Eminent scientists are well-placed to bring the novel works of others, even if not in their own areas of expertise, to general attention. In so doing, they may be able to extend original accounts or introduce new terminologies, but they are basically messengers, not innovators. In the 1940s an evolutionary theory of biological aging was explained by Peter Medawar, and informational concepts relating to DNA were explained by Erwin Schrödinger. Both explanations were eventually traced back to the Victorian polymath Samuel (...) Butler—one by Medawar’s research associate Alex Comfort, and the other, albeit indirectly, by Schrödinger himself. In his time Butler’s works were too erudite for general readers and too laden with populist jargon for contemporary experts to take seriously. However, today it appears counterfactually plausible that an early acceptance of his ideas would have greatly quickened the pace of research. (shrink)

Knowing how introns originated should greatly enhance our understanding of the information we carry in our DNA. Gilbert’s suggestion that introns initially arose to facilitate recombination still stands, though not for the reason he gave. Reanney’s alternative, that evolution, from the early “RNA world” to today’s DNA-based world, would require the ability to detect and correct errors by recombination, now seems more likely. Consistent with this, introns are richer than exons in the potential to extrude the stem-loop structures needed for (...) the homology search that can lead to heteroduplex formation and the recognition of base mismatches. In nucleic acid sequences that were unable concomitantly to encode sufficient stem-loop potential, protein-encoding potential was constrained to arise as segments (exons) interrupted by segments rich in stem-loop potential (introns). Thus, sequences with properties that we now deem intronic are likely to have preceded the emergence of exons. (shrink)

In contrast to the two X chromosomes that participate equally in oogenic meiosis in mammals, during spermatogenesis the solitary X chromosome can be regarded as an inadequate pairing partner for the Y chromosome. Hence it is epigenetically silenced and consigned to the XY body. This silenced state can transfer between generations. The sleeping X will awake when in a female cell with an accompanying maternally donated X chromosome. Transgene experiments in nematodes indicate that a similar process can operate at the (...) level of chromosomal segments. A gene that mispairs at meiosis is epigenetically silenced and transferred to the next generation where its awakening is conditional on the presence of a meiotic pairing partner. These intergenerational transfers of epigenetic labelling, and intragenerational reversals thereof, might apply at the level of individual bases when confronted with inadequate pairing partners. During meiotic recombination, homologous DNA sequences of maternal and paternal origin pair to form a mutual duplex, and mismatches can be detected and corrected. But there is only a 50 % chance that the correction will favor a particular allele. There is information that a DNA duplex segment is in need of correction, but not how correction could asymmetrically favor one allele. If the segment were epigenetically marked as “suspect,” this information could be used in a future generation to favorably correct should more information, in the form of a homologous unmutated duplex, became available. So fundamental would this mechanism be that it would have provided a selection pressure for the emergence of epigenetic marking early in evolution. (shrink)