Apoptosis Is Unchanged from Cambrian Corals to Humans
Science progresses when investigators boldly question assumptions. Look at the assumption that a group of scientists questioned: Darwinian evolution. Eight scientists from San Diego State University, Scripps Institution of Oceanography, and Cedars-Sinai Heart Institute published a bombshell in the Proceedings of the National Academy of Sciences:
The Precambrian explosion [they mean the Cambrian explosion] led to the rapid appearance of most major animal phyla alive today. It has been argued that the complexity of life has steadily increased since that event. Here we challenge this hypothesis through the characterization of apoptosis in reef-building corals, representatives of some of the earliest animals. Bioinformatic analysis reveals that all of the major components of the death receptor pathway are present in coral with high-predicted structural conservation with Homo sapiens. (Emphasis added.)
Apoptosis is "programmed cell death." When a cell becomes unstable or diseased, genetic algorithms kill it in an orderly way, to prevent further harm to the organism. Specialized enzymes (especially the TNF superfamilies) switch on the program, setting locked-up destroyers called caspases loose in the cell. The microbiologist can see bubbles and blisters forming (blebbing), followed by complete disruption of the cell and all its parts (this is animated in a sequence in Metamorphosis: The Beauty and Design of Butterflies, where the caterpillar parts are shown breaking down inside the chrysalis).
Corals have many of the same TNF enzymes that humans do. This got the team wondering:
The TNF receptor-ligand superfamilies (TNFRSF/TNFSF) are central mediators of the death receptor pathway, and the predicted proteome of Acropora digitifera contains more putative coral TNFRSF members than any organism described thus far, including humans. This high abundance of TNFRSF members, as well as the predicted structural conservation of other death receptor signaling proteins, led us to wonder what would happen if corals were exposed to a member of the human TNFSF (HuTNF?).
In a series of experiments, they inserted coral enzymes into human cells. The human cells died. Then they ran the reciprocal experiment, putting human TNF enzymes into coral, and its cells died too. Even the bleaching process was seen using human enzymes. The agents of death were perfectly interchangeable, despite 550 million years for evolution to have increased the complexity of the system.
HuTNF? was found to bind directly to coral cells, increase caspase activity, cause apoptotic blebbing and cell death, and finally induce coral bleaching. Next, immortalized human T cells (Jurkats) expressing a functional death receptor pathway (WT) and a corresponding Fas-associated death domain protein (FADD) KO cell line were exposed to a coral TNFSF member (AdTNF1) identified and purified here. AdTNF1 treatment resulted in significantly higher cell death (P < 0.0001) in WT Jurkats compared with the corresponding FADD KO, demonstrating that coral AdTNF1 activates the H. sapiens death receptor pathway. Taken together, these data show remarkable conservation of the TNF-induced apoptotic response representing 550 My of functional conservation.
Obviously, conservation is not evolution. This is evidence against Darwinian evolution on both sides of the coin: it shows no evolutionary "progress" despite all that time, and it shows a complex system appearing abruptly right at the beginning of complex animal origins. The significance of this discovery was not lost on the team: "Here we show that TNF induced apoptosis has been functionally maintained for more than half a billion years of evolution."
Abrupt appearance, and remarkable stasis: it's a common theme in biology. Can they rescue Darwinism from this evidence?
Phylogenetic analysis indicates a deep evolutionary origin of the TNFSF and TNFRSF that precedes the divergence of vertebrates and invertebrates. The most ancient and well-defined invertebrate TNF ligand-receptor system that has been described to date is that of the fruit fly Drosophila melangastor [melanogaster, sic passim]. D. melangastor posseses just one member of both the TNFRSF/TNFSF, in contrast to humans who have 18 and 29, respectively. This difference has led to the widely accepted hypothesis that the TNF ligand-receptor superfamily expanded after the divergence of invertebrates and vertebrates.
In this paper, we describe the annotation of 40 members of the TNFRSF and 13 members of the TNFSF in the reef building coral A. digitifera, suggesting that key parts of the TNF receptor ligand superfamily have been lost in D. melangastor but maintained in coral. Comparison of these coral TNFSF/TNFRSF members to those of Homo sapiens reveals high genetic and predicted structural conservation.
Instead of confirming Darwinian expectations, they debunked "the widely accepted hypothesis" that the complexity of the TNF ligand system should have increased. No; it was there from the beginning. Some animals lost some of it, but the most "primitive" Cambrian animals had it, and it works in human cells today.
This is no small matter. Most of the 53 proteins (containing 228 to 533 amino acids apiece) show "high amino acid conservation" with their human counterparts, especially at the active sites. From extreme ends of the animal complexity scale, tens of thousands of amino acids in these families of enzymes show no evolution at all. What's more, the coral's system appears even more complex than ours. "Compared with previously published work on members of the TNFRSF," they say, "corals contain the most diverse TNFRSF repertoire of any organism described to date, including humans."
About the only thing they could say in support of Darwinian evolution from these data is that evolution is a "non-linear process." If so, that is very different from the vision Darwin had of the slow, gradual accumulation of small variations.
This is but one more instance in a huge body of evidence supporting intelligent design for the origin of animal body plans, as Stephen Meyer explains further in Darwin's Doubt (now in paperback with an added chapter answering critics of the first edition). Apoptosis is but one mechanism that makes an organism work. It plays important roles in embryonic development as well as disease prevention. When you add up all the other systems required to build and maintain an animal, on so many levels, Darwinism seems clearly inadequate to the account for them. The only cause we know of that is able to explain the observations, from the overall forms down to the specific amino acids, is intelligent design.
Photo source: Wikipedia.