Why Sexual Reproduction? What'sNEW
In spite of the number of ways bacteria can exchange genetic instructions, many of them haven't evolved very far — not as bacteria anyway. There are many modern bacteria that look very similar to fossils of the earliest bacteria of over 3 billion years ago. Eukaryotes are much better at evolving than prokaryotes. Eukaryotes first appeared on Earth about 1.7 billion years ago. They contain complex subunits, some of which — mitochondria and plastids — have their own DNA. With the appearance of eukaryotes, evolution began to accelerate. All multicelled animals and plants are made of eukaryotic cells. Where did they come from?
Eukaryotes by Symbiosis
Research biologist Lynn Margulis has finally won acceptance for the theory that eukaryotic cells formed by symbiosis among bacterial cells. Under the theory Margulis advocates, mitochondria and plastids did not originate within the eukaryotic cells that now carry them. Rather, these subunits were once free-living prokaryotic cells that infected other bacterial cells and came to reside in them with benefits for both parties. Even the bounded nucleus that characterizes all eukaryotic cells may have evolved this way. This is a whole new kind of evolution. Not just new genes, but new whole cells were incorporated into existing cells. This kind of evolution has already been confirmed by experiment (2). This theory represents a significant amendment to the prevailing paradigm of evolution. Now we know that evolution can proceed by assembling subunits. This mechanism would help evolution to take the giant step from prokaryotes to eukaryotes relatively quickly.
This symbiotic system has an additional consequence — as evolution proceeds, genes originally in the mitochondria and plastids apparently tend to be lost. In May, 1998, molecular biologists who analyzed 210 protein-coding genes from nine fully sequenced chloroplast genomes reported, "Some of these genes have been lost altogether,... whereas others have been transferred to the nucleus. We have documented 44 bona fide cases of functional plant nuclear genes among the 210 genes examined ..." (2.5). If mitochondria and plastids tend to lose genes, one can reason backward to a time when they had genomes as large as free-living bacteria do. This evidence strengthens the case for the symbiotic evolution Margulis advocates. And if some of those genes are transferred to the nucleus, we have another mechanism for importing whole genes into the nuclear genomes of eukaryotes.
If you had to name one development in all of evolution that was the most important single development, it would definitely be the evolution of eukaryotic cells. This step is apparently the prerequisite for any more highly organized forms of life to evolve. That the mitochondria and plastids in eukaryotes probably got there by symbiosis is a welcome insight. But we still have many other steps to explain. How did the structural system within eukaryotic cells evolve? How did eukaryotes evolve into a multitude of species with the wide variety of features they have? How do multicelled eukaryotes acquire new complex features? Where do the new genes for these steps come from? How do they get installed and activated?
Viruses and The Origin of Species
Charles Darwin named his greatest work The Origin of Species. Of course, the species is only one level of biological hierarchy. Darwin could have named his book The Origin of Phyla or The Origin of Kingdoms. A species is defined by being reproductively isolated from every other species. Darwin was able to see that if a sexually reproducing animal or plant were ever to take a an evolutionary step big enough to create a new species, it would be necessary for at least a complete breeding pair — one male and one female — to take the step simultaneously. If only one member of a breeding pair, say the female, acquired a speciating new feature, she would be reproductively isolated from the male. They would be unable to reproduce.
Sometimes new species can be produced by hybridization: closely related species can produce hybrid offspring that are able to sexually reproduce with other, similarly produced hybrids but not with members of either of the parents' species. Hybridization alone cannot, however, produce new features; it can only add existing ones together.
Today, with our understanding of DNA, we would state the problem differently: new features require new genetic instructions. And small steps are clearly possible without coordination between two members of a breeding pair. But big, speciating steps are still problematic for neo-Darwinism. If only one individual undergoes a mutation of speciating effect, the remaining population is either unable or unlikely to follow this "hopeful monster."
However, if new genetic instructions are inserted by infectious viruses, then the problem of finding breeding pairs equipped for big evolutionary steps is solved. Viruses typically infect whole populations, or substantial parts of them, so many breeding pairs may carry the same new instructions. This is a profound new way for evolution to advance, and in potentially larger steps than Darwin imagined. This proposed mechanism for evolution was already understood by the farseeing genetic researcher Susumo Ohno in 1970. He wrote (3):
Uniform transformation from an old species to a new species can occur only if the heritable traits responsible for the speciation are carried by a viral genome. Only then can widespread infection and subsequent incorporation of the viral genome into the host genome transform a majority of the previous species members to members of a new species.
The Germ Line
If new genetic programs are as common as viral infections, wouldn't they be more likely to wreak havoc than to improve things — especially in the larger animals and plants, for whom the genome is more complicated and individuals are less expendable? For example, suppose the genetic programs for antlers or antennae got installed and activated in people. That would cause a real-life horror show. The evolutionary world would be much better if each virus infected only a narrow range of hosts. Fortunately, that is how viruses usually work. With a few exceptions, each virus infects only one species or group of closely related species. But there are important exceptions to this rule. For example, arboviruses have two classes of carriers, vertebrate and invertebrate. Sometimes one class of host may not become infected, but usually both do. Over 500 arboviruses are known (4).
Some viruses infect their hosts with no harm to the host. Other viral infections can cause diseases, occasionally lethal ones. One wishes the immune system would keep them out completely. But if evolution depends on viruses, that capability would inhibit evolution. The situation is especially complex in sexually reproducing multicelled animals, where the "germ line" is carefully protected. The germ line, the gametes and their ancestral cells that give rise to the next generation, are isolated early in the life cycle from the rest of the (somatic) cells. In order for a virus to cause evolution in sexually reproducing creatures, it must infect the germ line and become integrated into the genome there. This process has been proven to occur already. "If, for example, the DNA is injected into the nucleus of a mouse's fertilized egg, the genes will be found in many cells of the adult animal and sometimes even in its germ cells" (5). And the descendants of newborn mice infected with a virus have been shown to carry the genes of the infecting virus in their own genomes (6). Also, "When DNA from a retrovirus is inserted into fetal lambs, their offspring inherit the retroviral DNA — a clear sign that the foreign genes had entered the sheep germline" (7). Furthermore, we now know that such insertion can happen in nature at a rate approaching one entire viral genome per host generation (8). By the time the textbook Retroviruses was published, in 1997, this question is settled. "...Retroviruses can become integrated into the germ line as endogenous viruses, leading to permanent genetic consequences for the descendents of the original host, a property they share with a variety of nonviral, but related, reverse-transcriptase-containing elements..." (9).
To accomplish this integration in nature the virus probably would have to spread by lytic infection throughout much of the body. This process will probably have side effects that may appear as symptoms of disease. Perhaps it would be a reasonable compromise if a new virus were able to establish a lytic infection and become widespread within the individual host's body one time only, and never again. Guess what. That's the way our mammalian immune system often handles viruses.
Sometimes retroviruses cause other genes in the host's genome to become "oncogenes" (10). That means they cause cancer. If evolution involves trial and error, cancer seems to be in the error category. However, perhaps it would make evolutionary sense, under some circumstances, for cells carrying newly acquired genes to begin to multiply rapidly.
Cosmic Ancestry assumes that the function of a virus is to install its genes into the germ line of its host. After this mission has been accomplished, it serves no purpose for the host to remain susceptible to lytic infection by the virus. It would make sense if the host's descendant inheriting the new genes were born with immunity to lytic, or disease-causing, infection by the virus.
In fact, it has been known since 1933 that resistance to a disease caused by a virus can be inherited (11). Now there is some reason to believe that even resistance to AIDS may be inheritable. AIDS is an incurable viral disease to which, we once thought, no one is immune. Studies are now suggesting, however, that some children of mothers with AIDS are born immune to the disease. This is the subject of a recent  story in Science, "Can Some Infants Beat HIV?" (12)
Among hundreds of children born to HIV-positive mothers, the studies found 21 who initially tested positive on HIV antibody and virus tests, but later came out negative. Referring to one of the studies, Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, says: "It's pretty compelling evidence that they were able to clear the infection, or were exposed to it, got transient infection, and then cleared it."
Gene ConversionAnother vital advantage comes with sexual reproduction. It depends on a process of genetic recombination called "gene conversion." Consider the following problem: as we know, in multicelled animals most DNA is silent. Neo-Darwinists call it "junk DNA," assumed to be the leftovers of previous evolution. Natural selection cannot prevent mistakes from accumulating in silent DNA — there's no expressed feature to affect the struggle for survival. Nor can having two copies of the gene offer any protection, by itself — neither copy is expressed so there's no "working" copy to be dominant. Both copies would be equally subject to the accumulation of errors. Of course, if the silent DNA will always be silent, it won't ever matter. But if any of the silent DNA is ever to be used in the future, it needs protection against the accumulation of errors. Cosmic Ancestry holds that at least some of the silent DNA is for future use.
The Cosmic Ancestry paradigm proposes that the genetic instructions for big evolutionary steps are installed by viruses or other lateral transfer mechanisms, and that some of the steps require several genes — so many that they cannot be installed all at once but only in stages. During the long installation process, the not-yet-activated DNA would be silent. To be useful in the future, this silent DNA would definitely need protection against the accumulation of errors.
Among the working genes of sexually reproducing creatures, gene conversion can alter one version of a gene to match the other version. A defective gene can be edited to match the nondefective version of the gene by this process (12.5):
Occasionally... one of the two copies of the paternal allele [version] has been changed to a copy of the maternal allele. This phenomenon is known as gene conversion. It often occurs in association with genetic recombination events, and it is thought to be important in the evolution of certain genes.... Gene conversion is thought to be a straightforward consequence of the mechanisms of general recombination and DNA repair.
So if an error develops in one copy of the gene, the process of gene conversion could compare it to the undamaged copy and fix it. In the above example, gene conversion has been demonstrated for working genes. Is there any reason to think that gene conversion also works on silent DNA? Yes. There is indirect evidence based on an otherwise unexplained similarity between silent DNA in humans and mice (13):
Koop and Hood have found that the DNA of the T cell receptor complex... shows 71% identity between humans and mice. That finding is startling, since only 6% of the DNA encodes for the actual protein sequence, while the rest consists of introns and noncoding regions.
The last common ancestor of humans and mice died at least 80 million years ago. Somehow the silent DNA has been maintained over many millions of replications. Gene conversion could be the mechanism. Something is.
If gene conversion works for silent DNA, it becomes possible for very large genetic programs to be installed in stages, without loss of fidelity. The parts installed first would be silent until the whole program had been installed. With gene conversion, this silent part could get continually debugged. The process of gene conversion could clean it up, as necessary, every time it is replicated. Thus, when the whole new genetic program is fully installed and ready to activate, it would be far more likely to be fully functional. The process of gene conversion could make it possible to install big genetic programs in pieces, over many generations.
Additional evidence for the longterm maintenance of silent genes comes from research on certain "retrotransposons" by biologists at The University of Rochester. They studied two related sequences that have remained stable in diverse lineages for over 500 million years. The sequences are always inserted at the same two precise locations in a certain (28S rRNA) gene, inactivating it. "How then do we account for their remarkable stability?" they wonder (14).
SummarySo it is necessary, at least intermittently..., this thing called sex. As of course you and I knew it must be. Otherwise surely, by now, we mammals and dragonflies would have come up with something more dignified. — David Quammen (15)
Evolution can proceed by the assembly of subunits.
References1. Mark Ridley, "Case Studies," p 269-270, Evolution, Mark Ridley, editor. Oxford University Press, 1997.
2. Lynn Margulis and Dorion Sagan, What Is Life? Simon and Schuster, 1995. p 107.
2.5. William Martin, Bettina Stoebe, Vadim Goremykin, Sabine Hansmann, Masami Hasegawa and Klaus V. Kowallik, "Gene transfer to the nucleus and the evolution of chloroplasts," p 162-165 v 393, Nature, 14 May 1998.
3. Susumu Ohno, Evolution by Gene Duplication, Springer-Verlag Publishing Company, 1970. p 55.
4. Frederick A. Murphy, "Epidemiology of Viral Diseases," p 398-404, Encyclopedia of Virology, Robert G. Webster and Allan Granoff, eds., Academic Press, 1994.
5. Renato Dulbecco, The Design of Life, Yale University Press, 1987. p 120.
6. Jean-Jacques Panthier, Hubert Condamine and François Jacob, "Inoculation of newborn SWR/J females with an ecotropic murine leukemia virus can produce transgenic mice," p 1156-1160 v 85, Proc. Natl. Acad Sci. USA, February 1988.
7. Richard Stone, "NIH to Study 'Germ-line' Therapy," p 1631 v 266, Science, 9 December 1994.
8. Jonothan Stoye, "Endogenous proviruses as 'mementos'?" p 840 v 388, Nature, 28 August 1997.
9. John M. Coffin, Stephen H. Hughes and Harold E. Varmus, eds., Retroviruses, Cold Spring Harbor Laboratory Press, 1997. p 336.
10. Michal J. Bishop, "Oncogenes," Scientific American, March, 1982.
11. David G. Brownstein, "Host Genetic Resistance," p 664-669, Encyclopedia of Virology, Robert G. Webster and Allan Granoff, eds., Academic Press. 1994.
12. Clare Thompson, "Can Some Infants Beat HIV?" p 441 v 271, Science, 26 January 1996.
12.5. Bruce Alberts, Dennis Bray, Julian Lewis, Martin Raff, Keith Roberts and James D. Watson, The Molecular Biology of the Cell, 3rd edition, New York: Garland Publishing, Inc., 1994. p 268.
13. Rachel Nowak, "Mining Treasures From 'Junk DNA'," p 608-610 v 263, Science, 4 February 1994.
14. William D. Burke, Harmit S. Malik, Warren C. Lathe III and Thomas H. Eickbush, "Are retrotransposons long-term hitchhikers?" p 141-142 v 392, Nature, 12 March 1998.
15. David Quammen, "Is Sex Necessary?" p 169-174, Natural Acts: A Sidelong View of Science and Nature, Avon Books, 1985. p 174.
16. Clifford Zeyl and Graham Bell, "The advantage of sex in evolving yeast populations," p 465-468 v 388, Nature, 31 July 1997. See also Evolutionary Advantage Found For Sex by Wayne Thompson, EurekAlert!, 30 July 1997.
17. Virginia Morell, "Sex Frees Viruses From Genetic Ratchet" and "Viruses Scout Evolution's Path," p 1562-1564 v 278, Science. 28 November, 1997.