Anyway, here is the article.
Extending Darwinism
Is there more to heredity, natural selection, and evolution than genes and DNA?
Image courtesy of Bitforms Gallery, NYC (detail of "Path 25, 2001" by C.E.B. Reas).
Like Charles Darwin, Jean-Baptiste Lamarck suggested that living organisms are products of a long process of transformation. But instead of asserting, as Darwin did, that diversity emerges through the natural selection and accumulation of heritable variations over time, Lamarck proposed two mechanisms of evolutionary change: an inherent tendency in living matter to become increasingly more complex and the inheritance of acquired characteristics — environmentally induced or learned individual adaptations that accrue over time and pass to offspring. Many biologists at the time, including Darwin himself, believed such "soft" inheritance was complementary to the theory of natural selection.
Soft inheritance was passionately debated for decades but fell from favor in the 20th century with the forging of the Modern Evolutionary Synthesis (MS), a version of Darwinism that unified the theory of natural selection with Mendelian genetics, and, later, the myriad discoveries from the midcentury molecular biology revolution of the 1950s, '60s, and '70s. For the past 60 years, it has provided the theoretical basis for evolutionary studies.
In the MS, Lamarck's soft inheritance is effectively impossible. It explains biological heredity only in terms of the blind variation of genes (which are DNA base sequences). Gene exchange through either sexual production or some rare genetic mutations accounts for inherited differences between individuals; any and all bodily changes acquired or induced during an individual's lifetime, such as muscles enlarged through exercise, cannot be passed to offspring. Macroevolutionary changes (such as new species) are simply the gradually accumulated effects of genetic variations; sudden evolutionary changes are rare and insignificant.
I and several other biologists believe the MS is in need of serious revision. Growing evidence indicates there is more to heredity than DNA, that heritable non-DNA variations can take place during development, sometimes in response to an organism's environment. The notion of soft inheritance is returning to reputable scientific inquiry. Moreover, there seem to be cellular mechanisms activated during periods of extreme stress that trigger bursts of genetic and non-genetic heritable variations, inducing rapid evolutionary change. These realizations promise to profoundly alter our view of evolutionary dynamics.
Collectively, the processes that we believe have been neglected in evolutionary studies are known as epigenetic mechanisms. Epigenetics is a term that includes all the processes underlying developmental flexibility and stability, and epigenetic inheritance is part of this. Epigenetic inheritance is the transmission of developmental variations that have nothing to do with changes in DNA base sequences. In its broad sense, it covers the transmission of any differences that do not depend on gene differences, so it encompasses the cultural inheritance of different religious beliefs in humans and song dialects in birds. It even includes the developmental legacies that a young mammal may receive from its mother through her placenta or milk — transmitted antibodies, for example, or chemical traces that tell the youngsters what the mother has been eating and, therefore, what they should eat. But epigenetic inheritance is commonly associated with cellular heredity, in which differences that arise among genetically identical cells are transmitted to daughter cells.
Biologists have long suspected that mechanisms for epigenetic cell heredity must exist. Take, for example, our own embryonic development, when cells assume different roles. Some become kidney cells, others liver cells, and so on. Although they have the same DNA, liver cells and kidney cells look different and have different functions. In biologist jargon, they have the same genotype but different phenotypes. Moreover, they "breed true": Kidney cells generate more kidney cells, and liver cells generate more liver cells, even though the stimuli that induced the different phenotypes in embryonic precursor cells are long gone. There must be some epigenetic mechanisms to ensure that a cell "remembers" what it was induced to be and transmit this "memory" of its altered state to daughter cells. This much is obvious. But surprisingly, we now know that cellular epigenetic variations are transmitted not only within organisms, but sometimes also between generations of organisms, via their sperm and eggs.
So if cells pass on information in epigenetic memories as well as in their DNA sequences, how are the two types of inheritance related? Marion Lamb and I have hit upon a helpful analogy. An organism's genotype (DNA) is like a musical score; phenotypes are particular interpretations and performances of that score. Like DNA's replication, a score can be copied and transmitted from generation to generation through high-fidelity duplication processes, and although small mistakes (mutations) crop up from time to time, the score remains essentially unchanged. But nowadays music is not transmitted solely through the score: Interpretations can be passed to future generations using the very different technology of recording and broadcasting (analogous to epigenetic inheritance mechanisms). Even with identical musical scores, performances differ, since they depend on the culture, conductor, musicians, and instruments. In the same way, DNA 's performance depends on conditions within the cell. Because of recordings, the musical interpretations of one generation may influence the subsequent performances of later generations. Similarly, because of epigenetic inheritance, the characteristics acquired in one generation can affect what happens in the next. Interesting interactions can occur between the two routes of music transmission — changes in the score will obviously affect the performance, but some performances may actually modify the score that later musicians use. There are comparable interactions between genetic and epigenetic inheritance.
In the 1990s the evidence that epigenetic variants can be transmitted between generations of organisms was rather sparse, but this is no longer true. Epigenetic cell inheritance has become a major topic in molecular biology, and more and more examples of transgenerational inheritance are emerging. Gal Raz and I recently went through the scientific literature and found more than a hundred well-documented cases. They include inherited differences in the cortex; the surface structures of the protozoan Paramecium; self-reproducing architectural variants of proteins (prions) in fungi; inherited variations in flower morphology and color; inherited diseases in rats, induced during pregnancy by administering one dose of a male hormone suppressor to their mothers; inherited heart deformities in mice that were associated with transmissible, regulatory small RNA molecules. Our list isn't endless, but it shows that heritable epigenetic variations occur in all types of organisms and affect many different types of traits. Our findings may be the tip of a very large iceberg. The variations had certain stabilities — some lasting for many generations, some for only a few — and they involved several molecular mechanisms.
The mechanism about which we know the most is DNA methylation. Certain genes are "silenced," or rendered inactive, when small chemical groups (methyls) bond to some of the Cs of the four-letter alphabet (TAG C) that encodes information in DNA. These are not mutations because the coding properties of these Cs do not change, and if methyls are removed, the genes can become active again. This is not only an epigenetic control mechanism but also an epigenetic inheritance system, since a gene's pattern of methylation, and hence its state of activity, can be replicated and passed on to daughter cells.
One interesting and important discovery is that stresses — unusual conditions difficult for organisms to cope with, such as extreme heat, starvation, toxic chemicals, or drastic hormonal changes — are potent inducers of heritable epigenetic change. They can, for instance, alter patterns of methylation at many different DNA sites. Genomic stresses can have a similar effect, such as those from hybridization between plant species. Two recently formed natural hybrids between American and European species of the cordgrass Spartina had 30 percent of their parental DNA methylation patterns altered. This is an extreme example, but there are many others showing that stress conditions cause genome-wide effects and are sometimes associated with extensive changes in DNA sequences. It seems that stress can lead to a repatterning of the genome.
What does all of this mean for our view of heredity and evolution? The first implication is that when we see different heritable types in a population, we should not automatically assume they are genetically different; the differences may well be epigenetic. When they are, they might have been induced by environmental conditions. Unfortunately, at present we do not know how much epigenetic variation exists in natural populations, although botanists are beginning to study this in plants. If there is as much natural variation induced by environmental factors as lab studies suggest, then rapid evolutionary change could occur without any genetic change at all.
Further, induced and heritable epigenetic changes may guide genetic changes. Imagine that an environmental change repeatedly leads to a particular developmental adjustment — hot conditions induce thin fur in a population of mammals, for example. This epigenetic change could persist in the population until a genetic change occurred and rendered the thin-hair phenotype "inborn." In this way induced phenotypic changes, including epigenetically heritable ones, may precede and direct the selection of genetic changes. As Mary Jane West-Eberhard has aptly put it, "Genes are followers in evolution."
In the light of epigenetics, old views of macroevolution must change. If wide-ranging epigenetic and genetic changes occur in stressful conditions, they are likely to have many effects on an organism's form and function, its phenotype. This implies that conditions requiring novel adaptations to cope with them are often the very same ones that spur the massive epigenetic and genetic alterations conducive to rapid evolutionary change. A firm linkage between the production of new variation and its subsequent selection, something forbidden within the MS, grows ever clearer.
My colleagues and I have argued that various types of epigenetic inheritance have played key roles in all the major evolutionary transitions. For example, the symbiotic relations with bacteria that gave rise to modern cells would have been impossible without epigenetic mechanisms allowing their cell membranes to reproduce; cellular epigenetic inheritance mechanisms were necessary for the transition from single-celled creatures to complex multicellular organisms with many cell types; a new non-genetic system of information transmission (symbolic language) was crucial for the transition to human culture.
There is no doubt that acknowledging epigenetic inheritance alters our perspective on heredity and evolution. It eliminates the "negatives" in the MS and produces a broader theoretical framework, which puts the development horse firmly in front of the genetic cart. The origin of phenotypic variations takes a central position, sudden generational evolutionary changes assume significance, and soft inheritance gains recognition as part of heredity and evolution. Once again, Darwinian evolutionary theory is extending its boundaries and inspiring new studies that will further enrich our understanding of life, its history, and its future.
Here is the excerpt from my article related to the role of the epigenetic control system of the organism in biological evolution. The whole article and the book is presented at MISAHA’s site: www.misaha.com
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Savely Savva
Biofield Control System and Biological Evolution
In the current discussion between promoters of ‘Intelligent Design’ (ID) and Neo-Darwinists, M. Behe is absolutely persuasive in showing the “irreducible complexity” of the blocks of a living organism such as the eye, cellular cilium or bacterial flagellum, etc16. These and other most complex organizations could not possibly emerge by random (undirected) mutations. Emergence of a new species is associated not with just one mutation but with a long chain of mutations that are clearly not random and must occur simultaneously. Until the whole chain is accomplished, the individual, let alone a population or the whole species, would not have any advantage in adaptation selection, as J. Bockris noted in his book.17 This was understood by many distinguished biologists like Lev S. Berg who wrote his Nomogenesis in 1922—there must be laws determining ontogenesis as well as phylogenesis and there is no place for randomness in the biological evolution.18
The problem with the current discussion is that it seems more ideological than scientific. Darwinism from the beginning enjoyed an overwhelming support of the scientific community because it presented an alternative to the religious creationism. Then, it became a dogma with the same function as any religious dogma—to keep the social organization stable, in this case the scientific community. However, the actual alternative to Darwinism is not Intelligent Design but the broadening of the scientific paradigm. To paraphrase Einstein, an Omnipotent Designer would not “play dice,” he would know what he wants to begin with. He would not leave abundant dead ends on the branches of the evolutionary tree still providing a reasonable food chain—the omega point in terms of Teilhard d’Chardin. And indeed in the religion mythology he starts with Adam and Eve.
One cannot exclude some intelligence behind the whole Universe, but this intelligence must have produced all the physical forces, laws of their interactions and universal constants, including those yet unknown interaction that are responsible for emergence of life. This idea is not anymore unreal than the Big Bang or Chaos as the starting point of the Universe (I. Prigogine would not claim that life started out of chaos).
The postulated concept of the biofield control system may bring biological evolution back into the realm of science. Considering the obvious role of the “mother”—the egg, the ants colony, etc. in the embryonic development (see development program above), one can assume that the mother’s BCS (its reproduction program) can cause changes in the biofield control system of the embryo and consequent simultaneous genetic changes in the embryo. This is what can explain not only the Lamarckian examples of the giraffe’s neck and the bird’s legs elongation but the whole evolutionary process. Back in 1954 biologist Curt Stern mentioned the possibility of the biofield participation in the mutagenesis and evolution.19 Thus, the proverbial question “What came first—the chicken or the egg?” remains open: the chicken’s mother might have been a pre-chicken with a transformed BCS.
The adaptation selection at the population level may play a more significant role in the intraspecies evolution. V. Geodakian suggested that the gene pool of the male part of a population has a broader distribution with respect to the sensitivity to environmental changes than that of the female part. Changes in the environment eliminate a part of the male population causing the shift of the population gene pool toward greater resistance to that environmental factor.20
What might have occurred in biological evolution is that some global factor(s) periodically interfered with the biofield control systems of many living organisms changing the “mothers’” reproductive programs and these, in turn, substantially and simultaneously changed genomes of the prodigy organisms. Global forces that caused directed mutagenesis, for instance during the Cambrian period, most likely worked not at the chemical (genes) level. This is another reason to learn the physics of the BCS.