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September 22, 2012

How Did Bilaterian Evolution Happen? (Continued)




Although in Part One I used the legitimate analytical device of limiting to actual breeders my introductory examination of the historical evolution of Bilaterians, in reality throughout their long history of ~550 million years all Bilaterian gene pools were producing complete populations of animals, including those juveniles that did not survive development. And to understand how the actual breeders could have produced those unbroken chains of perfection we need to consider what mechanisms, operating on entire populations, could have favored that outcome. Before doing that I need to explain why I find certain terms favored by many biologists less than useful in this exercise.

I consider “negative selection” and “positive selection” unnecessary and misleading in considering, as I am, evolution over deep time. Yes, there were “victims” of selection (animals that died as juveniles) and “beneficiaries” of selection (the breeders) but they were all products of the same force: natural selection operating on the entire population. Juveniles afflicted with mal-formed vital organs died from those specific mal-developments and juveniles with perfectly formed organs (barring, of course, other causes of early death) passed their “genes for perfection” to offspring.

Some refer to the elimination of mal-formed juveniles as “stabilizing” selection. Again, I consider attempts to narrow the definition of selection by such gratuitous parsing not only unhelpful but profoundly misleading. If one thinks that lethal juvenile cancer was only an instrument of “stabilizing” selection because it eliminated imperfectly formed developing animals, it misses entirely the role played by selection pressure resulting from such deaths, pressure that enabled the affected gene pools to produce with great precision the most complex things known to exist in the universe. 


As I wrote in my August 27th posting I was perplexed by the reaction of two scientists to my idea; they said I was probably correct but I was wrong to insist that my idea was a radical departure from Neo-Darwinism. Here’s where I think they may have erred: they applied short-term thinking to the problem I address which is the entire history of Bilaterian evolution. They were probably thinking that cancer-caused deaths of individual juveniles was just another form of “stabilizing selection” and that I was therefore wrong to insist that without those deaths Bilaterians would not exist.

It is counter-intuitive in the extreme to insist that something that never occurred to any ancestor of any animal that ever existed—not a single one of them died of juvenile cancer—had a direct effect on the genetic makeup of all surviving Bilaterians, but sufficient thought will demonstrate that the phenomenon is not limited to cancer selection. For example the gene pool of any lineage that produced animals subjected to heavy predation by sighted predators either “learned” to modify the preyed-upon animals (improved camouflage, quicker detection of threat, faster flight speed, etc.) or that lineage ceased to exist. Similarly, any lineages subjected to heavy losses from lethal juvenile cancer initiated as a result of imprecise mitosis during development either learned to minimize imprecision or it went out of existence. My theory claims that lethal juvenile cancer did cause cumulatively enormous losses in all Bilaterian gene pools and that the surviving gene pools survived by producing animals equipped with a variety of characters that avoided cancer deaths in young animals. I refer to the genes that introduced these cancer defenses as “anti-oncogenes.”     


Selection pressure to accumulate defenses against cancer not only increased the likelihood that the lineage would survive, it enhanced that gene pool’s ability to express in every somatic cell all the characteristics embedded in the genotype. This idea—that anti-oncogenes were the primary enablers of developmental precision and thus of complexity—has been central to my theory from the beginning.

In 1984 I wrote the following in my Letter in the Journal of Theoretical Biology:

“Because the process leading to such genetic deaths [from lethal juvenile cancer] is believed to begin with imprecise replication of the genetic program in a single cell, I conclude that all anti-oncogenes also function as enhancers of precise replication.” [Emphasis in original.]

Without precision in the construction of all individual somatic cells the Bilaterian gene pools could not have produced animals with complex organs, and it is my conclusion that without selection pressure caused by the cancer deaths of uncountable juveniles the level of precision evident in all Bilaterians could not have emerged. This is what I wrote in Chapter Three (page 35) of my 1992 book:

“All [Bilaterian] lineages, having endured significant genetic losses to mutagen-induced cancer in juveniles, now possess a powerful array of anti-oncogenes.  The reason those germ lines produce animals of exquisite com­plexity lies in the abun­dance of anti-oncogenes—every one of them devel­opment-enhan­cive—that were col­lected be­cause the lineages en­dured losses from cancer.

So convinced am I that cancer defenses enabled the emergence of precise development I offered in Chapter Thirteen (page 167) of Cancer Selection the following as a proposed refutation of my theory:

“Find a morphophysiological character in any [juvenile Bilaterian] that would putatively protect it from cancer but would not also enhance precise execution of the development program.” 


It is my position that any plausible theory of Bilaterian evolution must explain—mechanistically—the emergence of the hyper-efficient mitosis required to produce all the descendants of the Ur-Bilaterians.  Genetics can explain how germ-line mutations and the rules of inheritance account for the genetic makeup of zygotes, and developmental biology can describe in detail the precise steps needed to construct the adult, but zygotes are not mature animals and description is not evolutionarily explicative.

The collective silence of evolutionary biologists on this subject reminds me of the famous “Then a miracle occurs” cartoon except that, unlike the fellow in the cartoon, the evolutionists haven’t even recognized the need for a miracle; the enormous challenge to their theory presented by the unbroken chains of perfect development is not even identified as a problem.

Because the origin of hyper-efficient mitosis in juveniles is not addressed by conventional theory it does not, in my opinion, explain the unbroken chains of perfect development and thus cannot explain the existence of a single Bilaterian.

The subject of these two postings is covered, in a somewhat different manner and at greater length, in Chapters Two and Three of Cancer Selection. A complete pdf of those two chapters is now available through links on this page.  (Scroll down to the lower portion.)  The same page provides links to the 1983 and 1984 Letters to JTB, the Google ebook version of CS, the Nature review and to some of the research papers citing my work.  

Comments and questions are welcomed here.

At this site you will find links to additional material including my original Letters to the Journal of Theoretical Biology and  the 1992 Nature review of my book.

Copyright © by James Graham 2012

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