by DeViL DriVeR 76 46 Replies latest watchtower bible
Well if thats the case why are australians white? I know the natives were not, I know the whites there were prisoners cast onto that island, and what about south africans?
I heard a lecture by a geneticist who addresses this very question, and she says that it would take 10,000 years (all other things being equal) for white Australians to become as dark as the aborigines (who have been there for 40,000 or so).
Beneficial mutation has never been proven.
Would the corrupted hemoglobin DNA in icefish be a positive, neutral, or negative mutation?
You know, I never heard of the icefish.
I will go through a process:
Google!!!
Wikipedia!!!
etc.
OK.
Is there DEFINITIVE proof that these animals EVER had hemoglobin in the first place? No. So it can't be a mutation. Mutate = change.
Since they were DESIGNED to live in their hyper-oxygenated environment, that is the end of that.
Assumptions that they should be exactly like other animals with blood would be spurious.
The argument about "beneficial" or "harmful" mutations is mute. As long as mutations happen and are heritable, evolution occurs. Most of the time the evolution does not result in a better anything. It just results in difference. As long as the new population are capable of existing in the given environment and breed true it may exist alongside its ancestral forms. In my lake I have bluegill, white crappie, pumpkinseed and largemouth bass. They are all closely related and are all the result of genetic mutations from ancestral forms of sunfish. In total there are presently about 30 species of sunfish, all of which exist only in North America. However its fair to ask is the pumpkinseed necessarily better than the bluegill? No, they both taste good. So the question of beneficial vs harmful mutation begins to become less purtenant. To break it down even further, there are bluegills where the male is monogomous through the spawning period and there are what you might call giggalo bluegills. The best part is the fact that the giggalo bluegills mimic females in order to gain close access to the females. Unfortunately these males have to spend time being wooed by other more aggressive males and waste time they'd perfer to be spending with the girls. These reproductive strategies each have pros and cons and therefore in most lakes there continues both genetically determined behaviors. Its an evolutionary draw. However if you introduce a new key predator or disease in the North American environment and one strategy will likely prevail rather quickly. This would then be properly called 'survival of the fittest'. However as I was trying to impress is that for many years the heritable genetic difference, aka evolution, may have presented no obvious advantage or disadvantage. And naturally then given a different set of environmental factors the genetic differences produce differently adaptive species. Hence we have warmouth bass, green sunfish, rock bass, smallmouth bass etc....living contemporaneously despite having separately evolved over millions of years. Largmouth bass represent a break in the family about 40-50 million years old while bluegill and bream are only about 2-4 million years separated.
The mighty Muskellunge, the walleyed pike and the yellow perch are similarly all cousins, and many creationists have no problem accepting that but when its stated that humans and chimpanzees had a common ancestry they get all bothered by the notion.
Most of your post is correct (I have fished for about 31 years), except for one thing:
They were made that way. There are no transitional forms in historical evidence to substantiate any evolution.
They were made that way.
Humans are similar to many animals. Same Designer = similar solutions, oftentimes.
Every living thing is a "transitional form".
Mad Tiger writes: " Beneficial mutation has never been proven. NEVER. "
You are COMPLETELY WRONG. This is bullshit propagated by the Watchtower society and their creationist brethren. Beneficial mutations have been demonstrated many, many times in controlled laboratory settings and within natural environments. These studies have been published in reputable scientific journals. Check the references, they are all available at your local library.
1.) Adaptation to High and Low Temperatures by E. coli.
A single clone of E. coli was cultured at 37 C (that is 37 degrees Celsius) for 2000 generations. A single clone was then extracted from this population and divided into replicates that were then cultured at either 32 C , 37 C, or 42 C for a total of another 2000 generations. Adaptation of the new lines was periodically measured by competing these selection lines against the ancestor population. By the end of the experiment, the lines cultured at 32 C were shown to be 10% fitter that the ancestor population (at 32 C), and the line cultured at 42 C was shown to be 20% more fit than the ancestor population. The replicate line that was cultured at 37 C showed little improvement over the ancestral line.Bennett, A.F., Lenski, R.E., & Mittler, J.E. (1992). Evolutionary adaptation to temperature I. Fitness responses of Escherichia coli to changes in its thermal environment. Evolution, 46:16-30.
2.) Adaptation to Growth in the Dark by Chlamydomonas.
Chlamydomonas is a unicellular green algae capable of photosynthesis in light, but also somewhat capable of growth in the dark by using acetate as a carbon source. Graham Bell cultured several clonal lines of Chlamydomonas in the dark for several hundred generations. Some of the lines grew well in the dark, but other lines were almost unable to grow at all. The poor growth lines improved throughout the course of the experiment until by 600 generations they were well adapted to growth in the dark. This experiment showed that new, beneficial mutations are capable of quickly (in hundreds of generations) adapting an organism that almost required light for survival to growth in the complete absence of light.
3.) Selection for Large Size in Chlamydomomas
Bell also selected clonal lines of Chlamydomonas for size by passing cultures through a fine filter and discarding the cells that were not retained on the filter. He reports that although this method was not very effective at retaining the largest cells (due to inconsistencies in the filter pore size), after forty generations of this selection technique, the cell diameter had increased by an average of about 1 phenotypic standard deviation.
4.) Adaptation to a Low Phosphate Chemostat Environment by a Clonal Line of Yeast
P.E. Hansche and J.C. Francis set up chemosats to allow evolution of a single clonal line of beer yeast in a phosphate limited (due to high pH) environment. (A chemostat is a device that allows the propagation of microorganisms in an extremely constant environment.) The yeast clones grew slowly for about the first 180 generations when there was an abrupt increase in population density. This was later shown to be due to better assimilation of the phosphate, presumably due to an improvement in the permease molecule. (Permease is an enzyme that controls what is allowed to come into the cell through the yeast's cell membrane.) After about 400 generations, a second improvement in cell growth rates occurred because of a mutation to the yeast's phosphatase (an enzyme that improves the cells ability to use phosphate). The phosphatase became more active overall, and its optimal pH (the pH where it is most active) was raised. Finally, a third mutant appeared after 800 generations that caused the yeast cells to clump. This raised the population density in the chemostat because individual cells were no longer being washed out of chemostat (which is one of the methods that the chemostat uses to maintain very uniform conditions) as quickly as they had prior to the mutation. (This is just speculation on my part, but I wonder if it wasn't under some similar conditions that multi-cellularity became favored over unicellularity - perhaps on a sea bed or river bottom.)This experiment was repeated, and the same mutations occurred, but in different orders. Also, in one replication, the processing of phosphate was improved by a duplication of the gene that produces phosphatase. This is experimental evidence of an extremely important mechanism in evolutionary history! It is also a particularly elegant experiment because not only was all of this adaptation shown to occur in clonal lines (descended from a single individual), but the authors also determined the exact mutations that caused the improved adaptations by sequencing the genes and proteins involved.
Francis, J.E., & Hansche, P.E. (1972) Directed evolution of metabolic pathways in microbial populations. I. Modification of the acid phosphatase pH optimum in Saccharaomyces cervisiae. Genetics, 70: 59-73.
Francis, J.E., & Hansche, P.E. (1973) Directed evolution of metabolic pathways in microbial populations. II. A repeatable adaptation in Saccharaomyces cervisiae. Genetics, 74:259-265.
Hansche, P.E. (1975) Gene duplication as a mechanism of genetic adaptation in Saccharaomyces cervisiae. Genetics, 79: 661-674.
5.) Evidence of genetic divergence and beneficial mutations in bacteria after 10,000 generations
Papadopoulos, D., Schneider, D., Meier-Eiss, J., Arber, W., Lenski, R. E., Blot, M. (1999). Genomic evolution during a 10,000-generation
experiment with bacteria. Proc. Natl. Acad. Sci. U. S. A. 96: 3807-3812Edited by John R. Roth, University of Utah, Salt Lake City, UT, and approved February 3, 1999 (received for review July 21, 1998)
Molecular methods are used widely to measure genetic diversity within populations and determine relationships among species. However, it is difficult to observe genomic evolution in action because these dynamics are too slow in most organisms. To overcome this limitation, we sampled genomes from populations of Escherichia coli evolving in the laboratory for 10,000 generations. We analyzed the genomes for restriction fragment length polymorphisms (RFLP) using seven insertion sequences (IS) as probes; most polymorphisms detected by this approach reflect rearrangements (including transpositions) rather than point mutations. The evolving genomes became increasingly different from their ancestor over time. Moreover, tremendous diversity accumulated within each population, such that almost every individual had a different genetic fingerprint after 10,000 generations. As has been often suggested, but not previously shown by experiment, the rates of phenotypic and genomic change were discordant, both across replicate populations and over time within a population. Certain pivotal mutations were shared by all descendants in a population, and these are candidates for beneficial mutations, which are rare and difficult to find. More generally, these data show that the genome is highly dynamic even over a time scale that is, from an evolutionary perspective, very brief.
6.) Adaptation of yeast to a glucose limited environment via gene duplications and natural selection
When microbes evolve in a continuous, nutrient-limited environment, natural selection can be predicted to favor genetic changes that give cells greater access to limiting substrate. We analyzed a population of baker's yeast that underwent 450 generations of glucose-limited growth. Relative to the strain used as the inoculum, the predominant cell type at the end of this experiment sustains growth at significantly lower steady-state glucose concentrations and demonstrates markedly enhanced cell yield per mole glucose, significantly enhanced high-affinity glucose transport, and greater relative fitness in pairwise competition. These changes are correlated with increased levels of mRNA hybridizing to probe generated from the hexose transport locus HXT6. Further analysis of the evolved strain reveals the existence of multiple tandem duplications involving two highly similar, high-affinity hexose transport loci, HXT6 and HXT7. Selection appears to have favored changes that result in the formation of more than three chimeric genes derived from the upstream promoter of the HXT7 gene and the coding sequence of HXT6. We propose a genetic mechanism to account for these changes and speculate as to their adaptive significance in the context of gene duplication as a common response of microorganisms to nutrient limitation.Brown CJ, Todd KM, Rosenzweig RF (1998) Multiple duplications of yeast hexose transport genes in response to selection in a glucose-limited environment. Mol Biol Evol 1998 Aug;15(8):931-42 Nature 387, 708 - 713 (1997)
7.) Molecular evidence for an ancient duplication of the entire yeast genome
KENNETH H. WOLFE AND DENIS C. SHIELDS
Gene duplication is an important source of evolutionary novelty. Most duplications are of just a single gene, but Ohno proposed that whole-genome duplication (polyploidy) is an important evolutionary mechanism. Many duplicate genes have been found in Saccharomyces cerevisiae, and these often seem to be phenotypically redundant. Here we show that the arrangement of duplicated genes in the S. cerevisiae genome is consistent with Ohno's hypothesis. We propose a model in which this species is a degenerate tetraploid resulting from a whole-genome duplication that occurred after the divergence of Saccharomyces from Kluyveromyces. Only a small fraction of the genes were subsequently retained in duplicate (most were deleted), and gene order was rearranged by many reciprocal translocations between chromosomes. Protein pairs derived from this duplication event make up 13% of all yeast proteins, and include pairs of transcription factors, protein kinases, myosins, cyclins and pheromones. Tetraploidy may have facilitated the evolution of anaerobic fermentation in Saccharomyces.
8.) Evolution of a new enzymatic function by recombination within a gene.
Hall BG, Zuzel T
Proc Natl Acad Sci U S A 1980 Jun 77:6 3529-33
Abstract Mutations that alter the ebgA gene so that the evolved beta-galactosidase (ebg) enzyme of Escherichia coli can hydrolyze lactose fall into two classes: class I mutants use only lactose, whereas class II mutants use lactulose as well as lactose. Neither class uses galactosylarabinose effectively. In this paper we show that when both a class I and a class II mutation are present in the same ebgA gene, ebg enzyme acquires a specificity for galactosylarabinose. Although galactosylarbinose utilization can evolve as the consequence of sequential spontaneous mutations, it can also evolve via intragenic recombination in crosses between class I and class II ebgA+ mutant strains. We show that the sites for class I and class II mutations lie about 1 kilobase, or about a third of the gene, apart in ebgA. Implications of these findings with respect to the evolution of new metabolic functions discussed.
9.) Changes in the substrate specificities of an enzyme during directed evolution of new functions.
Hall BG
Biochemistry 1981 Jul 7 20:14 4042-9
Abstract Wild-type ebg enzyme, the second beta-galactosidase of Escherichia coli K12, does not permit growth on lactose. As part of a study of the evolution of new enzymatic functions, I have selected, from a lacZ deletion strain, a variety of spontaneous mutants that grow on lactose and other beta-galactoside sugars. Single point mutations in the structural gene ebgA alter the enzyme so that it hydrolyzes lactose or lactulose effectively; two mutations in ebgA permit galactosylarabinose hydrolysis, while three mutations are required for lactobionic acid hydrolysis. Wild-type ebg enzyme and 16 functional mutant ebg enzymes were purified and analyzed kinetically to determine how the substrate specificities had changed during the directed evolution of these new functions. The specificities for the biologically selected substrates generally increased by at least an order of magnitude via increased Vmax and decreased Km for the substrate. These changes were very specific for the selected substrate, often being accompanied by decreased specificities for other related substrates. The single, double, or triple substitutions in the enzymes did not detectably alter the thermal stability of ebg enzyme.
10.) 12% (3 out of 26) random mutations in a strain of bacteria improved fitness in a particular environment.
Contribution of individual random mutations to genotype-by-environment interactions in Escherichia coli
Susanna K. Remold* and Richard E. LenskiCenter for Microbial Ecology, Michigan State University, East Lansing, MI 48824
Edited by M. T. Clegg, University of California, Riverside, CA, and approved July 30, 2001 (received for review March 22, 2001)
Numerous studies have shown genotype-by-environment (G×E) interactions for traits related to organismal fitness. However, the genetic architecture of the interaction is usually unknown because these studies used genotypes that differ from one another by many unknown mutations. These mutations were also present as standing variation in populations and hence had been subject to prior selection. Based on such studies, it is therefore impossible to say what fraction of new, random mutations contributes to G×E interactions. In this study, we measured the fitness in four environments of 26 genotypes of Escherichia coli, each containing a single random insertion mutation. Fitness was measured relative to their common progenitor, which had evolved on glucose at 37°C for the preceding 10,000 generations. The four assay environments differed in limiting resource and temperature (glucose, 28°C; maltose, 28°C; glucose, 37°C; and maltose, 37°C). A highly significant interaction between mutation and resource was found. In contrast, there was no interaction involving temperature. The resource interaction reflected much higher among mutation variation for fitness in maltose than in glucose. At least 11 mutations (42%) contributed to this G×E interaction through their differential fitness effects across resources. Beneficial mutations are generally thought to be rare but, surprisingly, at least three mutations (12%) significantly improved fitness in maltose, a resource novel to the progenitor. More generally, our findings demonstrate that G×E interactions can be quite common, even for genotypes that differ by only one mutation and in environments differing by only a single factor.
Evolution of a Unicellular Organism into a Multicellular Species
Starting from single celled animals, each of which has the capability to reproduce there is no sex in the sense that we think of the term. Selective pressure has been observed to convert single-cellular forms into multicellular forms. A case was observed in which a single celled form changed to multicellularity.
Boxhorn, a student of Boraas,writes:Coloniality in Chlorella vulgaris
Boraas (1983) reported the induction of multicellularity in a strain of Chlorella pyrenoidosa (since reclassified as C. vulgaris) by predation. He was growing the unicellular green alga in the first stage of a two stage continuous culture system as for food for a flagellate predator, Ochromonas sp., that was growing in the second stage. Due to the failure of a pump, flagellates washed back into the first stage. Within five days a colonial form of the Chlorella appeared. It rapidly came to dominate the culture. The colony size ranged from 4 cells to 32 cells. Eventually it stabilized at 8 cells. This colonial form has persisted in culture for about a decade. The new form has been keyed out using a number of algal taxonomic keys. They key out now as being in the genus Coelosphaerium, which is in a different family from Chlorella. "Boraas, M. E. 1983. Predator induced evolution in chemostat culture. EOS. Transactions of the American Geophysical Union. 64:1102.
from Observed Instances of Speciation
Evolution of New Metabolic Pathways
Some of the experiments that I described previously could be said to have one weakness - they each only cover minor changes to an existing metabolic pathway. Pages 229 - 243 of Graham Bell's book ("Selection - The Mechanism of Evolution" Alexander Bell, 1997) also describe experiments that have demonstrated that organisms are capable of evolving whole new metabolic pathways, not just improving existing pathways. This is important to me because it shows that evolution is capable of producing something new, not just making minor improvements to existing pathways.
The most common experimental process that leads to evolution of a new pathway is this. An organism (usually bacteria) is put in a novel environment - an environment that contains some resource (chemical) that the organism has not been exposed to in the past. If that new chemical is the sole source of some chemical the organism requires for survival (e.g. carbon or nitrogen), most of the time, the organism will die. However, if any of the organisms' existing enzymes have the slightest ability to enhance reactions with the new resource, selection will strongly favor the duplication of the gene that produces that enzyme, and future mutations will improve the ability of the newly duplicated enzyme to process the new chemical resource. It's not very hard to see that the same factors that are manipulated in these experiments are going to occur in nature as well in the very long term. This duplication and divergence "strategy" (in quotes because evolution doesn't really have a strategy) of evolution appears to be capable of driving evolution from the first pre biotic self-replicators to the present incredibly complex and diverse life forms that occupy every imaginable niche of the planet earth.
1.) Modifying the fucose pathway to metabolize propanediol.
In normal anaerobic E. coli metabolism L-fucose is transported into the cell and converted into dihydroxyacetone phosphate (which is used for further metabolism) and lactaldehyde (which is a waste product). The lactaldehyde is then converted to propanediol which is actively excreted from the cell by a "facilitator" - a chemical that eases movement of another chemical through the cell membrane in either direction. When E. coli lines are exposed to an aerobic environment rich in propanediol, some individuals are able to utilize this former waste as a food source. This is made possible by a change to the enzyme that formerly converted the lactaldehyde to propanediol to reverse its action and convert the propanediol to lactaldehyde. The lactaldehyde can then be processed by the previously existing aerobic pathways that use lactaldehyde as a carbon and energy source.Lin, E.C.C., & Wu, T.T. (1984) Functional divergence of the L-Fucose system in Escherichia coli. In R.P. Mortlock (ed.), "Microorganisms as Model Systems for Studying Evolution" (pp. 135-164) Plenum, New York.
2.) Exotic five-carbon sugars
Some five carbon sugars are very rare in nature, so very few organisms have the ability to use these exotic compounds in their metabolism. Robert Mortlock determined that the bacteria Klebsiella aerogenes was not immediately able to metabolize D-arabinose and xylitol by growing strains in media containing those compounds and noting the strains that were able to grow only after a lag time. This indicated that the original strain did not have the ability to process the compounds, but was able to evolve such a capability. Mortlock then went on to see how this capability was evolved.In the case of D-arabinose, Mortlock showed that the arabinose could be utilized if it could be converted to D-ribulose by an enzyme (an isomerase). Unfortunately, K. aerogenes has no such isomerase for the conversion of D-arabinose. However, the isomerase for L-fucose has a low activity for D-arabinose. But, the bad news is that the L-fucose isomerase is normally produced only when the cell is exposed to fucose. Nonetheless, in a few individuals, mutations occurred that allowed the fucose isomerase to be produced at all times - not just when L-fucose is present. This is normally a bad thing and would be selected against because it wastes the cells resources by constantly producing an unneeded enzyme. In this situation though, the mutation is a very good thing, and allows the cell to survive because it can now metabolize arabinose (albeit rather poorly). Although production of the fucose isomerase has been deregulated, the structure of the isomerase itself has not been changed. The next mutation was a change to the isomerase to make it more effective in the conversion of arabitol to ribulose. Finally (although I can't tell from Bell's description if this was actually done in the experiments), the culture could be selected to regain control of the expression of the isomerase - so that it is produced only when arabitol is present.
Xylitol is also not normally metabolized, but Mortlock and his colleagues were able to develop strains (generally through spontaneous mutations, but sometimes with u.v. ray or chemical induced mutations) that could use it because ribitol dehydrogenase (which is usually present in the cells to convert ribitol to D-ribulose) was able to slightly speed up the conversion of xylitol to D-xylulose, for which metabolic pathways already exist. The ability of the strains to utilize xylitol was increased as much as 20 fold when first production of ribitol dehydrogenase was deregulated (the enzyme was produced all the time, not just when ribitol was present), then duplication of the ribitol dehydrogenase genes occurred, then the structure of the enzyme was changed such that its efficiency at working with xylitol was improved, and finally, in at least one case, a line regained control of the modified ribitol dehydrogenase gene so that the enzyme was only produced in the presence of xylitol. Here we have a complete example of a new metabolic pathway being developed through duplication and modification of an existing pathway.
Many papers were published concerning this group of experiments. For a review, see:
Hartley, B.S. (1984), Experimental evolution of ribitol dehydrogenase. In R.P. Mortlock (ed.), "Microorganisms as Model Systems for Studying Evolution" (pp. 23 - 54) Plenum, New York.Bell goes on to give at least two more examples of the evolution of new metabolic pathways.
Adaptation does not equal mutation.
The author's journal article used the term "adaptation" multiple times.
Adaptation does not equal mutation.
If creation did not involve a pristine infusion of live organic material onto a lifeless earth then maybe we are looking at the story the wrong way round and making too simplistic an interpretation of the record (applying modern journalistic standards to an ancient history that may or may not have been recognised at the time as historical fact) here's some maybes to soften the edges:
1/ Maybe the myth was used to describe evolution in a way that made sense when no empirical scientific data/tools existed.
2/ Maybe the 'creation' was God's appearance to one of the races of man and the bestowal of some spiritual knowledge - a revelation that was occluded in a story.
3/ Maybe there was a creation/organisation , one of many creations by an external intelligence a creation that continues today whereby the an incredible battery of dna failsafes and backup systems where spliced into the previous creation. The ability to adapt to localised conditions seems to be very rapid as opposed to the more fundamental changes required to gain altered functionality - we seem full of back-ups and dormant potentials awaiting the correct moment to be triggered.
4/ Maybe a species was once smarter than the local hominids and this is the mythical tale of its defeat at the hands of mankind who rose to dominance.
5/ Maybe the earth really was created but the bible just records a mash of data - some of it spurious (like the ages of death/genealogies etc..) So God may have created life billions of years ago and then organised a selected species, Adam (meaning many) to be given a greater intelligence (represented by Gods breath) and becoming self aware (the man is become as one of us knowing good and evil - also recognising individual nudity.)
6/ Maybe its just a made up story with little value.
I tend to see truth behind the stories, there was probably an enormous catastrophic flood in the middle east that survived as the flood story of the bible, there was a period when man began to write (perhaps the singular most important invention ever) and he wrote down the most important things he could and in a non-scientific world everything becomes fable and so the Eden story was understood by them but we cannot know what it really meant and so on.
The daft thing is we still argue as though it matters one jot what it means.
Hi MadTiger,
I have not gotten a response from other creationists but I'll try with you. Why would God create whales, dolphins, and manatees which are fully aquatic but must come to the ocean's surface to breath air when He already knew how to make fish which can get their oxygen directly from the water? Why did God create land plants and animals with a vital need for water since it is often difficult to find and billions of land organisms have died due to its lack and much of the earth's land space is wasted because there is no water available? Why not just design land plants and animals that don't need water or that could at least use sea water? Why is most of the water in the world salty if land plants and animals can't use it? Why didn't God just make all water fresh? Why do we need to eat when we could easily be designed to just use sun light for energy? Billions have starved because they could not find enough food so why design things that need it? Why are so many things designed to kill so that they can eat? Why design parasites and pathenogenes? Why design things to get old, ugly, weak, and sickly that die a long painful death? Even if death was needed why not be strong and healthy and then just die instantly and painlessly. Even if I bought into the punishment for sin for humans then why are animals punished too with old age and long, painful deaths?
Why did God create monotremes( the platypus and echidna), mammel-like animals which produce milk through skin pores but have no nipples, have fur, yet are semi-ectothermic, and lay eggs like reptiles and birds? They are strangely like transitional animals you would expect in evolution much like amphibians which start out as fish and then develop the organs of land animals? or worms that change into flying insects? it seems there are alot of transitional animals afterall, why if they were created directly, do we see so much evidence for bad design and evolution-like steps??
