Skip to comments.Darwinist Ideologues Are on the Run
Posted on 01/30/2006 10:27:35 PM PST by Sweetjustusnow
The two scariest words in the English language? Intelligent Design! That phrase tends to produce a nasty rash and night sweats among our elitist class.
Should some impressionable teenager ever hear those words from a public school teacher, we are led to believe, that student may embrace a secular heresy: that some intelligent force or energy, maybe even a god, rather than Darwinian blind chance, has been responsible for the gazillions of magnificently designed life forms that populate our privileged planet.
Will has nothing but scorn for the lower human life forms who think ID should be mentioned, even if just shyly whispered, in a public school setting. When the Kansas State Board of Education decided to allowbut not requireID discussions in science classes, Will raged that the board is controlled by the kind of conservatives who make conservatism repulsive to temperate people. (Are these the words of a temperate man?) Those repugnant conservatives had the audacity to proclaim that evolution is not a fact But it is, Will sniffed.
Really? Well, lets just see if only dimwitted (and repulsive) conservatives think the case for Darwinian theory is weak. Literally hundreds of geneticists, biologists, paleontologists, chemists, mathematicians and other scientistswhose religious views vary from agnostic to evangelicalsay the theory is not a fact. Among them: Lev. V. Beloussov and Vladimir L. Voelkov, two prominent Russian biologists from Moscow State University; Dr. Richard Sternberg, an evolutionary biologist at the Smithsonian Institution; and Dr. David Berlinski, a mathematician with post-doctoral training in molecular biology. (Berlinksis scholarly article in the February issue of Commentary will prove an unpleasant read for evolutionists.)
The Discovery Institute recently produced a list of over 400 scientists of varying faith and non-faithincluding those from such prestigious institutions as Princeton, MIT and Cornellwho signed onto a statement stressing they were skeptical of claims for the ability of random mutation and natural selection to account for the complexity of life.
Even many evolutionists, it seems, are uncertain that Darwinian theory is scientific fact. There is the famous story of the late Colin Patterson, who had been a senior paleontologist at the British Natural History Museum and the author of the museums general text on evolution. Patterson gave a remarkable lecture in 1981 at the American Museum of Natural History in New York Cityall of it nicely retold by Tom Bethell in his book, The Politically Incorrect Guide to Science (Regnerya HUMAN EVENTS sister company). A brilliant essayist and scholar, Bethell has been a long-time critic of evolution and, unlike Will, has a science degree from Oxford University.
Patterson informed his audience of mostly expert biologists that he had studied evolution for some 20 years and suddenly realized that there was not one thing I knew about it. So either there was something wrong with me, or there was something wrong with evolutionary theory.
Thus he decided to put this question to various groups of experts: Can you tell me anything you know about evolution, any one thing, any one thing that you think is true? I tried that question on the geology staff at the Field Museum of Natural History and the only answer I got was silence. I tried it on the members of the Evolutionary Morphology seminar at the University of Chicago, a very prestigious body of evolutionists, and all I got there was silence for a long time and eventually one person said: I do know one thingit ought not to be taught in high school. Bethell stresses that Patterson never repudiated his statements, though he never truly repudiated evolution either.
Irving Kristol is a prominent, brainy, Jewish social critic and the godfather of neoconservatism. He can hardly be accused of being a literalist when it comes to the Bible, as evolutionists so frequently try to portray their critics. In a Sept. 30, 1986, article in the New York Times, Kristol observed the following:
Though Darwins theory on how man and animals were created is usually taught as an established scientific fact, it is nothing of the sort. It has too many lacunae. Geological evidence does not provide us with the spectrum of intermediate species we would expect. Moreover, laboratory experiments reveal how close to impossible it is for one species to evolve into another, even allowing for selective breeding and some genetic mutation. Does anyone have the nerve to suggest Kristol is a close-minded, religious dogmatist as well?
So heres the crux of the matter: If a theory as shaky as Darwins is a mandatory subject in the public schools, why shouldnt public school teachers be at least allowed, if not compelled, to inform their students that many reputable scientists, although still a distinct minority, believe that something else, including Intelligent Design, is worthy of some consideration?
The Kansas school board that caused poor George Will to unravel did not try to impose a single view of creation on the states public school system. The board majority is very unlike the rigid Darwinists in that regard. In November 2005, the board, by a 6-to-4 vote, drafted new scientific standards for education in the high schools. Far from eradicating the study of evolution, these intemperate board members made it a requirement, explaining that the new curriculum standards call for students to learn about the best evidence for modern evolutionary theory But the members also called for students to learn about areas where scientists are raising scientific criticisms of the theory.
These serious criticisms have now risen to a level where the board majority felt it would be positively remiss if those views werent also discussed in the classrooms. Isnt this as American as apple pie? (Interestingly, Board Chairman Steve Abrams, a veterinarian, informed this writer that he set aside three days of hearings for pro-evolutionist experts, and three days for the skeptics, with each side allowed to cross-examine the other. The pro-evolutionist experts refused to testify and be questioned. The skeptics testified and faced cross-examination.)
What scares the pants off the Darwinians today is that the Bush Supreme Court may validate the Kansas-style scientific standards that have already been embraced by at least four other states. The Darwinians were deliriously happy when the High Court ruled against a Louisiana statute in 1987 requiring the states public schools to give balanced treatment to creation science (sometimes equated with intelligent design) and evolution science. It amounted to imposing religion, said the court majority. But Antonin Scalia, with Chief Justice William Rehnquist in agreement, said this was nonsense. The evidence, said Scalia, was overwhelming that the laws framers were not trying to impose religion in the classrooms.
The acts reference to creation is not convincing evidence of religious purpose, said Scalia, because the proponents and witnesses repeatedly stressed that the subject can and should be presented without religious content. We have no basis on the record to conclude that creation science need be anything other than a collection of scientific data supporting the theory that life abruptly appeared on Earth. (Emphasis added.)
Scalia, in short, blew both Krauthammers and Wills reasoning about the teaching of creation science and intelligent design out of the water. Kansas and the other states, in truth, have done nothing more odious than attempt to permit a whiff of scientific freedom to enter the classrooms. With the High Court now about to have four justices in the Scalia mode, the Darwinist ideologues, including George Will, have a right to feel insecure.
Truth is argued - not settled - in courts, schools, bibles, churches, and textbooks.
Only in the mind is truth settled, and nowhere else.
Very well said, Irving Kristol!
I've never understood why conservatives are so infatuated by George Will. He's not all that in touch with the real world.
To say that the theory of evolution has lacunae is one thing, but that doesn't justify ID. Many other theories are conceivable. I don't mind teaching the uncertainties within the theory of evolution, but I do object to teaching ID in science classes.
Too bad Colin Patterson was not able to post his question on FR he would have recieved several pages of sarcastic responses full of insults and vitrolic condemnation.
Nobody would have been able to answer the question...but still...he at least would have gotten responses.
Too bad Colin Patterson was not able to post his question on FR he would have recieved several pages of sarcastic responses full of insults and vitrolic condemnation.
Nobody would have been able to answer the question...but still...he at least would have gotten responses.
Why? Teach it and present the best possible refutations of it. That's real education. Education is always a dialogue between opposing viewpoints. Indoctrination is presenting the "truth."
1001001 1000100 0100000 1101001 1110011 1101110 1110100 100000 1110011 1100011 1101001 1100101 1101110 1100011 1100101 100001
But the theory of man coming from apes is much more logical..../sarcasm.
Only someone grossly ignorant of the actual fossil record could say something this amazingly false with a straight face:
Moreover, laboratory experiments reveal how close to impossible it is for one species to evolve into another,
Gee, really? Let's see the citations to those "laboratory experiments", shall we? I just won't hold my breath, the IDers never provide any when asked, because they're just making this stuff up as they go along. When they say, "laboratory experiments reveal", it really means, "as an uninformed anti-evolutionist, I'm posting my presumption that some experiment must support my empty presumptions, because I've never actually read any that I can cite if asked."
Meanwhile, here are some *real* citations on speciation -- including dozens of OBSERVED cases of actual speciation:
Why don't you anti-evolutionists go read some science journals for a change, instead of parroting the lies of the creationist pamphlets written by people ignorant of science?
Ahearn, J. N. 1980. Evolution of behavioral reproductive isolation in a laboratory stock of Drosophila silvestris. Experientia. 36:63-64.
Barton, N. H., J. S. Jones and J. Mallet. 1988. No barriers to speciation. Nature. 336:13-14.
Baum, D. 1992. Phylogenetic species concepts. Trends in Ecology and Evolution. 7:1-3.
Boraas, M. E. 1983. Predator induced evolution in chemostat culture. EOS. Transactions of the American Geophysical Union. 64:1102.
Breeuwer, J. A. J. and J. H. Werren. 1990. Microorganisms associated with chromosome destruction and reproductive isolation between two insect species. Nature. 346:558-560.
Budd, A. F. and B. D. Mishler. 1990. Species and evolution in clonal organisms -- a summary and discussion. Systematic Botany 15:166-171.
Bullini, L. and G. Nascetti. 1990. Speciation by hybridization in phasmids and other insects. Canadian Journal of Zoology. 68:1747-1760.
Butters, F. K. 1941. Hybrid Woodsias in Minnesota. Amer. Fern. J. 31:15-21.
Butters, F. K. and R. M. Tryon, jr. 1948. A fertile mutant of a Woodsia hybrid. American Journal of Botany. 35:138.
Brock, T. D. and M. T. Madigan. 1988. Biology of Microorganisms (5th edition). Prentice Hall, Englewood, NJ.
Callaghan, C. A. 1987. Instances of observed speciation. The American Biology Teacher. 49:3436.
Castenholz, R. W. 1992. Species usage, concept, and evolution in the cyanobacteria (blue-green algae). Journal of Phycology 28:737-745.
Clausen, J., D. D. Keck and W. M. Hiesey. 1945. Experimental studies on the nature of species. II. Plant evolution through amphiploidy and autoploidy, with examples from the Madiinae. Carnegie Institute Washington Publication, 564:1-174.
Cracraft, J. 1989. Speciation and its ontology: the empirical consequences of alternative species concepts for understanding patterns and processes of differentiation. In Otte, E. and J. A. Endler [eds.] Speciation and its consequences. Sinauer Associates, Sunderland, MA. pp. 28-59.
Craig, T. P., J. K. Itami, W. G. Abrahamson and J. D. Horner. 1993. Behavioral evidence for host-race fromation in Eurosta solidaginis. Evolution. 47:1696-1710.
Cronquist, A. 1978. Once again, what is a species? Biosystematics in agriculture. Beltsville Symposia in Agricultural Research 2:3-20.
Cronquist, A. 1988. The evolution and classification of flowering plants (2nd edition). The New York Botanical Garden, Bronx, NY.
Crossley, S. A. 1974. Changes in mating behavior produced by selection for ethological isolation between ebony and vestigial mutants of Drosophilia melanogaster. Evolution. 28:631-647.
de Oliveira, A. K. and A. R. Cordeiro. 1980. Adaptation of Drosophila willistoni experimental populations to extreme pH medium. II. Development of incipient reproductive isolation. Heredity. 44:123-130.
de Queiroz, K. and M. Donoghue. 1988. Phylogenetic systematics and the species problem. Cladistics. 4:317-338.
de Queiroz, K. and M. Donoghue. 1990. Phylogenetic systematics and species revisited. Cladistics. 6:83-90.
de Vries, H. 1905. Species and varieties, their origin by mutation.
de Wet, J. M. J. 1971. Polyploidy and evolution in plants. Taxon. 20:29-35.
del Solar, E. 1966. Sexual isolation caused by selection for positive and negative phototaxis and geotaxis in Drosophila pseudoobscura. Proceedings of the National Academy of Sciences (US). 56:484-487.
Digby, L. 1912. The cytology of Primula kewensis and of other related Primula hybrids. Ann. Bot. 26:357-388.
Dobzhansky, T. 1937. Genetics and the origin of species. Columbia University Press, New York.
Dobzhansky, T. 1951. Genetics and the origin of species (3rd edition). Columbia University Press, New York.
Dobzhansky, T. and O. Pavlovsky. 1971. Experimentally created incipient species of Drosophila. Nature. 230:289-292.
Dobzhansky, T. 1972. Species of Drosophila: new excitement in an old field. Science. 177:664-669.
Dodd, D. M. B. 1989. Reproductive isolation as a consequence of adaptive divergence in Drosophila melanogaster. Evolution 43:1308-1311.
Dodd, D. M. B. and J. R. Powell. 1985. Founder-flush speciation: an update of experimental results with Drosophila. Evolution 39:1388-1392.
Donoghue, M. J. 1985. A critique of the biological species concept and recommendations for a phylogenetic alternative. Bryologist 88:172-181.
Du Rietz, G. E. 1930. The fundamental units of biological taxonomy. Svensk. Bot. Tidskr. 24:333-428.
Ehrman, E. 1971. Natural selection for the origin of reproductive isolation. The American Naturalist. 105:479-483.
Ehrman, E. 1973. More on natural selection for the origin of reproductive isolation. The American Naturalist. 107:318-319.
Feder, J. L., C. A. Chilcote and G. L. Bush. 1988. Genetic differentiation between sympatric host races of the apple maggot fly, Rhagoletis pomonella. Nature. 336:61-64.
Feder, J. L. and G. L. Bush. 1989. A field test of differential host-plant usage between two sibling species of Rhagoletis pomonella fruit flies (Diptera:Tephritidae) and its consequences for sympatric models of speciation. Evolution 43:1813-1819.
Frandsen, K. J. 1943. The experimental formation of Brassica juncea Czern. et Coss. Dansk. Bot. Arkiv., No. 4, 11:1-17.
Frandsen, K. J. 1947. The experimental formation of Brassica napus L. var. oleifera DC and Brassica carinata Braun. Dansk. Bot. Arkiv., No. 7, 12:1-16.
Galiana, A., A. Moya and F. J. Alaya. 1993. Founder-flush speciation in Drosophila pseudoobscura: a large scale experiment. Evolution. 47432-444.
Gottleib, L. D. 1973. Genetic differentiation, sympatric speciation, and the origin of a diploid species of Stephanomeira. American Journal of Botany. 60: 545-553.
Halliburton, R. and G. A. E. Gall. 1981. Disruptive selection and assortative mating in Tribolium castaneum. Evolution. 35:829-843.
Hurd, L. E., and R. M. Eisenberg. 1975. Divergent selection for geotactic response and evolution of reproductive isolation in sympatric and allopatric populations of houseflies. The American Naturalist. 109:353-358.
Karpchenko, G. D. 1927. Polyploid hybrids of Raphanus sativus L. X Brassica oleraceae L. Bull. Appl. Botany. 17:305-408.
Karpchenko, G. D. 1928. Polyploid hybrids of Raphanus sativus L. X Brassica oleraceae L. Z. Indukt. Abstami-a Verenbungsi. 48:1-85.
Kilias, G., S. N. Alahiotis and M. Delecanos. 1980. A multifactorial investigation of speciation theory using Drosophila melanogaster. Evolution. 34:730-737.
Knight, G. R., A. Robertson and C. H. Waddington. 1956. Selection for sexual isolation within a species. Evolution. 10:14-22.
Koopman, K. F. 1950. Natural selection for reproductive isolation between Drosophila pseudoobscura and Drosophila persimilis. Evolution. 4:135-148.
Lee, R. E. 1989. Phycology (2nd edition) Cambridge University Press, Cambridge, UK
Levin, D. A. 1979. The nature of plant species. Science 204:381-384.
Lokki, J. and A. Saura. 1980. Polyploidy in insect evolution. In: W. H. Lewis (ed.) Polyploidy: Biological Relevance. Plenum Press, New York.
Macnair, M. R. 1981. Tolerance of higher plants to toxic materials. In: J. A. Bishop and L. M. Cook (eds.). Genetic consequences of man made change. Pp.177-297. Academic Press, New York.
Macnair, M. R. and P. Christie. 1983. Reproductive isolation as a pleiotropic effect of copper tolerance in Mimulus guttatus. Heredity. 50:295-302.
Manhart, J. R. and R. M. McCourt. 1992. Molecular data and species concepts in the algae. Journal of Phycology. 28:730-737.
Mayr, E. 1942. Systematics and the origin of species from the viewpoint of a zoologist. Columbia University Press, New York.
Mayr, E. 1982. The growth of biological thought: diversity, evolution and inheritance. Harvard University Press, Cambridge, MA. McCourt, R. M. and R. W. Hoshaw. 1990. Noncorrespondence of breeding groups, morphology and monophyletic groups in Spirogyra (Zygnemataceae; Chlorophyta) and the application of species concepts. Systematic Botany. 15:69-78.
McPheron, B. A., D. C. Smith and S. H. Berlocher. 1988. Genetic differentiation between host races of Rhagoletis pomonella. Nature. 336:64-66.
Meffert, L. M. and E. H. Bryant. 1991. Mating propensity and courtship behavior in serially bottlenecked lines of the housefly. Evolution 45:293-306.
Mishler, B. D. 1985. The morphological, developmental and phylogenetic basis of species concepts in the bryophytes. Bryologist. 88:207-214.
Mishler, B. D. and M. J. Donoghue. 1982. Species concepts: a case for pluralism. Systematic Zoology. 31:491-503.
Muntzing, A. 1932. Cytogenetic investigations on the synthetic Galeopsis tetrahit. Hereditas. 16:105-154.
Nelson, G. 1989. Cladistics and evolutionary models. Cladistics. 5:275-289.
Newton, W. C. F. and C. Pellew. 1929. Primula kewensis and its derivatives. J. Genetics. 20:405-467.
Otte, E. and J. A. Endler (eds.). 1989. Speciation and its consequences. Sinauer Associates. Sunderland, MA.
Owenby, M. 1950. Natural hybridization and amphiploidy in the genus Tragopogon. Am. J. Bot. 37:487-499.
Pasterniani, E. 1969. Selection for reproductive isolation between two populations of maize, Zea mays L. Evolution. 23:534-547.
Powell, J. R. 1978. The founder-flush speciation theory: an experimental approach. Evolution. 32:465-474.
Prokopy, R. J., S. R. Diehl, and S. H. Cooley. 1988. Oecologia. 76:138.
Rabe, E. W. and C. H. Haufler. 1992. Incipient polyploid speciation in the maidenhair fern (Adiantum pedatum, adiantaceae)? American Journal of Botany. 79:701-707.
Rice, W. R. 1985. Disruptive selection on habitat preference and the evolution of reproductive isolation: an exploratory experiment. Evolution. 39:645-646.
Rice, W. R. and E. E. Hostert. 1993. Laboratory experiments on speciation: What have we learned in forty years? Evolution. 47:1637-1653.
Rice, W. R. and G. W. Salt. 1988. Speciation via disruptive selection on habitat preference: experimental evidence. The American Naturalist. 131:911-917.
Rice, W. R. and G. W. Salt. 1990. The evolution of reproductive isolation as a correlated character under sympatric conditions: experimental evidence. Evolution. 44:1140-1152.
Ringo, J., D. Wood, R. Rockwell, and H. Dowse. 1989. An experiment testing two hypotheses of speciation. The American Naturalist. 126:642-661.
Schluter, D. and L. M. Nagel. 1995. Parallel speciation by natural selection. American Naturalist. 146:292-301.
Shikano, S., L. S. Luckinbill and Y. Kurihara. 1990. Changes of traits in a bacterial population associated with protozoal predation. Microbial Ecology. 20:75-84.
Smith, D. C. 1988. Heritable divergence of Rhagoletis pomonella host races by seasonal asynchrony. Nature. 336:66-67.
Soans, A. B., D. Pimentel and J. S. Soans. 1974. Evolution of reproductive isolation in allopatric and sympatric populations. The American Naturalist. 108:117-124.
Sokal, R. R. and T. J. Crovello. 1970. The biological species concept: a critical evaluation. The American Naturalist. 104:127-153.
Soltis, D. E. and P. S. Soltis. 1989. Allopolyploid speciation in Tragopogon: Insights from chloroplast DNA. American Journal of Botany. 76:1119-1124.
Stuessy, T. F. 1990. Plant taxonomy. Columbia University Press, New York.
Thoday, J. M. and J. B. Gibson. 1962. Isolation by disruptive selection. Nature. 193:1164-1166.
Thoday, J. M. and J. B. Gibson. 1970. The probability of isolation by disruptive selection. The American Naturalist. 104:219-230.
Thompson, J. N. 1987. Symbiont-induced speciation. Biological Journal of the Linnean Society. 32:385-393.
Vrijenhoek, R. C. 1994. Unisexual fish: Model systems for studying ecology and evolution. Annual Review of Ecology and Systematics. 25:71-96.
Waring, G. L., W. G. Abrahamson and D. J. Howard. 1990. Genetic differentiation in the gall former Eurosta solidaginis (Diptera:Tephritidae) along host plant lines. Evolution. 44:1648-1655.
Weinberg, J. R., V. R. Starczak and P. Jora. 1992. Evidence for rapid speciation following a founder event in the laboratory. Evolution. 46:1214-1220.
Wood, A. M. and T. Leatham. 1992. The species concept in phytoplankton ecology. Journal of Phycology. 28:723-729.
Yen, J. H. and A. R. Barr. 1971. New hypotheses of the cause of cytoplasmic incompatability in Culex pipiens L.
Just a smattering of a huge database of articles (1991 only):
- Bullini, L and Nascetti, G, 1991, Speciation by Hybridization in phasmids and other insects, Canadian Journal of Zoology, Volume 68(8), pages 1747-1760.
- Ramadevon, S and Deaken, M.A.B., 1991, The Gibbons speciation mechanism, Journal of Theoretical Biology, Volume 145(4) pages 447-456.
- Sharman, G.B., Close, R.L, Maynes, G.M., 1991, Chromosome evolution, phylogeny, and speciation of rock wallabies, Australian Journal of Zoology, Volume 37(2-4), pages 351-363.
- Werth, C. R., and Windham, M.D., 1991, A model for divergent, allopatric, speciation of polyploid pteridophytes resulting from silencing of duplicate- gene expression, AM-Natural, Volume 137(4):515-526.
- Spooner, D.M., Sytsma, K.J., Smith, J., A Molecular reexamination of diploid hybrid speciation of Solanum raphanifolium, Evolution, Volume 45, Number 3, pages 757-764.
- Arnold, M.L., Buckner, C.M., Robinson, J.J., 1991, Pollen-mediated introgression and hybrid speciation in Louisiana Irises, P-NAS-US, Volume 88, Number 4, pages 1398-1402.
- Nevo, E., 1991, Evolutionary Theory and process of active speciation and adaptive radiation in subterranean mole rats, spalax-ehrenbergi superspecies, in Israel, Evolutionary Biology, Volume 25, pages 1-125.
... on and on to about #50 if you like...
There are about 100 each for every year before 1991 to 1987 in my database.
By L. Drew Davis
A List of Speciation References
- Weiberg, James R.. Starczak, Victoria R.. Jorg, Daniele. Evidence for rapid speciation following a founder event in the laboratory. Evolution. V46. P1214(7) August, 1992.
- Kluger, Jeffrey. Go fish. (rapid fish speciation in African lakes). Discover. V13. P18(1) March, 1992.
- Hauffe, Heidi C.. Searle, Jeremy B.. A disappearing speciation event? (response to J.A. Coyne, Nature, vol. 355, p. 511, 1992). Nature. V357. P26(1) May 7, 1992.
Analysis of contact between two chromosomal races of house mice in northern Italy show that natural selection will produce alleles that bar interracial matings if the resulting offspring are unfit hybrids. This is an important exception to the general rule that intermixing races will not tend to become separate species because the constant sharing of genes minimizes the genetic diversity requisite for speciation.
- Barrowclough, George F.. Speciation and Geographic Variation in Black-tailed Gnatcatchers. (book reviews) The Condor. V94. P555(2) May, 1992.
- Rabe, Eric W.. Haufler, Christopher H.. Incipient polyploid speciation in the maidenhair fern (Adiantum pedatum; Adiantaceae)? The American Journal of Botany. V79. P701(7) June, 1992.
- Nores, Manuel. Bird speciation in subtropical South America in relation to forest expansion and retraction. The Auk. V109. P346(12) April, 1992.
The climatic and geographic history of the Pleistocene and Holocene periods modified the distribution of the bird population in the South American forests. Forest birds are found dispersed in the Yungas and Paranese areas with only minimal infiltration of the Chaco woodland, indicating an atmospheric change during the interglacial periods. In the Chaco lowlands, the interactions between non-forest birds reveal the existence of presence of a forest belt along the Bermejo and Pilcomayo rivers.
- Kondrashov, Alexey S.. Jablonka, Eva. Lamb, Marion J.. Species and speciation. (response to J.A. Coyne, Nature, vol. 355, p. 511, 1992). Nature. V356. P752(1) April 30, 1992.
J.A. Coyne wrongly asserted that neodarwinism includes allopatric evolution but not sympatric evolution. Allopatric evolution occurs among geographically isolated populations, whereas sympatric evolution occurs within one species' entire population. Both are neodarwinian since each results from natural selection of genetic variation. Also, Coyne failed to recognize that the molecular models used to illustrate how genetic changes bring on speciation are most useful when researchers acknowledge that both inherited epigenetic and genetic changes affect speciation.
- Spooner, David M.. Sytsma, Kenneth J.. Smith, James F.. A molecular reexamination of diploid hybrid speciation of Solanum raphanifolium. Evolution. V45. P757(8) May, 1991.
- Orr, H. Allen. Is single-gene speciation possible?. Evolution. V45. P764(6) May, 1991.
- Miller, Julie Ann. Pathogens and speciation. (Research Update). BioScience. V40. P714(1) Nov, 1990.
- Barton, N.H. Hewitt, G.M. Adaptation, speciation and hybrid zones; many species are divided into a mosaic of genetically distinct populations, separated by narrow zones of hybridization. Studies of hybrid zones allow us to quantify the genetic differences responsible for speciation, to measure the diffusion of genes between diverging taxa, and to understand the spread of alternative adaptations. (includes related information) Nature. V341. P497(7) Oct 12, 1989.
- Wright, Karen. A breed apart; finicky flies lend credence to a theory of speciation. Scientific American. V260. P22(2) Feb, 1989.
- Coyne, Jerry A. Orr, H. Allen. Patterns of speciation in Drosophila. Evolution. V43. P362(20) March, 1989.
- Feder, Jeffrey L. Bush, Guy L. A field test of differential host-plant usage between two sibling species of Rhagoletis pomonella fruit flies (Diptera: Tephritidae) and its consequences for sympatric models of speciation. Evolution. V43. P1813(7) Dec, 1989.
- Soltis, Douglas E. Soltis, Pamela S. Allopolyploid speciation in Tragopogon: insights from chloroplast DNA. The American Journal of Botany. V76. P1119(6) August, 1989.
- Coyne, J.A. Barton, N.H. What do we know about speciation?. Nature. V331. P485(2) Feb 11, 1988.
- Barton, N.H. Jones, J.S. Mallet, J. No barriers to speciation. (morphological evolution). Nature. V336. P13(2) Nov 3, 1988.
- Kaneshiro, Kenneth Y. Speciation in the Hawaiian drosophila: sexual selection appears to play an important role. BioScience. V38. P258(6) April, 1988.
A talk.origins participant writes:
1) Speciation occured in a strain of Drosophila paulistorum sometime between 1958 and 1963 in Theodosius Dobzhansky's lab. He wrote this up in:
Dobzhansky, T. 1973. Species of Drosophila: New Excitement in an Old Field. Science 177:664-669
2) A naturally occurring speciation of a plant species, Stephanomeria malheurensis, was observed in Burns County, Oregon. The citing is:
Gottlieb, L. D. 1973. Genetic differentiation, sympatric speciation, and the origin of a diploid species of Stephanomeria. American Journal of Botany 60(6):545-553
3) In the 1940's a fertile species was produced through chromosome doubling (allopolyploidy) in a hybrid of two primrose species. The new species was Primula kewensis. The story is recounted in:
Stebbins, G. L. 1950. Variation and Evolution in Plants. Columbia University Press. New York
4) Finally, two workers produced reproductive isolation between two strains of fruit flies in a lab setting within 25 generations. I don't have the paper handy, so I can't give the species. The partial citing of the paper is:
Rice and Salt 1988. American Naturalist 131:911-
Dobzhansky got a subpopulation of D. paulistorum to speciate in his lab. The reference is:
Dobzhansky and Pavlovsky, 1957 An experimentally created incipient species of Drosophila, Nature 23: 289- 292
Weinberg, et. al, 1992 Evidence for rapid speciation following a founder event in the laboratory, Evolution 46: 1214. (This isn't a full paper, just a note -- it describes what is probably speciation of a type of polychaete worm.)
Background: Retroviruses reproduce by entering a cell of a host (like, say, a human), then embedding their own viral DNA into the cell's own DNA, which has the effect of adding a "recipe" for manufacturing more viruses to the cell's "instruction book". The cell then follows those instructions because it has no reason (or way) to "mistrust" the DNA instructions it contains. So the virus has converted the cell into a virus factory, and the new viruses leave the cell, and go find more cells to infect, etc.
However, every once in a while a virus's invasion plans don't function exactly as they should, and the virus's DNA (or portions of it) gets embedded into the cell's DNA in a "broken" manner. It's stuck into there, becoming part of the cell's DNA, but it's unable to produce new viruses. So there it remains, embedded in the DNA. If this happens in a regular body cell, it just remains there for life as a "fossil" of the past infection and goes to the grave with the individual it's stuck in. All of us almost certainly contain countless such relics of the past viral infections we've fought off.
However... By chance this sometimes happens to a special cell in the body, a gametocyte cell that's one of the ones responsible for making sperm in males and egg cells in females, and if so subsequent sperm/eggs produced by that cell will contain copies of the "fossil" virus, since now it's just a portion of the entire DNA package of the cell. And once in a blue moon such a sperm or egg is lucky enough to be one of the few which participate in fertilization and are used to produce a child -- who will now inherit copies of the "fossilized" viral DNA in every cell of his/her body, since all are copied from the DNA of the original modified sperm/egg.
So now the "fossilized" viral DNA sequence will be passed on to *their* children, and their children's children, and so on. Through a process called neutral genetic drift, given enough time (it happens faster in smaller populations than large) the "fossil" viral DNA will either be flushed out of the population eventually, *or* by luck of the draw end up in every member of the population X generations down the road. It all depends on a roll of the genetic dice.
Due to the hurdles, "fossil" retroviral DNA strings (known by the technical name of "endogenous retroviruses") don't end up ubiquitous in a species very often, but it provably *does* happen. In fact, the Human DNA project has identified literally *thousands* of such fossilized "relics" of long-ago ancestral infections in the human DNA.
And several features of these DNA relics can be used to demonstrate common descent, including their *location*. The reason is that retroviruses aren't very picky about where their DNA gets inserted into the host DNA. Even in an infection in a *single* individual, each infected cell has the retroviral DNA inserted into different locations than any other cell. Because the host DNA is so enormous (billions of basepairs in humans, for example), the odds of any retroviral insertion event matching the insertion location of any other insertion event are astronomically low. The only plausible mechanism by which two individuals could have retroviral DNA inserted into exactly the same location in their respective DNAs is if they inherited copies of that DNA from the same source -- a common ancestor.
Thus, shared endogenous retroviruses between, say, ape and man is almost irrefutable evidence that they descended from a common ancestor. *Unless* you want to suggest that they were created separately, and then a virus they were both susceptible to infected both a man and an ape in EXACTLY the same location in their DNAs (the odds of such a match by luck are literally on the order of 1,000,000,000,000 to 1...), *and* that the infections both happened in their gametocyte cells (combined odds on the order of 1,000,000 to 1) *and* that the one particular affected gametocyte is the one which produces the egg or sperm which is destined to produce an offspring (*HUGE* odds against), and *then* the resulting modified genome of the offspring becomes "fixed" in each respective population (1 out of population_size^squared)...
Then repeat that for *each* shared endogenous retrovirus (there are many) you'd like to claim was acquired independently and *not* from a shared ancestor...
Finally, you'd have to explain why, for say species A, B, and C, the pattern of shared same-location retroviruses is always *nested*, never *overlapped*. For example, all three will share some retroviruses, then A and B will both share several more, but if so then B *never* shares one with C that A doesn't also have (or at least remnants of).
In your "shared infection due to genetic similarities" suggestion, even leaving aside the near statistical impossibility of the infections leaving genetic "scars" in *exactly* the same locations in independent infections, one would expect to find cases of three species X, Y, and Z, where the degree of similarity was such that Y was "between" X and Z on some similarity scale, causing the same disease to befall X and Y but not Z, and another disease to affect Y and Z but not X. And yet, we don't find this in genetic markers. The markers are found in nested sequence, which is precisely what we would expect to see in cases of inheritance from common ancestry.
Here, for example, is an ancestry tree showing the pattern of shared same-location endogenous retroviruses of type HERV-K among primates:
This is just a partial list for illustration purposes -- there are many more.
Each labeled arrow on the chart shows an ERV shared in common by all the branches to the right, and *not* the branches that are "left-and-down". This is the pattern that common descent would make. And common descent is the *only* plausible explanation for it. Furthermore, similar findings tie together larger mammal groups into successively larger "superfamilies" of creatures all descended from a common ancestor.
Any presumption of independent acquisition is literally astronomically unlikely. And "God chose to put broken relics of viral infections that never actually happened into our DNA and line them up only in patterns that would provide incredibly strong evidence of common descent which hadn't actually happened" just strains credulity (not to mention would raise troubling questions about God's motives for such a misleading act).
Once again, the evidence for common descent -- as opposed to any other conceivable alternative explanation -- is clear and overwhelming.
Wait, want more? Endogenous retroviruses are just *one* type of genetic "tag" that makes perfect sense evolutionary and *no* sense under any other scenario. In addition to ERV's, there are also similar arguments for the patterns across species of Protein functional redundancies, DNA coding redundancies, shared Processed pseudogenes, shared Transposons (including *several* independent varieties, such as SINEs and LINEs), shared redundant pseudogenes, etc. etc. Here, for example, is a small map of shared SINE events among various mammal groups:
Like ERV's, any scenario which suggests that these shared DNA features were acquired separately strains the laws of probability beyond the breaking point, but they make perfect sense from an evolutionary common-descent scenario. In the above data, it is clear that the only logical conclusion is that, for example, the cetaceans, hippos, and ruminants shared a common ancestor, in which SINE events B and C entered its DNA and then was passed on to its descendants, yet this occurred after the point in time where an earlier common ancestor had given rise both to that species, and to the lineage which later became pigs.
And this pattern (giving the *same* results) is repeated over and over and over again when various kinds of molecular evidence from DNA is examined in detail.
The molecular evidence for evolution and common descent is overwhelming. The only alternative is for creationists to deny the obvious and say, "well maybe God decided to set up all DNA in *only* ways that were consistent with an evolutionary result even though He'd have a lot more options open to him, even including parts which by every measure are useless and exactly mimic copy errors, ancient infections, stutters, and other garbage inherited from nonexistent shared ancestors"...
And since a couple times when I've posted this, clueless anti-evolutionists have mistaken their presumptions for reality and tried to declare that ERV insertion or analysis was just "speculative", here are a few relevant papers to chew on establishing their validity:
And, as usual, that's just the tiniest *tip* of the iceberg. My PubMed searches on endogenous retroviruses turned up over a *thousand* papers. These are just some of the more useful ones.
Humans have 23 pairs of chromosomes ---chimps and gorillas have 24 pairs. How many pairs of chromosomes did the "common ancestor" have? Was it 23 or 24 pairs? How do you "evolve" missing or added chromosomes ---that would happen all at one time.And:
The common ancestor had 24 chromosomes.
If you look at the gene sequences, you'll find that Chromosome 2 in humans is pretty much just 2 shorter chimpanzee chromosomes pasted end-to-end, with perhaps a slight bit of lost overlap:
(H=Human, C=Chimpanzee, G=Gorilla, O=Orangutan)
Somewhere along the line, after humans split off from the other great apes, or during the split itself, there was an accidental fusion of two chromosomes, end-to-end. Where there used to be 24 chromosomes, now there were 23, but containing the same total genes, so other than a "repackaging", the DNA "instructions" remained the same.
If a chimpanzee gives birth to a creature with 23 chromosomes, that offspring isn't going to be a well-formed chimpanzee able to survive well.
It is if the same genes are present, which they would be in the case of a chromosome fusion.
Evolve would imply the genetic material changes little by little --not some big loss of two chromosomes at once but I don't see how they'd go away gene by gene.
Tacking two chromosomes together end-to-end is not a "big loss" of genes, and it really is a "little by little" change in the total genetic code. It's just been "regrouped" a bit. Instead of coming in 24 "packages", it's now contained in 23, but the contents are the same.
So how, you might ask, would the chromosomes from the first 23-chromosome "fused" individual match up with the 24 chromosomes from its mate when it tried to produce offspring? Very well, thanks for asking. The "top half" of the new extra-long Chromosome 2 would adhere to the original chromosome (call it "2p") from which it was formed, and likewise for the "bottom half" which would adhere to the other original shorter chromosome (call it "2q"). In the picture above, imagine the two chimp chromosomes sliding over to "match up" against the human chromosome. The chimp chromosomes would end up butting ends with each other, or slightly overlapping in a "kink", but chromosomes have overcome worse mismatches (just consider the XY pair in every human male -- the X and the Y chromosome are *very* different in shape, length, and structure, but they still pair up).
In fact, the "rubbing ends" of the matched-up chimp chromosomes, adhering to the double-long human-type chromosome, would be more likely to become fused together themselves.
For studies in which recent chromosome fusions have been discovered and found not to cause infertility, see:Chromosomal heterozygosity and fertility in house mice (Mus musculus domesticus) from Northern Italy. Hauffe HC, Searle JB Department of Zoology, University of Oxford, Oxford OX1 3PS, United Kingdom. firstname.lastname@example.orgIn that last reference, the Przewalski horse, which has 33 chromosomes, and the domestic horse, with 32 chromosomes (due to a fusion), are able to mate and produce fertile offspring.
An observed chromosome fusion: Hereditas 1998;129(2):177-80 A new centric fusion translocation in cattle: rob (13;19). Molteni L, De Giovanni-Macchi A, Succi G, Cremonesi F, Stacchezzini S, Di Meo GP, Iannuzzi L Institute of Animal Husbandry, Faculty of Agricultural Science, Milan, Italy.
J Reprod Fertil 1979 Nov;57(2):363-75 Cytogenetics and reproduction of sheep with multiple centric fusions (Robertsonian translocations). Bruere AN, Ellis PM
J Reprod Fertil Suppl 1975 Oct;(23):356-70 Cytogenetic studies of three equine hybrids. Chandley AC, Short RV, Allen WR.
Meanwhile, the question may be asked, how do we know that the human Chromosome 2 is actually the result of a chromsome fusion at/since a common ancestor, and not simply a matter of "different design"?
Well, if two chromsomes accidentally merged, there should be molecular remnants of the original chromosomal structures (while a chromosome designed from scratch would have no need for such leftover "train-wreck" pieces).
Ends of chromosomes have characteristic DNA base-pair sequences called "telomeres". And there are indeed remnants of telomeres at the point of presumed fusion on human Chromosome 2 (i.e., where the two ancestral ape chromosomes merged end-to-end). If I may crib from a web page:Telomeres in humans have been shown to consist of head to tail repeats of the bases 5'TTAGGG running toward the end of the chromosome. Furthermore, there is a characteristic pattern of the base pairs in what is called the pre-telomeric region, the region just before the telomere. When the vicinity of chromosome 2 where the fusion is expected to occur (based on comparison to chimp chromosomes 2p and 2q) is examined, we see first sequences that are characteristic of the pre-telomeric region, then a section of telomeric sequences, and then another section of pre-telomeric sequences. Furthermore, in the telomeric section, it is observed that there is a point where instead of being arranged head to tail, the telomeric repeats suddenly reverse direction - becoming (CCCTAA)3' instead of 5'(TTAGGG), and the second pre-telomeric section is also the reverse of the first telomeric section. This pattern is precisely as predicted by a telomere to telomere fusion of the chimpanzee (ancestor) 2p and 2q chromosomes, and in precisely the expected location. Note that the CCCTAA sequence is the reversed complement of TTAGGG (C pairs with G, and T pairs with A).Another piece of evidence is that if human Chromosome 2 had formed by chromosome fusion in an ancestor instead of being designed "as is", it should have evidence of 2 centromeres (the "pinched waist" in the picture above -- chromosomes have centromeres to aid in cell division). A "designed" chromosome would need only 1 centromere. An accidentally "merged" chromosome would show evidence of the 2 centromeres from the two chromosomes it merged from (one from each). And indeed, as documented in (Avarello R, Pedicini A, Caiulo A, Zuffardi O, Fraccaro M, Evidence for an ancestral alphoid domain on the long arm of human chromosome 2. Hum Genet 1992 May;89(2):247-9), the functional centromere found on human Chromosome 2 lines up with the centromere of the chimp 2p chromosome, while there are non-functional remnants of the chimp 2q centromere at the expected location on the human chromosome.
As an aside, the next time some creationist claims that there is "no evidence" for common ancestry or evolution, keep in mind that the sort of detailed "detective story" discussed above is repeated literally COUNTLESS times in the ordinary pursuit of scientific research and examination of biological and other types of evidence. Common ancestry and evolution is confirmed in bit and little ways over and over and over again. It's not just something that a couple of whacky anti-religionists dream up out of thin air and promulgate for no reason, as the creationists would have you believe.
[The poster known as Mr. LLLICHY wrote:] Here is that Vitamin C dataAnd:
After discovering this same data on another thread along with more discussion than has appeared here (I've taken the liberty of pinging the participants of that discussion), I see what the "mystery" is supposed to be -- it's supposed be why did some sites have multiple mutations while (small) stretches of other sites had none? In other words, why do the mutations appear clustered?
(You know, it would really help if people explained their points and questions in more detail, instead of leaving people to guess what the poster was thinking...)
[LLLICHY wrote:] "U238" that decays thrice, pretty good trick when there is "U238" that does not decay at all in 50,000,000 years.
Actually, no site had mutations "thrice". Three different bases at a given site is only *two* mutations (one original base, plus two mutations from it to something else).
Here's the "mutation map" from the actual DNA data:--1-12--1-1-1-1--------1112112--1---1-11-1--------1 ALL/nNo mutations ("-") in about half the sites, one mutation at several (17) sites, two mutations at three sites.
The first thing to keep in mind that random processes tend to "cluster" more than people expect anyway. People expect "randomness" to "spread out" somewhat evenly, but instead it's usually more "clumped", for statistical reasons that would be a diversion to go into right now. So "that looks uneven" isn't always a good indication that something truly is non-random.
If you don't believe me on that, I wrote a program which made 23 mutations totally at random on a 51-site sequence, then repeated the process to see what different random outcomes would look like:10 X$=STRING$(51,"-") 20 FOR I=1 TO 23 30 J%=INT(RND*51)+1 40 C$=MID$(X$,J%,1) 50 IF C$="-" THEN MID$(X$,J%,1)="1" ELSE MID$(X$,J%,1)=CHR$(ASC(C$)+1) 60 NEXT I 70 PRINT X$ 80 GOTO 10Yeah, it's BASIC, so sue me. Here's a typical screenful of the results:-21---1---2---111----2-----2-1121-------1---1--11-1 -1--1--21-11---1-1--1-1---1----1---21-11111---11--- 3-11---3-----1-----11-2-1---1--1----3--2---1--1---- ---1-1--22--1-1--2-2111--1-1111---1------1-------1- ---32----1-11-1-----1---2-231----1------1-----11--1 ----2---21--1---4----1-------------11-1--111-11-211 11--1-1---1-----1--1------1----3111--1----111-2-1-2 1112---1-3-1----1-1-----1-1------121--111-------1-1 -111121--1----1----1-1-1-1-11-2---1-1-------1-111-- -----------11-1---11-11--------21----12211--1---131 --1-211-1-1----21--11-1-2----1--1----11---11-----11 12---1-13------------2---21-21---11-1-1-1--2------- -----2-1---1-1----21--11-11-1---111-1--111-----2--1 -----1-----1-1-1-1---1-2----11-21-11--1-111---1-21- ---11--1-1-122-1-1-1--1-----2-1-1-1-------1-1---111 --2--11----2--1---12-2----1-1---1-1--1--12----1-1-1 -111-1-----1-1----------1-21111--1-2-11-11-1----11- 11-1--211-1221-----1--1-----11--1-2-1----------11-- -----1-12-11---2-1---11--1-2--1----11---111-1----11 11----1--12---12----1---31---1-11----2--1-11-1----- ---1--111-1--1-1-111----1-21----1-1-3---1------2--1 -2-11----1-1------1------2-1-1--111-111-1-1----1111 1--1--1-1---1-111111--2--1-1------112----2---11----Notice how oddly "clustered" most of them look, including one run which left a 13-site stretch "absolutely untouched", contrary to intuition (while having *4* mutations at a single site!)
Frankly, I don't see anything in the real-life DNA mutation map which looks any different from these truly random runs. Random events tend to cluster more than people expect. That solves the "mystery" right there.
Also, there may be a selection factor -- the GLO gene is a *lot* bigger than this. One has to wonder if this small 51-bp section was presented just because it was the one that looked "least random". That would be a no-no, since one can always hand-select the most deviant subset out of larger sample in order to artificially skew the picture.
However, since there are some interesting evolutionary observations to be made, let's look at that DNA data again, slightly rearranged:TAC CCC GTG GAG GTG CGC TTC ACT CGG GCG GAC GAC ATC CTG CTG AGC CCC PIG TAC CCC GTG GAG GTA CGC TTC ACT CGC GGG GAC GAC ATC CTG CTG AGC CCC BOS TAC CCC GTA GAG GTG CGC TTC ACC CGA GGC GAT GAC ATT CTG CTG AGC CCC RAT TAC CCC GTG GAG GTG CGC TTC ACC CGA GGT GAT GAC ATC CTG CTG AGC CCG MOUSE TAC CCT GTG GGG GTG CGC TTC ACC CGG GGG GAC GAC ATC CTG CTG AGC CCC GUIN PIG TAC CTG GTG GGG GTA CGC TTC ACC TGG AG* GAT GAC ATC CTA CTG AGC CCC HUMAN TAC CTG GTG GGG CTA CGC TTC ACC TGG AG* GAT GAC ATC CTA CTG AGC CCC CHIMPANZEE TAC CCG GTG GGG GTG CGC TTC ACC CAG AG* GAT GAC GTC CTA CTG AGC CCC ORANGUTAN TAA CCG GTG GGG GTG CGC TTC ACC CAA GG* GAT GAC ATC ATA CTG AGC CCC MACAQUEHere I've put spaces between codons, and clustered the closely-related species together: pig/cow as ungulates, rat/mouse for their obvious relationship, guinea pig right below them but separated because of the pseudogene nature of its GLO gene, then primates all in a group, with man's closest relative, the chimp, immediately below him, followed by the more distant orangutan, and the even more distant macaque. Also note that the top four have "working" GLO genes, and the bottom five have "broken" GLO pseudogenes.
First, let's consider just the four species with working GLO genes. Evolution predicts that even over large periods of time, these genes will be "highly conserved", with natural selection weeding out mutations that could "break" the gene. Note that the mutations will still have occurred in individuals of the population, but natural selection will "discourage" that mutation from spreading into the general population.
And before we go any further, let's talk about the "universal genetic code". In all mammals (indeed, in almost all living organisms), each triplet of DNA sites cause a particular amino acid to be formed. The mapping of triplets (called "codons") to amino acids is as follows:
Second Position of Codon T C A G F
TTT Phe [F] TTC Phe [F] TTA Leu [L] TTG Leu [L]
TCT Ser [S] TCC Ser [S] TCA Ser [S] TCG Ser [S]
TAT Tyr [Y] TAC Tyr [Y] TAA Ter [end] TAG Ter [end]
TGT Cys [C] TGC Cys [C] TGA Ter [end] TGG Trp [W]
T C A G T
CTT Leu [L] CTC Leu [L] CTA Leu [L] CTG Leu [L]
CCT Pro [P] CCC Pro [P] CCA Pro [P] CCG Pro [P]
CAT His [H] CAC His [H] CAA Gln [Q] CAG Gln [Q]
CGT Arg [R] CGC Arg [R] CGA Arg [R] CGG Arg [R]
T C A G A
ATT Ile [I] ATC Ile [I] ATA Ile [I] ATG Met [M]
ACT Thr [T] ACC Thr [T] ACA Thr [T] ACG Thr [T]
AAT Asn [N] AAC Asn [N] AAA Lys [K] AAG Lys [K]
AGT Ser [S] AGC Ser [S] AGA Arg [R] AGG Arg [R]
T C A G G
GTT Val [V] GTC Val [V] GTA Val [V] GTG Val [V]
GCT Ala [A] GCC Ala [A] GCA Ala [A] GCG Ala [A]
GAT Asp [D] GAC Asp [D] GAA Glu [E] GAG Glu [E]
GGT Gly [G] GGC Gly [G] GGA Gly [G] GGG Gly [G]
T C A G
(The above table imported from http://psyche.uthct.edu/shaun/SBlack/geneticd.html, which also has a nice introduction to the genetic code.)
Another version of the same table with nifty Java features and DNA database lookups can be found here.
The thing which is most relevant to the following discussion is the fact that most of the genetic codes are "redundant" -- more than one codon (triplet) encodes to exactly the same amino acid. This means that even in genes which are required for the organism, certain basepair mutations make absolutely no difference if the change is from one codon which maps into amino acid X to another codon which still maps into amino acid X. (This fact allows certain kinds of evolutionary "tracers" to be "read" from the DNA, as described here).
Now back to our DNA data. The redundancy in the genetic code means that some basepair sites will have more "degrees of freedom" than others (i.e., ways in which they can mutate without disrupting the gene's biological function in any way). Let's look at the four species with working GLO genes again:TAC CCC GTG GAG GTG CGC TTC ACT CGG GCG GAC GAC ATC CTG CTG AGC CCC PIG TAC CCC GTG GAG GTA CGC TTC ACT CGC GGG GAC GAC ATC CTG CTG AGC CCC BOS TAC CCC GTA GAG GTG CGC TTC ACC CGA GGC GAT GAC ATT CTG CTG AGC CCC RAT TAC CCC GTG GAG GTG CGC TTC ACC CGA GGT GAT GAC ATC CTG CTG AGC CCG MOUSE T T T A T A T T T A T C C T T T T T T T T A A A A A C A A A A A G C G G G G G C C C --- --- --1 --- --1 --- --- --1 --2 -12 --1 --- --1 --- --- --- --1Under each site of the mouse DNA, I've listed the "alternative" bases which could be be substituted for the mouse base at that site WITHOUT ALTERING THE GENE'S FUNCTION (because of genetic code redundancy). And under that I show the "mutation map" of just those four species.
Note that most of the "alternative" bases are in the third base of each codon, *and* that this is where all but one of the mutations have appeared. This is because these were the sites which were "free" to mutate in the way they did, because the mutation was genetically neutral. That doesn't mean that the first and second sites of each codon were immune from mutation, it's just that when mutations did occur at those sites, natural selection weeded them out quickly because they most likely "broke" the GLO gene for the individuals which received that mutuation. What we see above is the results after natural selection has already "filtered" the undesirable mutations and left the ones which "do no harm".
Additionally, the two sites which have mutated twice (i.e. have a "2" in the mutation map) are ones which had more "allowable" mutations. Also note that the sites which had the fewest allowable alternatives (only one alternate letter allowed) didn't have any mutations fix at those sites, which is unsurprising since a "safe" mutation would be less likely to occur there versus a site that "allowed" two or three alternatives.
All this is as predicted by evolutionary theory, you'll note.
It also explains the one anomoly of the original mutation map, which is that the mutation counts do tend to be higher at the third base of a codon.
However... What about the one exception? The pig DNA has had one mutation at a site which does not encode to exactly the same amino acid (which is the case for *all* the other ones). In the pig DNA, the GGG codon (mapping to Glycine) has changed to a GCG codon (mapping to Alanine). What's up with that? Well, one of two things. First and most likely, just as base values in codons have a built-in redundancy, so do the amino acids which make up the proteins which result from the DNA templates. In other words, certain amino acids can be substituted for other ones at some sites in given proteins without making any functional difference. (This "protein functional redundancy" also has implications for "evolutionary tracer" analysis, see here.) That may well be the case for Alanine versus Glycine in the GLO protein, but I'm not enough of a biochemist to be able to say. The other option is that it *does* make some difference in the function of the pig GLO protein, but not enough to "break" the vitamin-C synthesis (as proven by the fact that pigs *can* synthesize vitamin C). So one way or another, it's not a deal-breaker even though pig GLO will not be 100% identical to cow/mouse/rat GLO. It's yet another "allowable" mutation.
More interesting evolutionary observations: The number of mutational differences between pig/cow is 3, the number between mouse/rat is 4, and the difference between rat/cow is 7 -- all roughly as one would expect from the evolutionary relatedness of these animals (cows/pigs and rats/mice are each closer to each other than the rodents are to the ungulates).
Now let's take a close look at the guinea pig:TAC CCT GTG GGG GTG CGC TTC ACC CGG GGG GAC GAC ATC CTG CTG AGC CCC GUIN PIG --- --1 --- -1- --- --- --- --- --1 --1 --1 --- --- --- --- --- ---The "mutation map" under the guinea pig DNA is compared to the mouse DNA. Fascinating: Note that four of the five mutations are in the third base of a codon, *and* are of the type "allowed" by the genetic code redundancy. This indicates strongly that most of the evolutionary divergence between guinea pigs and mice likely occurred while the guinea pig's ancestors still had a working GLO gene. This is the sort of prediction implied by the evolutionary theory which could be cross-checked by further research of various types, and if verified, would be yet further confirmation that evolutionary theory is likely correct. So far, evolutionary theory has been subjected to literally countless tests like this, large and small, and the vast majority of results have confirmed the evolutionary prediction. This track record is hard to explain if evolution is an invalid theory, as some assert...
Finally, let's look over the primate DNA and mutation map (relative to each other):TAC CTG GTG GGG GTA CGC TTC ACC TGG AG* GAT GAC ATC CTA CTG AGC CCC HUMAN TAC CTG GTG GGG CTA CGC TTC ACC TGG AG* GAT GAC ATC CTA CTG AGC CCC CHIMPANZEE TAC CCG GTG GGG GTG CGC TTC ACC CAG AG* GAT GAC GTC CTA CTG AGC CCC ORANGUTAN TAA CCG GTG GGG GTG CGC TTC ACC CAA GG* GAT GAC ATC ATA CTG AGC CCC MACAQUE --1 -1- --- --- 1-1 --- --- --- 111 1-- --- --- 1-- 1-- --- --- ---Evolutionary theory predicts that because the GLO gene is "broken" in primates (i.e. is a pseudogene), mutations in it are highly likely to be neutral (i.e., make no difference, since it can't get much more broken), and thus mutations are just as likely to accumulate at any site as any other. Is that what we see? Yup. There's no obvious pattern to the mutations between primates in the above mutation map, and unlike the pig/cow/mouse/rat mutation map, the mutations aren't predominantly at the "safer" third base of a codon, nor of a type that would be "safe". In fact, one base has vanished entirely, but no biggie, the gene's already broken.
Also, although primates share a more recent common ancestor than cows/pigs/mice/rats, note that they've already racked up almost as many relative mutations as the cow/pig/mouse/rat DNA. This too is just as evolutionary theory predicts, because many mutations in a functional gene (GLO in this case) will be "non-safe" and weeded out by natural selection, making for a slower mutation fixation rate overall than in a pseudogene (as GLO is in primates) where natural selection doesn't "care" about the vast majority of mutations since *most* are neutral. So pseudogenes accumulate mutations faster than functional genes (even though rate of mutation *occurence* in both are likely the same).
Finally, note that there are ZERO mutational differences between the human DNA and the chimpanzee DNA, our nearest living relative.
I also see some interesting implications in the DNA sequences concerning which specific mutation fixed during what branch of the common-descent evolutionary tree for all the species represented, but reconstructing that would not only take another couple hours, at least, but would be a major bear to code in HTML, since I'd have to draw trees with annotations on the nodes... Bleugh.
In any case, I hope I've clarified some of the methods by which biologists find countless confirmations of evolution in DNA data. This is just a "baby" example, and to be more statistically valid would have to be done over much vaster sections of DNA sequences, but my intent was to demonstrate some of the concepts.
And if such a small amount of DNA as this can make small confirmations of evolutionary predictions, imagine the amount of confirmation from billion-basepair DNA data from each species compared across thousands of species... The amount of confirmatory discoveries for evolution from DNA analysis has already been vast, and promises to only grow in the future. For an overview of some of the different lines of evidence being studied, see The Journal of Molecular Evolution -- abstracts of all articles, current and back issues, can be browsed free online.
Where exactly is the "missing" transition in the following sequence? It looks pretty complete and gradual to me -- certainly there's no sudden "jump", no discontinuity, no pair between which a creationist would have any trouble dismissing such a small amount of change as "just microevolution", "just variation within a kind":(The above is from 29 Evidences for Macroevolution -- Part 1: The Unique Universal Phylogenetic Tree)
Figure 1.4.4. Fossil hominid skulls. Some of the figures have been modified for ease of comparison (only left-right mirroring or removal of a jawbone). (Images © 2000 Smithsonian Institution.)
- (A) Pan troglodytes, chimpanzee, modern
- (B) Australopithecus africanus, STS 5, 2.6 My
- (C) Australopithecus africanus, STS 71, 2.5 My
- (D) Homo habilis, KNM-ER 1813, 1.9 My
- (E) Homo habilis, OH24, 1.8 My
- (F) Homo rudolfensis, KNM-ER 1470, 1.8 My
- (G) Homo erectus, Dmanisi cranium D2700, 1.75 My
- (H) Homo ergaster (early H. erectus), KNM-ER 3733, 1.75 My
- (I) Homo heidelbergensis, "Rhodesia man," 300,000 - 125,000 y
- (J) Homo sapiens neanderthalensis, La Ferrassie 1, 70,000 y
- (K) Homo sapiens neanderthalensis, La Chappelle-aux-Saints, 60,000 y
- (L) Homo sapiens neanderthalensis, Le Moustier, 45,000 y
- (M) Homo sapiens sapiens, Cro-Magnon I, 30,000 y
- (N) Homo sapiens sapiens, modern
Accelerated Evolution of the ASPM Gene Controlling Brain Size Begins Prior to Human Brain ExpansionEtc., Etc., Etc. How many more thousands of papers would you like to see covering the overwhelming evidence for the human/ape common ancestry?Abstract: Primary microcephaly (MCPH) is a neurodevelopmental disorder characterized by global reduction in cerebral cortical volume. The microcephalic brain has a volume comparable to that of early hominids, raising the possibility that some MCPH genes may have been evolutionary targets in the expansion of the cerebral cortex in mammals and especially primates. Mutations in ASPM, which encodes the human homologue of a fly protein essential for spindle function, are the most common known cause of MCPH. Here we have isolated large genomic clones containing the complete ASPM gene, including promoter regions and introns, from chimpanzee, gorilla, orangutan, and rhesus macaque by transformation-associated recombination cloning in yeast. We have sequenced these clones and show that whereas much of the sequence of ASPM is substantially conserved among primates, specific segments are subject to high Ka/Ks ratios (nonsynonymous/synonymous DNA changes) consistent with strong positive selection for evolutionary change. The ASPM gene sequence shows accelerated evolution in the African hominoid clade, and this precedes hominid brain expansion by several million years. Gorilla and human lineages show particularly accelerated evolution in the IQ domain of ASPM. Moreover, ASPM regions under positive selection in primates are also the most highly diverged regions between primates and nonprimate mammals. We report the first direct application of TAR cloning technology to the study of human evolution. Our data suggest that evolutionary selection of specific segments of the ASPM sequence strongly relates to differences in cerebral cortical size.Identification of paralogous HERV-K LTRs on human chromosomes 3, 4, 7 and 11 in regions containing clusters of olfactory receptor genesAbstract: A locus harboring a human endogenous retroviral LTR (long terminal repeat) was mapped on the short arm of human chromosome 7 (7p22), and its evolutionary history was investigated. Sequences of two human genome fragments that were homologous to the LTR-flanking sequences were found in human genome databases: (1) an LTR-containing DNA fragment from region 3p13 of the human genome, which includes clusters of olfactory receptor genes and pseudogenes; and (2) a fragment of region 21q22.1 lacking LTR sequences. PCR analysis demonstrated that LTRs with highly homologous flanking sequences could be found in the genomes of human, chimp, gorilla, and orangutan, but were absent from the genomes of gibbon and New World monkeys. A PCR assay with a primer set corresponding to the sequence from human Chr 3 allowed us to detect LTR-containing paralogous sequences on human chromosomes 3, 4, 7, and 11. The divergence times for the LTR-flanking sequences on chromosomes 3 and 7, and the paralogous sequence on chromosome 21, were evaluated and used to reconstruct the order of duplication events and retroviral insertions. (1) An initial duplication event that occurred 14-17 Mya and before LTR insertion - produced two loci, one corresponding to that located on Chr 21, while the second was the ancestor of the loci on chromosomes 3 and 7. (2) Insertion of the LTR (most probably as a provirus) into this ancestral locus took place 13 Mya. (3) Duplication of the LTR-containing ancestral locus occurred 11 Mya, forming the paralogous modern loci on Chr 3 and 7.Birth and adaptive evolution of a hominoid gene that supports high neurotransmitter fluxAbstract: The enzyme glutamate dehydrogenase (GDH) is important for recycling the chief excitatory neurotransmitter, glutamate, during neurotransmission. Human GDH exists in housekeeping and brain-specific isotypes encoded by the genes GLUD1 and GLUD2, respectively. Here we show that GLUD2 originated by retroposition from GLUD1 in the hominoid ancestor less than 23 million years ago. The amino acid changes responsible for the unique brain-specific properties of the enzyme derived from GLUD2 occurred during a period of positive selection after the duplication event.A uniquely human consequence of domain-specific functional adaptation in a sialic acidbinding receptorAbstract: Most mammalian cell surfaces display two major sialic acids (Sias), N-acetylneuraminic acid (Neu5Ac) and N-glycolylneuraminic acid (Neu5Gc). Humans lack Neu5Gc due to a mutation in CMP-Neu5Ac hydroxylase, which occurred after evolutionary divergence from great apes. We describe an apparent consequence of human Neu5Gc loss: domain-specific functional adaptation of Siglec-9, a member of the family of sialic acidbinding receptors of innate immune cells designated the CD33-related Siglecs (CD33rSiglecs). Binding studies on recombinant human Siglec-9 show recognition of both Neu5Ac and Neu5Gc. In striking contrast, chimpanzee and gorilla Siglec-9 strongly prefer binding Neu5Gc. Simultaneous probing of multiple endogenous CD33rSiglecs on circulating blood cells of human, chimp, or gorilla suggests that the binding differences observed for Siglec-9 are representative of multiple CD33rSiglecs. We conclude that Neu5Ac-binding ability of at least some human CD33rSiglecs is a derived state selected for following loss of Neu5Gc in the hominid lineage. These data also indicate that endogenous Sias (rather than surface Sias of bacterial pathogens) are the functional ligands of CD33rSiglecs and suggest that the endogenous Sia landscape is the major factor directing evolution of CD33rSiglec binding specificity. Exon-1-encoded Sia-recognizing domains of human and ape Siglec-9 share only 9395% amino acid identity. In contrast, the immediately adjacent intron and exon 2 have the 98100% identity typically observed among these species. Together, our findings suggest ongoing adaptive evolution specific to the Sia-binding domain, possibly of an episodic nature. Such domain-specific divergences should also be considered in upcoming comparisons of human and chimpanzee genomes.Lineage-Specific Gene Duplication and Loss in Human and Great Ape EvolutionAbstract: Given that gene duplication is a major driving force of evolutionary change and the key mechanism underlying the emergence of new genes and biological processes, this study sought to use a novel genome-wide approach to identify genes that have undergone lineage-specific duplications or contractions among several hominoid lineages. Interspecies cDNA array-based comparative genomic hybridization was used to individually compare copy number variation for 39,711 cDNAs, representing 29,619 human genes, across five hominoid species, including human. We identified 1,005 genes, either as isolated genes or in clusters positionally biased toward rearrangement-prone genomic regions, that produced relative hybridization signals unique to one or more of the hominoid lineages. Measured as a function of the evolutionary age of each lineage, genes showing copy number expansions were most pronounced in human (134) and include a number of genes thought to be involved in the structure and function of the brain. This work represents, to our knowledge, the first genome-wide gene-based survey of gene duplication across hominoid species. The genes identified here likely represent a significant majority of the major gene copy number changes that have occurred over the past 15 million years of human and great ape evolution and are likely to underlie some of the key phenotypic characteristics that distinguish these species.Sequence Variation Within the Fragile X LocusAbstract: The human genome provides a reference sequence, which is a template for resequencing studies that aim to discover and interpret the record of common ancestry that exists in extant genomes. To understand the nature and pattern of variation and linkage disequilibrium comprising this history, we present a study of ~31 kb spanning an ~70 kb region of FMR1, sequenced in a sample of 20 humans (worldwide sample) and four great apes (chimp, bonobo, and gorilla). Twenty-five polymorphic sites and two insertion/deletions, distributed in 11 unique haplotypes, were identified among humans. Africans are the only geographic group that do not share any haplotypes with other groups. Parsimony analysis reveals two main clades and suggests that the four major human geographic groups are distributed throughout the phylogenetic tree and within each major clade. An African sample appears to be most closely related to the common ancestor shared with the three other geographic groups. Nucleotide diversity, [pi], for this sample is 2.63 ± 6.28 × 10-4. The mutation rate, [mu], is 6.48 × 10-10 per base pair per year, giving an ancestral population size of ~6200 and a time to the most recent common ancestor of ~320,000 ± 72,000 per base pair per year. Linkage disequilibrium (LD) at the FMR1 locus, evaluated by conventional LD analysis and by the length of segment shared between any two chromosomes, is extensive across the region.Structural and evolutionary analysis of the two chimpanzee alpha-globin mRNAsAbstract: Two distinct alpha-globin mRNAs were detected in chimpanzee reticulocyte mRNA using a primer extension assay. DNA copies of these two mRNAs were cloned in the bacterial plasmid pBR322, and their sequence was determined. The two alpha-globin mRNAs have obvious structural homology to the two human alpha-globin mRNAs, alpha 1 and alpha 2. Comparison of the two chimpanzee alpha-globin mRNAs to each other and to their corresponding human counterparts revealed evidence of a recent gene conversion in the human alpha-globin complex and a marked heterogeneity in the rate of structural divergence within the alpha-globin gene.Differential Alu Mobilization and Polymorphism Among the Human and Chimpanzee LineagesAbstract: Alu elements are primate-specific members of the SINE (short interspersed element) retroposon family, which comprise 10% of the human genome. Here we report the first chromosomal-level comparison examining the Alu retroposition dynamics following the divergence of humans and chimpanzees. We find a twofold increase in Alu insertions in humans in comparison to the common chimpanzee (Pan troglodytes). The genomic diversity (polymorphism for presence or absence of the Alu insertion) associated with these inserts indicates that, analogous to recent nucleotide diversity studies, the level of chimpanzee Alu diversity is 1.7 times higher than that of humans. Evolutionarily recent Alu subfamily structure differs markedly between the human and chimpanzee lineages, with the major human subfamilies remaining largely inactive in the chimpanzee lineage. We propose a population-based model to account for the observed fluctuation in Alu retroposition rates across primate taxa.
I'll make you guys a deal -- if you'll actually learn something about biology for a change before you spew your uninformed opinions, I'll stop pointing out just how ignorant you're being.
Anyone that believes the theory of evolution claims that man came from apes doesn't know the theory enough to criticize it. You're obviously ignorant.
The theory claims that man and the apes evolved from a common ancestor.
George Will is usually right, but he is wrong on this one.
Ditto for Charles Krauthammer. I have the utmost respect for Krauthammer's political acumen, but he fumbled the ball on this one.
Both of them have fallen for the transparent lie that the only alternative to purely naturalistic evolution is biblical creationism.
If you get a chance, please check out a couple of articles I wrote at
Ah, yes, the creationists are fond of misquoting and misrepresenting Patterson. Read this, guys. Even Patterson himself agrees you folks are misrepresenting him.
Do you guys have *any* material which isn't based on a) misrepresentation, or b) falsehoods due to ignorance of the material?
Yeah, I'm particularly impressed with our appendixes and backwards-wired eyes. But we can't expect God to be perfect, can we?
The evidence, said Scalia, was overwhelming that the laws framers were not trying to impose religion in the classrooms.
Right, it's not religion, it's just a supernatural entity that operates outside physical laws. Gotcha.
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