show that bone cells are abnormally well protected from degradation, at least suggesting that abnormal survival times are possible.

In this vein the paper goes on to note that Autolysis (cell death via the enzymes it contains) “is self-limiting, and after reaching a certain threshold, the remaining cells are stable for long periods.” In addition:

The association with mineral affords other protections that are unavailable to non-biomineralized tissues and cells. The microcrystalline surfaces of apatite may act like clay grains, adsorbing degradative enzymes and inactivating them, and in addition to limiting access of microbes to osteocytes, the rigid bone matrix may also inhibit denaturation and molecular swelling that precedes autolysis.

What this all adds up to is that the natural processes that could be expected to destroy a cell under normal conditions wouldn’t happen – at least to such an extent and to all cells – as you would expect with ‘normal’ tissue. Then we can begin to talk about the long-term preservation of what makes up the cells:

In 2007, we hypothesized that iron, released post-mortem from hemoglobin and myoglobin through autolysis/degradation of red blood cells and muscle tissue, would act to “fix” both tissues and molecules, a hypothesis also put forth by others. Biologically active Fe (II), which is soluble, would rapidly convert to Fe (III) upon release from the cell, and precipitate out of solution. Iron is a reactive oxygen species (ROS), and this switch triggers the formation of hydroxyl radicals. Through a cascade of events referred to as Fenton chemistry, highly reactive hydroxyl radicals trigger both crosslinking of proteins and peroxidation and crosslinking of the fatty acids making up cell membranes. Because osteocytes are intimately linked through filopodia to the vascular system of bone, and because the iron-binding protein ferritin has been identified in this cell line [89] they would be susceptible to this chain reaction.

This, you’ll note, would not just preserve the proteins but the cell membrane as well. The section ends noting that iron has an “intimate association with the cell “membranes” in analytical TEM.” In addition, the proteins found (actin, tubulin, and PHEX – the latter of which I innacurately thought was one of the antibodies on Monday, my mistake) are all associated with the cell membrane, and their preservation would be enhanced if the membrane were “fixed.” The presence of the iron itself “may also function to bind oxygen, preventing oxidative damage to tissues and molecules,” and there are a few other aspects that they mention.

I remain undecided over whether the Schweitzer discoveries are the real deal, including whether or not they would be possible given the timeframe, as I do not know nearly enough about the subject to make a definitive judgement (neither do our friends at the ICR, I should think). I do think, however, that it is entirely unreasonable to both a) unquestionably accept that the finds are truly dinosaurian and especially b) completely disregard the above proposed mechanisms for preservation.Yet Mr Thomas has done both of those.

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Next, Brian’s latest article. In a shorter section immediately prior to the above the authors lay out their “Evidence for DNA.” Brian says:

The researchers applied two different DNA-sensitive stains to the osteocyte structures. The stains showed faint but visible DNA in a tight central location inside the long-dead cell remnant. This clearly corresponds to the remains of the cellular nucleus, although the study authors did not specify that.

The Bone study authors also applied an antibody that only binds to a DNA-packing protein called histone H4. It, too, bound to its target in the same central region within the dinosaur bone cell as the DNA showed. The stains and antibody did not bind other parts of the cell, nor the mineral matrix that originally surrounded the fossil.

The DNA is in exactly the right place to be dinosaur DNA, but without determining its sequence, it is difficult to be absolutely sure.

However, if it is dinosaur DNA—the most obvious explanation of the data—it cannot be millions of years old. This report was published on the heels of a separate study that determined the decay rate of DNA. It totally precludes the possibility that ancient DNA could last for a hundred thousand years at normal temperatures, much less millions of years.

Arguably the most important part of the two paragraphs in the paper is the following:

These data are not sufficient to support the claim that DNA visualized in these cells is dinosaurian in origin; only sequence data can testify to its source.

As Brian says, we can’t actually tell that it’s from a dinosaur unless we sequence it. Only he shouldn’t be saying that.

If we were to take the creationist view that extant birds are unrelated to dinosaurs, and dinosaurs make up a collection of equally unrelated “kinds,” then there we would have no way of determining what their sequence should look like to compare. If we found a bird-like sequence evolutionary biologists who accept the other evidence that birds are descended and thus most closely related to dinosaurs would be able to conclude that the DNA probably is from the bone. But a creationist would not be able to do the same.

There are other aspects worth noting. First, the “signal is greatly reduced from that seen in extant cells.” Secondly, “only about 15%–20% of cells from the dinosaurs reacted positively.” Both of these really show that a significant degree of degradation has occurred.

The recent DNA decay rate study that “totally precludes the possibility that ancient DNA could last for a hundred thousand years” (Brian’s emphasis) was, of course, the one covered here. What’s important is that the ‘decay’ discussed there was the breaking up of the DNA polymer into smaller and smaller subunits, down to single bases. I can not tell you at which point the techniques used by Schweitzer et al would be unable to pick up any remaining DNA strands, or even if that’s a relevant consideration. Schweitzer notes that amplifying and sequencing the small amount of DNA found may well not be possible with current technology, which the DNA decay paper more than agrees with. I don’t know if the dinosaur bones were preserved in “normal temperatures” or not, and the maximum length of time that the decay paper says a strand of DNA could last (at negative five degrees Celsius) is actually nearly seven million years.

So yes, we shall have to wait and see what comes of this. Jumping to conclusions at this point – especially creationist positions – is just silly.