Moss - What genes cant do - 2003 (522929), страница 48
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It is onlyafter this, in the context of such ongoing metabolizing enterprises thatRNA evolves as an intracellular, self-replicating parasite which eventually becomes symbiotically integrated into the life cycle of its host. Thehost provides the precursors for RNA replication and the RNA (andeventually DNA) comes to form through the evolution of translationmechanisms (and thus codons), an efficient repository of protein template information.5 Dyson takes his clue from “the strange fact thatthe two molecules, ATP and AMP, which have almost identical chemical structures, have totally different but equally essential functions inmodern cells.
ATP is the universal energy carrier. AMP is one of thenucleotides that make up RNA and function as bits of information inthe genetic apparatus” (Dyson 1999). Indeed ATP is a precursor in thesynthesis of RNA. How could one molecule come to be so central to twoentirely different roles? By Dyson’s schema, ATP had become establishedin its metabolic energy-carrying role. Various cells built up large quantities of it (as many cells still do).
In some cases it spontaneously polymerized into proto-RNA becoming, as it were, the first virus. Initiallycells would have become sick and died of this parasitic disease. But then,following the pattern of endosymbiosis described by Lynn Margulis6 forthe evolution of the eukaryotic cell, some infected cell would have developed the means to survive the infection and turn the relationship intoone of symbiotic mutualism.Dyson’s model has a number of benefits. Amino acids, the precursorsof proteins, are known to be capable of coming about spontaneouslyin a prebiotic environment. Indeed, they have even been found onmeteorites. Nucleic acids, like AMP, are much less likely to be spontaneously produced and much less stable afterwards if they are.Nucleotides would have a much better chance to accumulate andpolymerize inside of a metabolizing host.
But even more interesting (andunremarked upon by Dyson) is the heuristic perspective that Dyson’smodel suggests. That which began as a parasite because of its efficientself-replication capacity, brings along the perennial threat of newbouts of parasitism and new rounds of symbiotic accommodation.Nucleic acids (RNA and DNA) began as viruses and have never stoppedAfter the Gene193giving rise to viruses. Host cells have long since developed defense mechanisms against viruses marked as “other,” but what about new roundsof symbiosis?Almost half of human DNA (ten times more than that which is“coding”) is parasitic (Baltimore 2001). But it doesn’t constitute a sickness.
Why not? The uncontrolled expansion of transposable elements inthe genome is prevented through methylation (“epigenetic” chromatinmarking as discussed in chapter 3). And it is possible that the methylation system evolved for this purpose (Matzke et al. 2000, Symer andBender 2001). Eukaryotic cells have developed the capacity to recognizerepeat DNA and to prevent or regulate its transpositional spread throughmethylation. By the terms of the latest symbiotic modus vivendi (literally) parasitic DNA had become incorporated into the living enterprise,not for template-code stabilization but as a source of controlled destabilizaton for modularizing, complexity promoting, architectural restructuring of the genome.Evolution involves an ongoing symbiotic interplay between metabolichosts and perennially short-circuiting segments of nucleic acid. Thecreativity and volatility of the enterprise is realized in the interlockingdynamics of the systems of DNA repair, DNA recombination, DNAtransposition, and DNA methylation (Federoff 1999).
Turn on the faucetand reconfiguring forces begin to flow. Turn it on faster and, as Federoffsuggests, either evolution or cancer may ensue. Bacteria have been shownto turn on their “faucet,” referred to as an SOS system (Radman1973; Radman 1999) in response to conditions of stress. Metastaticcancer cells may well be reconstituting their own SOS system in(dynamic) response to becoming uncoupled from the stabilizing influences of a tissue matrix.From bacteria to humans it appears to be a universal ability of livingcells and living organisms to be able to turn on the faucet and allowsome destabilizing forces to flow. One may want to question whetherand how this may pertain to evolutionary dynamics that must cut acrossthe Weismannian barrier between the soma and the germ line (for thoseorganisms, like us, that sequester their germ line at any early stage ofdevelopment).
Evidence for the plausibility of this model can be gottenfrom the unfortunate example of Huntington’s disease. What turns a194Chapter 5certain Gene-D into a Huntington’s Gene-P is the inclusion of multiplecopies of the CAG trinucleotide (resulting in the inclusion of polyglutamine tracts in the translated protein known as “huntingtin”). Theseverity of the disease appears to be correlated with the number of suchrepeats,7 with the greater the number predicting an earlier age of onset.The finding that age of disease onset has had some tendency to decreasein subsequent generations has been referred to as “anticipation.” Whatis revealing is that anticipation results from a cross-generational expansion of the number of repeats, especially when the gene is passed fromfather to child. Male and female gametogenesis produce different patterns of chromatin methylation (imprinting) in the genomes of the resulting gametes.
Anticipation in the transmission of Huntington’s diseasethus has the earmarks of a process that involves the interlocking networkof DNA modulating enzyme systems proposed by Federoff: DNA repair,recombination, transposition, and methylation. Could it be thatHuntington’s and other CAG repeat-related diseases are tragic byproducts of those systems of genomic architectural reconstruction that occasionally give rise to evolutionary novelties? In any case the example ofHuntington’s disease provides a strong indication that even in humangametogenesis there is no ironclad barrier against forces of genomicreconstruction.Rebuking the Dawkinsonian ReplicatorTalk about parasitic DNA and its continuing role in the evolution of lifeforms may give some the impression of lending credence to trendy talkabout the selfish gene also known as “the replicator.” It shouldn’t.
ForRichard Dawkins and his epigones it is the parasite that invents the host(see table 1.1). Dawkins’s selfish replicator constitutes the quintessenceof conflationary confusion. His viewpoint does not build on the advancing elucidation of molecular biology but rather depends on an enforcedignorance of it. His is a biology built of ontotheology. His point of departure conditions all that follows. Dawkins and his followers take theirconflationary replicator (the so-called selfish gene) as an ontologicalbedrock. The “fact” of the primacy of the selfish replicator that standsin a creator-created relationship to all else is simply asserted as theAfter the Gene195grounds of all possible biological intelligibility.
The Dawkinsonians thenweave out the logic that follows from their ontology, and they defend itwith religious zeal.But why buy into such an ontology to begin with? The idea that a naturalistic account of evolution within a roughly Darwinian farmeworkrequires a fundamental replicator is patently false. The Darwinian tradition stakes its claim on the idea of descent with modification. Nowheredoes the need for either Xerox machines or Turing machines follow fromthis.
Now the idea of doing biology by way of ontologic has a strongappeal to bioideologues and philosophers who are good at logic andweak on biological details. But each time intellectually honest thinkersattempt to make good on a consistent and coherent notion of an evolutionary replicator they come to realize that boundaries become blurry,that whole organisms (Hull 1980) and even such things as nests and birdsongs (Sterelney, Smith and Dickison 1996) must also be classified asreplicators, and/or that in any event replicators are not necessary forDarwinian evolution (Godrey-Smith 2001).Parasitic DNA is just that. It is an ability of some chemicals to proliferate by chain reaction given the right conditions.
The parasite did notinvent the host, and it has only been the conflation of two nonoverlapping senses of the gene that have made it even tempting to think otherwise. When nucleic acids enter symbiotically into the enterprise of theliving system, they do so as one kind of resource among many. It is thewhole enterprise that will sink or swim and fail or succeed to leavedescendents that bear some resemblance, that inherit components andcontextualize them in a structurally and dynamically similar fashion.Evolutionary Developmental Biology (Evo-Devo) and theDevelopmental Basis of Evolvability (Devo-Evo)Aristotle approached reproduction as a continuation and outgrowth ofdevelopment (“generation”) and set the tone for centuries to come.During the “century of the gene” however, the processes of biologicalchange that take place during one generation and those across generations became radically dichotomized.8 Transgenerational change (evolution) was deemed to be the result of random point mutations that take196Chapter 5place, as it were, behind the backs of organisms and so are not teleological in any sense.
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