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Featured Is evolution a fact or theory?

Discussion in 'Creation & Theistic Evolution' started by mathinspiration, Jan 8, 2018.

  1. sfs

    sfs Senior Member

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    Don't be ridiculous. Biologists are no more publishing evidence for macroevolution than physicists are publishing evidence for the existence of atoms. Both ideas were established well over a century to the satisfaction of the relevant scientists.

    What you can find are lots of papers that use common descent in their studies (e.g. here and here, just off the top of my head), which could only be true if it were already the scientific consensus.
     
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  2. The Barbarian

    The Barbarian Crabby Old White Guy

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    Barbarian notes that microevolution and macroevolution are two different things with the same cause, a change in allele frequency in populations over time. hence, both are consequences of evolution, just as planetary orbits and apples falling from trees are two different things caused by gravity.

    For example, definition of planetary orbits are the movement of planets around a star, while apples falling from a tree, are objects falling to earth. Two different things, caused by the same thing. Likewise microevolution and macroevolution. As you learned it's even possible for microevolution to become retroactively macroevolution.

    Nope. Both speciation and changes within a speciation are directly observed.

    I just showed you directly:
    Leopard frogs exist in the US everywhere from the Gulf Coast to the Canadian border. As you go north, the alleles in those frogs governing maturation change to effect faster maturity (because of longer and colder winters in the north). Frogs from adjacent populations can interbreed, though. And this allows gene flow in the population. These changes are microevolution, and there is one species.

    However, if the leopard frogs in the center of the United States were to go extinct, leopard frogs in the far north could not interbreed with those from the Gulf coast. And suddenly, what was microevolution becomes (retroactively) macroevolution. This is why that error to which you referred is so wrong.


    It's not a surprise to any biologist. But some journal articles:


    BMC Genomics. 2018 Jan 3;19(1):12. doi: 10.1186/s12864-017-4382-2.
    The gonadal transcriptome of the unisexual Amazon molly Poecilia formosa in comparison to its sexual ancestors, Poecilia mexicana and Poecilia latipinna.

    Appl Environ Microbiol. 2017 Dec 8. pii: AEM.02015-17. doi: 10.1128/AEM.02015-17.
    Divergence in gene regulation contributes to sympatric speciation of Shewanella baltica strains.

    Genome Biol Evol. 2018 Jan 1;10(1):33-44. doi: 10.1093/gbe/evx245.
    Speciation Generates Mosaic Genomes in Kangaroos.

    Molecular investigation of genetic assimilation during the rapid adaptive radiations of East African cichlid fishes.
    Mol Ecol. 2017 Dec;26(23):6634-6653. doi: 10.1111/mec.14405. Epub 2017 Nov 23.

    Parasit Vectors. 2017 Sep 6;10(1):410. doi: 10.1186/s13071-017-2349-4.
    Holocentric chromosome evolution in kissing bugs (Hemiptera: Reduviidae: Triatominae): diversification of repeated sequences.

    Curr Opin Genet Dev. 2017 Dec;47:17-23. doi: 10.1016/j.gde.2017.07.014. Epub 2017 Aug 19.
    Beyond speciation genes: an overview of genome stability in evolution and speciation.

    Stud Hist Philos Sci. 2016 Feb;55:47-59. doi: 10.1016/j.shpsa.2015.08.013. Epub 2015 Sep 12.
    Testing hypotheses in macroevolution.
     
  3. GBTG

    GBTG Member

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    @sfs I disagree as physicists have moved to quantum mechanics... bosons, quarks, dark matter, but that is not relevant to the topic of this discussion. Thank you for demonstrating that Macroevolution is not being published, as there is no current understanding of the mechanism. That mechanism is inferred, it is not known, therefore not a fact. This is all I have tried to state from the beginning.

    In regard to the two papers you linked: I cut and pasted the conclusions and highlighted the key portions. This first paper linked second above, focuses specifically on human gene mapping and "microevolution", which is indeed proven! Even within the microevolution camp this paper is week as they discovered the alleles were already present and not expressed. This is not a new mutation (highlighted in red below).

    "Previous inferences about demographic history and the role of local adaptation in shaping human genetic variation made from genomewide genotype data4,36,37 have been limited by the partial and complex ascertainment of SNPs on genotyping arrays. Although data from the 1000 Genomes Project pilots are neither fully comprehensive nor fully free of ascertainment bias (issues include low power for rare variants, noise in allele frequency estimates, some false positives, non-random data collection across samples, platforms and populations, and the use of imputed genotypes), they can be used to address key questions about the extent of differentiation among populations, the presence of highly differentiated variants and the ability to fine-map signals of local adaptation. Although the average level of population differentiation is low (at sites genotyped in all populations the mean value ofWright’s Fst is 0.071 between CEU and YRI, 0.083 between YRI and CHB1JPT, and 0.052 between CHB1JPT and CEU), wefind several hundred thousand SNPs with large allele frequency differences in each population comparison (Fig. 5c). As seen in previous studies4,37, the most highly differentiated sites were enriched for non-synonymous variants, indicative of the action of local adaptation. The completeness of common variant discovery in the low-coverage resource enables new perspectives in the search for local adaptation. First, it provides a more comprehensive catalogue of fixed differences between populations, of which there are very few: two between CEU and CHB1JPT (including the A111T missense variant in SLC24A5 (ref. 38) contributing to light skin colour), four between CEU and YRI (including the 246 GATA box null mutation upstream of DARC39, the Duffy O allele leading to Plasmodium vivax malaria resistance) and 72 between CHB1JPT and YRI (including 24 around the exocyst complex component gene EXOC6B); see Supplementary Table 7 for a complete list. Second, it provides new candidates for selected variants, genes and pathways. For example, we identified 139 non-synonymous variants showing large allele frequency differences (at least 0.8) between populations (Supplementary Table 8), including at least two genes involved in meiotic recombination— FANCA (ninth most extreme non-synonymous SNP in CEU versus CHB1JPT) and TEX15 (thirteenth most extreme non-synonymous SNP inCEU versus YRI, and twenty-sixth most extreme non-synonymous SNP in CHB1JPT versus YRI). Because we are finding almost all common variants in each population, these lists should contain the vast majority of the near fixed differences among these populations. Finally, it improves the fine mapping of selective sweeps (Supplementary Fig. 14) and analysis of the dynamics of location adaptation. For example, we find that the signal of population differentiation around high Fst genic SNPs drops by half within, on average, less than 0.05 cM (typically 30–50 kb; Fig. 5d). Furthermore, 51% of such variants are polymorphic in both populations. These observations indicate that much local adaptation has occurred by selection acting on existing variation rather than new mutation. The effect of recombination on local sequence evolution We estimated a fine-scale genetic map from the phased low-coverage genotypes. Recombination hotspots were narrower than previously estimated4 (mean hotspot width of 2.3 kb compared to 5.5 kb in HapMap II; Fig. 6a), although, unexpectedly, the estimated average peak recombination rate in hotspots is lower in YRI (13 cM Mb21 ) than in CEU and CHB1JPT (20 cM Mb21 ). In addition, crossover activity is less concentrated in the genome in YRI, with 70% of recombination occurring in 10% of the sequence rather than 80% of the recombination for CEU and CHB1JPT (Fig. 6b). A possible biological basis for these differences is that PRDM9, which binds a DNA motif strongly enriched in hotspots and influences the activity of LD-defined hotspots40–43, shows length variation in its DNA-binding zinc fingers within populations, and substantial differentiation between African and non-African populations, with a greater allelic diversity in Africa43. This could mean greater diversity of hotspot locations within Africa and therefore a less concentrated picture in this data set of recombination and lower usage of LD-defined hotspots (which require evidence in at least two populations and therefore will not reflect hotspots present only in Africa). The low-coverage data also allowed us to address a long-standing debate about whether recombination has any local mutagenic effect. Direct examination of diversity around hotspots defined from LD data are potentially biased (because the detection of hotspots requires variation to be present), but we can, without bias, examine rates of SNP variation and recombination around the PRDM9 binding motif associated with hotspots. Figure 6c shows the local recombination rate and pattern of SNP variation around the motif compared to the same plots around a motif that is a single base difference away. Although the motif is associated with a sharp peak in recombination rate, there is no systematic effect on local rates of SNP variation. We infer that, although recombination may influence the fate of new mutations, for example through biased gene conversion, there is no evidence that it influences the rate at which new variants appear."

    Second paper linked first above: For everyone to read is the highlighted red portions of the second papers conclusions. Please explain how any of this bolsters the pro fact/theory camp? The first highlighted red portion state that 10-40% of the amino acids were adaptive (microevolution) between the 2 genomes. Essentially humans and chimpanzees are more different than previously thought, based on genetics. They tried to state this as politically correct as possible in the first sentence "This conclusion does not imply that humans have experienced few phenotypic adaptations, or that adaptations have not shaped genomic patterns of diversity." In other words human and chimp phenotype similarities may be coincidental and that the genetic differences we do see for diversity were bigger than previously thought.

    "This conclusion does not imply that humans have experienced few phenotypic adaptations, or that adaptations have not shaped genomic patterns of diversity. Comparisons of diversity and divergence levels at putatively functional versus neutral sites, for example, suggest that 10–15% (and possibly as many as 40% (29)) of amino acid differences between humans and chimpanzees were adaptive (e.g., (30)) as were 5% of substitutions in conserved non-coding regions (22, 29) and ~20% in UTRs (22). Given the paucity of classic sweeps revealed by our findings, an excess of functional divergence would point to the importance of other modes of adaptation. One way to categorize modes of adaptation is in terms of their effect on the allele frequencies at sites that affect the beneficial phenotype. In this view, classic sweeps bring new alleles to fixation; selection on standing variation or on multiple beneficial alleles brings rare or intermediate frequency alleles to fixation; and other forms of adaptation, such as selection on polygenic traits, increase or decrease allele frequencies to a lesser extent. Such changes in allele frequencies can decrease variation at closely linked sites - to a lesser extent than in a full sweep - and might therefore contribute to a reduction in diversity near functional elements (31), as well as to excess divergence. Alternatives to classic sweeps are likely for parameters applicable to human populations (7, 32); in particular, many phenotypes of interest are quantitative, and plausibly result from selection at many loci of small effect (8).

    An important implication is that in the search for targets of human adaptation, a change in focus is warranted. To date, selection scans have relied almost entirely on the sweep model, either explicitly by considering strict neutrality as the null hypothesis and a classic sweep as the alternative or implicitly, by ranking regions by a statistic thought to be sensitive to classic sweeps and focusing on the tails of the empirical distribution. It appears that few adaptations in humans took the form that these approaches are designed to detect, suggesting that low hanging fruits accessible by existing approaches may be largely depleted. Conversely, the more common modes of adaptation likely remain undetected. Thus, in order to dissect the genetic basis of human adaptations and assess what fraction of the genome was affected by positive selection, we need new tests to detect other modes of selection, such as comparisons between closely related populations that have adapted to drastically different environments (e.g., (33)) or methods that consider loci that contribute to the same phenotype jointly (e.g., (34)). Moreover, if alleles that contribute to recent adaptations are often polymorphic within a population, genome-wide association studies should be highly informative.

    At least we are looking at the right science!

    Regard, GBTG
     
    Last edited: Jan 13, 2018
  4. GBTG

    GBTG Member

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    They are still frogs correct? So still microevolution...

    As these were not provided as links I will look them up and get back to you... the "Testing hypothesis in macroevolution", appears by title alone to support my premise that evolution is devolving from theory to hypothesis...

    As I am not at work I don't have my pub med subscription. This will have to wait until Monday, unless you can provide links to these articles for all of us to read? If so thanks in advance!

    Regards, GBTG
     
    Last edited: Jan 13, 2018
  5. sfs

    sfs Senior Member

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    Your response does nothing to address my point. I repeat: macroevolution has been accepted as a fact among biologists for more than a century. Your challenge to find recent publications presenting evidence for macroevolution was completely wrong headed. Do you understand that or not?

    I'll also repeat my previous question, after you claimed to speak as a scientist: what kind of science do you do?

    You have missed my point with both papers. As I said, both papers used common descent -- that is, they assumed it was true in order to reach conclusions about other matters. If common descent were not already the consensus of the field, no reviewer would have let them get away with that kind of argument.

    If you want me to explain some of the evidence for common descent, I'm willing to do so, but that's not what you asked for.
     
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  6. sfs

    sfs Senior Member

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    Yikes. Microevolution refers to evolution within a single species. "Frogs" represents an entire order, containing 33 species and roughly 5000 species.
     
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  7. GBTG

    GBTG Member

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    Consensus of field also was a popular sentiment prior to Copernicus. Just because its popular does not mean its accurate. Macroevolution has been popularized and accepted based on phenotypic observations. I have stressed this numerous times. The more we study genetics the more baffling, not less so, this becomes.

    I have worked in basic biomedical research for 20+ years and hold an MS. I used to work in a transgenic core facility performing pronuclear injections. I have identified and specifically studied the phenotypical outcomes from genetic modifications for most of those years.

    Regards, GBTG
     
  8. The Barbarian

    The Barbarian Crabby Old White Guy

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    Leopard frogs exist in the US everywhere from the Gulf Coast to the Canadian border. As you go north, the alleles in those frogs governing maturation change to effect faster maturity (because of longer and colder winters in the north). Frogs from adjacent populations can interbreed, though. And this allows gene flow in the population. These changes are microevolution, and there is one species.

    However, if the leopard frogs in the center of the United States were to go extinct, leopard frogs in the far north could not interbreed with those from the Gulf coast. And suddenly, what was microevolution becomes (retroactively) macroevolution. This is why that error to which you referred is so wrong.

    They would just be then two difference species.

    Not by the standard you've given us. Speciation, by your definition is macroevolution.

    If you want to got to Pub Med, you can get the links rather easily. But since macroevolution is directly observed, it's a moot point.
     
  9. The Barbarian

    The Barbarian Crabby Old White Guy

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    No. It doesn't say that there are more differences than previously thought. It says that more of the relatively few differences may be adaptive. Which would please classical Dawinians, but offers little comfort to creationists.

    No. It says that more of the differences may be adaptive than previously thought. Exactly the opposite of what you say it says.

    Doesn't say that, either:
    "This conclusion does not imply that humans have experienced few phenotypic adaptations, or that adaptations have not shaped genomic patterns of diversity. Comparisons of diversity and divergence levels at putatively functional versus neutral sites, for example, suggest that 10–15% (and possibly as many as 40% (29)) of amino acid differences between humans and chimpanzees were adaptive (e.g., (30)) as were 5% of substitutions in conserved non-coding regions (22, 29) and ~20% in UTRs
     
    Last edited: Jan 13, 2018
  10. sfs

    sfs Senior Member

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    Of course it doesn't. But it does mean that your challenge to show recent papers presenting evidence for macroevolution was pointless -- and that's the issue I've actually been addressing.
    Macroevolution was initially accepted -- by the relevant scientists -- based on phenotypic observation, yes. It has been overwhelmingly supported by genetic evidence as well. Do you want to look at some of the evidence or not?
     
  11. The Barbarian

    The Barbarian Crabby Old White Guy

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    And notice that the phylogenies of evolutionary theory were first published by Linnaeus, a man who didn't even know about evolution.

    He had no real explanation why it looked like a family tree.
     
  12. Open Heart

    Open Heart Well-Known Member

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    This was worded so perfectly, that I need not respond to the OP! :)
     
  13. KomatiiteBIF

    KomatiiteBIF Well-Known Member

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    Thats 33 families, but good to point out...

    This is a good one because, when you start talking about things like arthropods, the number of species and families and genuses just blows out the roof. Some anti evolution people talk about "kinds" of animals, and then you point out the ridiculous number of species and genuses and families of arthropods and its just like...alright, so how did this whole ark thing happen again?
     
  14. sfs

    sfs Senior Member

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    Urf, yes. Sometimes the brain skips ahead of the fingers.
     
  15. ViaCrucis

    ViaCrucis Evangelical Catholic of the Augsburg Confession

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    And humans and chimps are still apes. And apes and monkeys are still primates. Primates and rodents are still mammals. Mammals and reptiles are still amniotes. Amniotes and amphibians are still tetrapods. Tetrapods and ray-finned fish are still vertibrates. Vertibrates and arthropods are still animals. Animals and plants are still eukaryotes.

    -CryptoLutheran
     
  16. The Barbarian

    The Barbarian Crabby Old White Guy

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    The "they are still (whatever taxon the two species share) dodge is easily countered. The important thing is to bring them back to the original subject. In this case, the attempt was to deny speciation, and when that failed, to reset the goal posts.
     
  17. dcalling

    dcalling Senior Member

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    It will be great if you could elaborate.

    Let's pick one for example.
    Do we have a lab test that shows how the fused Chromosome were done in natural conditions? How did the human one lose part of it (or fuse together as it is called)? Is it archival under natural conditions? Tests?

    Now look at my predication:
    We saw N chromosome for some primate and n-1 for humans, the sequence looks similar. God most likely fused one of those to make humans. Now predication is met.

    My other predication:
    Such situation can't happen naturally, and this fusing needs precision engineering work.
     
  18. dcalling

    dcalling Senior Member

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    I view common descent of life more like a code library, that God wrote sequence A, and used A to contruct B,C etc. Just like how our mordern code uses many many pre-existing libraries. DNA is just like code.

    So to the same point, code can't evolve randomly. Any mistype will make the program either malfunction or crash, so look at birth defects, they don't evolve, they crash. With the exception of per-defined parameters, you can change color, change size, amount of things etc.
     
  19. The Barbarian

    The Barbarian Crabby Old White Guy

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    I'll do that in a second post.

    We actually have a large number of known fusions from nature. Domesticated horses, for example, have one fusion, being otherwise closely related to Prezwalski's horse.

    There are also a lot of lab observations:
    Survival of Chromosomal Changes

    The whole-genome duplication (WGD) that occurred during yeast evolution changed the basal number of chromosomes from 8 to 16. However, the number of chromosomes in post-WGD species now ranges between 10 and 16, and the number in non-WGD species (Zygosaccharomyces, Kluyveromyces, Lachancea, and Ashbya) ranges between 6 and 8. To study the mechanism by which chromosome number changes, we traced the ancestry of centromeres and telomeres in each species. We observe only two mechanisms by which the number of chromosomes has decreased, as indicated by the loss of a centromere. The most frequent mechanism, seen 8 times, is telomere-to-telomere fusion between two chromosomes with the concomitant death of one centromere. The other mechanism, seen once, involves the breakage of a chromosome at its centromere, followed by the fusion of the two arms to the telomeres of two other chromosomes. The only mechanism by which chromosome number has increased in these species is WGD. Translocations and inversions have cycled telomere locations, internalizing some previously telomeric genes and creating novel telomeric locations. Comparison of centromere structures shows that the length of the CDEII region is variable between species but uniform within species. We trace the complete rearrangement history of the Lachancea kluyveri genome since its common ancestor with Saccharomyces and propose that its exceptionally low level of rearrangement is a consequence of the loss of the non-homologous end joining (NHEJ) DNA repair pathway in this species.
    Mechanisms of Chromosome Number Evolution in Yeast

    The fusion was first hypothesized, when it became clear that humans had one less chromosome pair than other apes. Then it was noted that one human chromosome looked very, very much like two ape chromosomes.

    All members of Hominidae except humans, Neanderthals, and Denisovans have 24 pairs of chromosomes.[7] Humans have only 23 pairs of chromosomes. Human chromosome 2 is a result of an end-to-end fusion of two ancestral chromosomes.[8][9]


    The evidence for this includes:


    • The correspondence of chromosome 2 to two ape chromosomes. The closest human relative, the chimpanzee, has near-identical DNA sequences to human chromosome 2, but they are found in two separate chromosomes. The same is true of the more distant gorilla and orangutan.[10][11]
    • The presence of a vestigial centromere. Normally a chromosome has just one centromere, but in chromosome 2 there are remnants of a second centromere in the q21.3–q22.1 region.[12]
    • The presence of vestigial telomeres. These are normally found only at the ends of a chromosome, but in chromosome 2 there are additional telomere sequences in the q13 band, far from either end of the chromosome.[13]
    According to researcher J. W. IJdo, "We conclude that the locus cloned in cosmids c8.1 and c29B is the relic of an ancient telomere-telomere fusion and marks the point at which two ancestral ape chromosomes fused to give rise to human chromosome 2." [13]
    Chromosome 2 (human) - Wikipedia

    If you can call in a non-scriptural miracle to cover every problem with your belief, than any belief is equally likely to be true.

    Since we observe numerous chromosome fusions in nature, that cannot be true.
     
  20. The Barbarian

    The Barbarian Crabby Old White Guy

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    We observe that it does. Most mutations don't do much of anything. A few are harmful. A very few are useful. Natural selection sorts it out.

    No. You have a few dozen "mistakes" in your DNA that were not in either of your parents.

    On the other hand, favorable mutations tend to persist. That's how evolution works. There are numerous useful human mutations. Would you like to learn about some of them?
     
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