Why Darwinism is wrong

Hi Jianyi,For some reason you didn't reply to my post, but that of Wounded King raised similar issues, so I hope it is okay for me to jump in here.You say that chromosomal mutations are .But this also applies to any mutation (including point mutations). Point mutations are also "instantaneous processes at individual level, which occur without NS, and subject to NS effect after they are generated". Who ever said that point mutations occur "because" of NS? You are imputing a teleology to population genetics which is a misrepresentation of the theory. If point mutations are teleological, then so are chromosomal mutations. But if chromosomal mutations are not teleological, then neither are point mutations. You need to get your story straight, one way or the other. The importance of chromosomal mutations is exaggerated here. There are plenty of closely related species that have identical chromosome numbers and formations, for example. I suspect that your invisible karyotypic mutations are just point mutations. If you can't identify them by karyotypic study, then how do you know they are what you say they are? The important point is that mutations such as inversions or repeats are generated by the same mechanism as any other mutation. An error in DNA replication may result in micro-level substitutions, or it may result in mid-level gene duplications, or it may result in whole genome duplications. The origin of genetic diversity in the genome doesn't make any difference to whether NS can result in speciation, as you have already pointed out NS only operates AFTER the mutation has occurred. You are making the same mistake again. We already agree that NS only operates after the mutation arises. polyploidy IS a random mutation, unless you are claiming that genome duplication in plants occurs by a non-random process (which you haven't explained and haven't provided any evidence for). natural selection doesn't predict or explain why polyploidization occurs. It may have something to say about the origin of proofreading systems that correct such errors after they have occurred. But the duplication of a genome during a malfunctioned cell division happens randomly, and then NS acts on the result. I've read some Mayr, and I think he says pretty much what I've said above. Can you elaborate? The national geographic article you cite give some possible explanations (i.e. long-term storage of sperm, or hermaphroditism). I couldn't find any mention of this shark in the scientific literature, and note that the zookeepers have yet to carry out any genetic analysis to try to identify what happened. it's already known that hermaphroditic sharks, such as the black dogfish, exist in the wild (i.e. http://web.ukonline.co.uk/aquarium/pages/lsd.html). What's your point? What are we meant to infer re. the importance of natural selection to speciation? speciation is usually considered to take longer than a single generation to occur, and I'm sure you know this. This is why reproductive isolation is necessary. But you are right, new species have arisen in oviparous clades (i.e. virtually every species of insect). here's a prediction for you: If physical barriers to gene flow are important in speciation, then we should find that "species richness" increases when the environment is variable and "patchy", compared to when it is uniform. We should also find that species richness declines for taxonomic groups that are able to travel large distances, because ability to travel will result in gene flow between divergent populations. The fact that I've made this prediction disproves your assertion.This message has been edited by mick, 04-27-2005 01:19 PMadded in edit:Your assertion the karyotype changes are necessary for speciation is wrong. I forgot about a useful review article that i should have mentioned. In Nature Reviews Genetics, Wu and Ting (2004, vol 5, p. 114-122) describe a number of "speciation genes" and give an overview of the theory. See Nature - Not FoundClark et al. (Science, 2003, Vol. 302, Issue 5652) describe the variety of genes that have undergone natural selection since divergence of chimps and humans. Some of these may be "speciation genes" (though I admit it's an ugly concept). Note that this natural selection is acting irrespective of karyotype differences.This message has been edited by mick, 04-27-2005 01:39 PM

Originlly posted by Percy EvC Forum Director You get frustrated, as you do not know evolution and mechanism of evolution two totally different things.

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Jianyi Zhang

You get frustrated, as you do not know evolution and evolution mechanism totally different issues.

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Jianyi Zhang

Not only would a truly altruisitic species falsify the theory, as Darwin and another posted noted, but so would a common creationist epithet for evolution.Have you ever heard of evolution through RMNS described as "Dogs giving birth to cats evolution"? I have, from one of my best friends. And I didn't say it at the time but I will next time she says it: such an event (in a repeatable or authortatively documented example) would completely falsify the entire New Synthesis of evolution, the dominant paradigm since the 1920's and 1930's. Animals are not supposed to change families in one go like that, according to the theory.Note that there is no necessary reason that either an Intelligent Designer or a literal Book of Genesis universe would need to obey such laws- in both cases it would be because the Designer/God made it so- so such an event would not falsify either theory. The search for a hypothetical fact that would falsify either of those theories continues.Chris

Originally posted by Mick: The key is changes of allele frequency a gradual process, also at population level; it occurs by NS, however, duplications, deletions, inversions, amplifications and insertion are instantaneous processes at individual level, which occur without NS, and subject to NS effect after they are generated. Yes, the existence of HGT challenges neither the existence of mutations nor the existence of natural selection; but it challenges Darwinian idea of RMNS. HGT is an instantaneous process, gene(s) were inserted into bacterial by viral vectors without any NS. The resulted bacteria is subjected to NS. HGT usually provides bacteria with antibiotics resistand property. Regardless of existence of antibiotics, bacteria obtain foreign gene resistent to various antibiotics. Antiobiotics kills other bacteria without the genes, the resistant bacteria proliferate. Even without NS, the resistant bacteria is likely there; however, there is no way to find out them. Can you think whole genome duplication by a gradual process? You should review some basic biology books, or Mayr (top Darwinist) books to find out what you says about polyploids. Of course, they did not come from dirt. I agree HIV derived from SIV. However, the very first HIV probably generated by combining several viruses including SIV.Visna sequencesI copy a part of it from the website:
Let's look at two hypotheses: a) the HIV virus was made by combining bovine leukemia virus (BLV) with sheep visna (VLV) virus
b) HIV, the green monkey virus (SIV), BLV, and VLV all evolved from a common ancestor. HIV and SIV evolved from a close ancestor; BLV and VLV are more distantly related.
The combination is an instantaneous process, can you think a virus gradually combined with other virus. It combined or not combined, there is no 1%, 2%, 5% combination. Even multiple endosymbiotic events, each of them are instantaneous events, not gradual ones. Plasmids containing mitochondria could infect bacteria and stayed inside, which was an instantaneous event.Please read Dr. Lynn Margulis book "Acquiring Genomes", who is the person to propose incorporation of mito. by symbosis and also against Darwin's theory of evolution. You will find out what she said.Population genetists do not explain speciation, even they think and claim so.

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Jianyi Zhang

Jianyi,Your post seems to rest on the idea that mutations are "caused" by natural selection. As an alternative to this view, you say Can we get it straight that mutations are not caused by natural selection? the "R" in RMNS stands for Random. That is, they are not "caused".Now I will give you the benefit of the doubt and assume that you mean the spread of a random mutation is due to NS, but not its initial occurrence. How does this differ from the spread of a karyotype change in a population? Like a point mutation, the karyotype change occurs in a single individual. What mechanism do you have other than NS (by which I include all aspects of the modern synthesis including drift) to explain the spread of the karyotype change within a population?mickThis message has been edited by mick, 04-27-2005 05:00 PM

Jianyi Zhang, How is this sequence of events significantly different to a scenario in which a point mutation to a particular gene confers antibiotic resistance, and then gets selected for within a population of bacteria? I don't see the difference. After all, how did the gene on your resistance plasmid evolve? Did it spring into the world all on it's own accord, or did it evolve by random mutation and selection in another bacteria? Before I ask you to go into why endosymbiotic events are a violation of the principle of random mutation and natural selection, can you clarify this statement? It might be a case of you not putting it in quite the best way, but as it stands it doesn't bare much resemblence to how I understand the evolution of mitochondria is meant to have happened.Also, on a slightly connected vein:On your website, you claim that one of the bourne out predictions of your model is that there will be two mitochondrial eves. I didn't quite understand this. Are you saying that speciation events always correlate with bottlenecks? If so, how can you reconcile the fact that mitochondrial eve never met (let alone mated with) Y chromosomal Adam?

Originally posted by Mick: Please read my post carefully: I said "changes of allele frequency a gradual process, also at population level; it occurs by NS, however, duplications, deletions, inversions, amplifications and insertion are instantaneous processes at individual level" Nobody said 'point mutations occur "because" of NS, except you. No, I did not mean only point mutations invisible karyotypic mutations. To be seen under microscope, ones need 1-2 million base pair changes, so it is possible that many smaller changes in chromosomes there, ranging thousands to upto 1 millions invisible.
There are huge differences if mutation occur at small scale or large-scale. Small mutations probably do not lead to speciation, their carriers consist of polymorphism in population. However, carriers with large-scale mutations would be seeds of new species, as their gemate might not pair with gemates from parental species. If carriers could have mate with ones with similar genetic structure and reproduce, they could become a new species. So new species is created by gross-mutation at the initial phase, which would be subject to NS after they were born. Polyploid is a random mutation, by it a new species is created. There is no NS involved. So speciation occur by gross mutation itself, not by Darwinian RM & NS (the random mutation usually means small mutation at allele level).
Look E. Mays book (This is biology) page 184. Polyploid is an exception to Darwinian mechanism. If you keep thinking polyploid plants generated by RM&NS, you really need reading more. If the shark can reproduce herself by virgin birth and it is a new species of shark, this species is created instantaneously, not by RM&NS or geographical isolation.
If you think it is, please elaborate. No, I do not agree. By my model, all speciation occurs in a single generation, it takes many generations for them to proliferate and for us to find out. Reproductive isolations could be generated at the speciation. Even if physical barriers to gene flow are NOT important in speciation, we also should find that "species richness" increases when the environment is variable and "patchy", compared to when it is uniform.
Because different individuals are adaptative to more variable condition by NS than it is uniform.
You did not show me a falsification of any Darwiniam mechanism, only show me a case of falsification of adaptation by NS, plus your confusion. I did not claim karyotype changes a must for speciation, I just say almost all species has distinct karyotic patterns, ones without could also have gross changes in chromosomes as they are invisible under microscope. With this in mind, all speciation might be involved with gross-mutations, plus few exceptions.This message has been edited by Jianyi Zhang, 04-28-2005 12:23 AM

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Jianyi Zhang

Originally posted by mick: Agree. Carriers with karyotypic changes might be new species, while carriers with different allele are probably members within same species.
Spread of changes at both levels are subject to NS, however, generation of both changes has nothing to do with NS. So, new species arrive not by RM+NS, just by random gross mutation itself.

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Jianyi Zhang

Originally posted by ooook: There is no differencs. Both point mutation or HGT occur randomly, which could provide drug-resistant regardless existence of antibiotics. Application of a particular antibiotics only kill others sensitive ones, let drug-resistant ones proliferate."Plasmids containing mitochondria could infect bacteria and stayed inside" The principle RM&NS means biodiversity only occur with BOTH RM and NS, my point is that biodiversity occur only by random gross changes in genetic materials. If you assume bacteria with mitochondria is biodiversity from its parental one without it, a plasmid infected a bacteria which stayed inside and become mitochondria, this is an event, not a process. It occurs instantanously. NS only works after they are generated. I do not think I say two mitochondrial Eves there. I say initial seeds of sexual animals might have two or more idential mothers, just like identical supertwins (step 3 in the model). Sexual animals all have bottleneck at the initial stage. The model provides reasonal explanation; as both Adam and Eve were born as fraternal twins or supertwins, it is very easy for them to mate. If only Eves were born, she did not have proper mate, she would die out, and we never know. What we see in the world are only winners even with very small lucky odds.This message has been edited by Jianyi Zhang, 04-28-2005 12:18 AM

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Jianyi Zhang

No it doesn't, it means that RM&NS can give rise to biodiversity, not that they are the only concievable mechanisms, although depending on how broadly you define random mutation a case could be made for that. In fact if you define biodiversity strictly in terms of genetic variation, at whatever level, then natural selection is entirely unneccesary. Natural selection becomes neccessary however if one wishes to come up with something that actually bears some relation to the biodiversity we see around us. As has already been suggested this is completely wrong. Plasmids have nothing to do with the endosymbiotic origin of mitochondria, except perhaps as intermediaries for gene transfer between the mitochondrial and nuclear genome.The protomitochondria, according to the traditional endosymbiotic hypothesis, would itself be a prokaryotic bacteria not a plasmid. This bacteria would exist as an intracellular endosymbiont providing the host cell with energy. Over time the internal endosymbiont would lose genetic information for a number of now redundant systems, such as perhaps locomotory or sensory systems. Eventually the mitochondrial genome may be no more than the barest minimum neccessary for the structure of the mitochondrion itself and its esential metabolic enzymes. Indeed many mitochondrial genes are thought to have been transferred to the nuclear genome over time, so even that bare minimum may be reduced even further.Using early bacteria in a discussion of speciation is totally pointless. The gaining of an endosymbiont would not preclude the exchange of genetic information with other bacteria, indeed it is a hard job trying to stop bacteria exchanging information. Well at least we all agree on that, but no one ever suggested otherwise. Any shred of evidence for that? That isn't an explanation, Oook was pointing out that the genetic evidence places the existences of mitochondrial Eve and y chromosome Adam about 80,000 years apart, unlikely for fraternal twins.TTFN,WK

Hi,Okay, I think I understand you now. Sorry if my earlier posts were slightly off-target.There are some areas we agree on. Polyploidy in plants plays an important role in speciation. Chromosomal changes, in general, may play an important role in speciation.What we disagree on is how a karyotypic mutation, once it occurs, spreads within a population.You seem to be saying that the existence of a chromosomal change (often?) results in instantaneous speciation. As I understand it, this can only hold for asexually-reproducing organisms. This is probably why you keep bringing up plants. Its notable that polyploidy in plants is far more common in species with some form of vegatative propogation, because this permits the polyploidization to be spread within a large asexual lineage.This is not the case for the vast majority of sexually-reproducing species. Perhaps this is why polyploidization is so rare in higher animals. I can think of a couple of polyploidizations in the fish, one in mammalia, a couple in reptiles, but not much more. Certainly nothing like the number of polyploidizations we can find in plants.In a sexual species, once an individual has a chromosomal mutation resulting in reproductive isolation, it is finished, an evolutionary dead end. I imagine that this is why you brought up the virgin birth of the shark. You need mechanisms like hermaphroditism, asexuality and virgin births to explain how the mutated individual does not simply go extinct.Unfortunately for you, hermaphroditism and virgin births are the exception rather than the rule in sexually reproducing species. (I might go so far as to say that the hermaphroditic black dogfish is a red herring )For strictly sexual species, your model requires a multiplication of very small probabilities. First, a chromosomal change has to happen in a single individual. Then, an identical chromosomal change has to happen in a different individual of the opposite sex. Next, the two individuals have to meet each other and mate successfully with each other. All of these events are vansihingly unlikely, and the multiplication of their likelihoods has to be pretty small.I would think a model permitting the accumulation of small chromosomal mutations with slightly negative fitness increment, in the presence of geographic isolation, would be a much more plausible hypothesis. Imagine that a small chromosomal mutation takes place. It has a slight fitness cost, or no fitness cost at all, and the individual can still reproduce. The chromosomal mutation spreads through the population by genetic drift. Many generations later, further, similarly small, mutations occur. These also spread (or not) by drift. Although none of these small changes results in reproductive isolation in and of itself, the long term accumulation of such small changes results in reproductive isolation between geographically separated populations, who have different histories of karyotype mutations that are not compatible with each other.Unlike your model, the model I've described doesn't require the multiplication of vanishingly small probabilities, and doesn't require lots of unlikely events to occur in a single generation. All it requires is time and population genetic structure.So I agree with you that chromosomal changes can result in speciation. But I don't agree that this happens instantaneously because of mutations resulting in complete reproductive isolation, in a single generation. And I don't agree that it is a likely general explanation for speciation in higher animals.mickThis message has been edited by mick, 04-28-2005 01:01 PM

Originally posted by mick: No, an identical chromosomal changes has to occur in twin zygotes in the same mother, not separate individuals, this is a huge different.
Twin zygotes are closed associated, and their deveopmental phase is very similar. As the supertwins or twins live together, it is very easy for them meet and mat. I copy a part of my website here:
In biology, almost everything plays by chance, not by certainty, so is the model.
By the model, speciation is an event, not a process; the number of the zygotes with gross mutation might be astronomical; whereas under NS only a few speciation might occur in millions years. Following is a hypothetical case:
There was a multiple-births animal long, long time ago that survived for one million years (10E6) in the world, during which there were one millions births yearly on average. So the number of the total births was 1 trillion (10E6 x 10E6).
In one trillion births, there were 1% or 10E2 gross mutations in zygotes, 1 out 1 million or 10E6 was identical mutation on twins zygotes, 1% or 10E2 survived and populated.
The number of species formed would be one hundred (10E12 x 10E-2 x 10E-6 x 10E-2 =10E2). Even in each step the probability is very small , it is still very easy for one multiple-births species have 100 speciation after considering all of probability factors.
All of species seen had or have passed the test, and are in the numerator; there are millions time more in the denominator that failed the test, you would never know them.
So what is wrong with the model? The model you present is very like Robertsonian translocation,there are similar models by Schwartz and Todd-Kolnicki (supported by Lynn Margulis), these models have similar scenario which advocates macromutation have to be present in either gametogenesis or zygotes, the products by these all macromutations are 'hopeful monster', so the following question is how the monster get mate to reproduce.
Usually, there are several steps to overcome the dilemma. I use a case that an organism with 48 chromosomes became one with 46 chromosomes. There was a small group of organism with 48 (24/24) chromosomes in geographical isolation, two chromosomal fusions in gametogenesis, resulting in gametes with 23 chromosomes. The gamete combines with ancestral gamete (24 chromosomes) with production of zygotes 47 chromosomes (23/24), and a baby born with corresponding organism (23/24).
The organism would survive and give birth the corresponding organism
(23/24), when it mated with ancestral organism (24/24), the resulted
organism (23/24) survived and was fixed with a certain percentage in
the small population by drifting or heterozygous advantages.
After organism (23/24) accumulated to a fixed percentage, they had
chance to mate among themselves, with production of a new organism
(23/23). This is how we, human beings (23/23) evolved from our ancestor
(24/24).
Beside some biological issue, for the unbalanced organism overcome reproductive barriers, ones need a bunch of assumptions. I list a few major ones in following:
By Geographical isolation (assumption 1), Robertsonian
translocation/fusion occurs in gametogenesis, the resulted organism
(23/24) was generated by mating ancestral with translocated gametes.
The organism survives well (assumption 2). The organism will pass its
genetic structure by mating between unbalanced organisms with balanced ancestors (assumption 3). The above process repeats until the unbalance organism accumulated to a certain level or percentage. The two unbalance organism mated to have the first balance organism (23/23) (assumption 4). The two-unbalanced organism mated to have the second balance organism (23/23). The two-balanced organism was close, and very lucky to find out each other to mate and have the second generation of balanced organism (assumption 5).
It is difficult to say why the Robertsonian or similar model never play any role in speciation; however they are all involved with multiple assumptions. In the twins model, only assumption is made, which is much more parsimonious than others.
We know allele frequencies and morphologies are modified by natural
selection, or geographical isolation, or sexual isolation. However,
nobody has followed any species to their splitting by imaginative
mechanisms.
But instantaneous biodiversity in plants, some animals, virus, and
bacteria are confirmed with little controversies. If these organisms
evolve by instantaneous mode, why cannot others organisms have the same process, even we cannot see them evolved? If the instantaneous mode alone can explain all biodiversity so far, why do ones still need gradual modes? This is against rule of Ocazam razor.
In fact, ones think over, the twins model is very simple with logical
necessity. There are three simple points: 1) every individual of sexual animals starts at zygotes, which have to contain all genetic
information needed for developments. 2) Mutation is a random process,
every mutation is unique, it is unthinkable for a group of zygote at
different body of animals to have similar mutation at the same time and location. Without the group of 'hopeful monsters' available for mating, individual will die out without reproduction. If ones agree the macromutation present in zygotes, they have to admit it not related with natural selection, or geographical isolation, both of them only work after mutants are born. 3) The twins model is the most
parsimonious model with one assumption.Another indirect support of the model is inverse relationship between
number of species and number of siblings in the same birth. Usually,
small animals have more species, large ones has less or none. Small
animals have more siblings in the same birth. Even within mammals, mice have four siblings in the same birth; there are reports for new
speciation of mice. However, there are a few dozens billion human being in last 200,000 years, there are no signs for them, or part of them become a new species.
Can any other models provide any reasonable explanation to it?

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Jianyi Zhang

Jianyi,Thanks for responding.In a previous post, I said that Rather than denying my challenge, you have now added "twinning" to the mix.Up to yet, your theory of instantaneous chromosomal speciation explains speciation in:1. plants (but only if they reproduce asexually, for example by vegetative propogation)2. sharks (but only in they are hermaphroditic or can have virgin births, or reproduce by vegetative propogation)3. mammals (but only when they give birth to twins, are hermaphroditic, have virgin births or reproduce by vegetative propogation)Why don't you give another ad hoc explanation for speciation in birds and reptiles (which don't twin and aren't hermaphroditic). Let's keep adding to the list!And all this from somebody who criticises evolutionary theory for not being parsimnious enough!

Basic population genetics tells us that population size and generation time account for such differences. Why don't you read "Why big fierce animals are rare" by Colinvaux, and read a good pop.gen textbook at the same time?