Why Darwinism is wrong

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?

Jianyi, I’d go back and read your website again if I were you:

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Every species has two Eves

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Prediction

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According to the GMCMI model, every species have two Eves. The first one is the single ancestral mother, who gave birth to a new species, the second Eve or ‘Eves is a group of females with very similar genetically structure, who are the first generation or seed of new species. In terms of human, most likely, its ancestor or first Eve was one member of ape-like animals; the second Eves was a group of mothers with identical human genetic structure and phenotype

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This shows a misunderstanding of the ‘mitochondrial eve’ concept. ‘Eve’ is the most recent individual to whom all living members of a species can trace their mitochondrial inheritance back to. This means:

To use the tag-line from Highlander — There can be only one! The keys words being most recent.If you could pinpoint a mitochondrial eve in your model she would either be ‘supermum’ or one of her descendents. Your prediction is therefore not a prediction: it could never happen

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Mitochondrial ‘Eve’ doesn’t have to be alone. There is nothing to suggest that any ‘Eve’ is the only female in her species. If you are saying that mitochondrial Eve’s are indicative of your ‘super-twinning’ events then following the male line of a species (ie Y chromosomal Adam) must lead back to the same point in time. As WK clarified quite nicely — in humans they spectacularly don’t! 80, 000 years is quite an age gap. Mitochondrial Eves therefore mean diddly squat in relation to your theory.

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As you have made a big deal about "RM+NS" not being falsifiable in your original post, and claim in your website that your model has been tested, I hope you won’t mind me asking a couple of questions about the other things you mention on it.

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Similarity of the initial genetic structure

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Prediction:

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By natural selection, at the beginning of any new species, diversity of genetic structures within the species existed, whereas in the GMCMI model, all species had similar genetic structure at the beginning.

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How exactly would you really test this? There certainly have been genetic bottlenecks — but how can you tie them specifically to your ‘super-twin’ speciation events?

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Prediction:

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In the GMCMI model, the ability to generate prolific novelties in any species is directly related to the number of fraternal births. The size of animals throughout evolution has increased, while the number of siblings in the same birth decreased. Many species only have a singleton birth, such as humans, elephants, and tigers; multiple siblings from the same births are only the exception

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In order for your idea to work, the ancestor of modern elephants, or of homo sapiens would have to be a twin factory. How can you possibly confirm/falsify this?

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According the GMCMI model, speciation is the outcome of gross mutations by a random process. There are no specific patterns regarding how, why, where the mutations occur, any genes could be involved in the gross mutation. Irregularity of involvement of genes would make the inconsistency of results in molecular phylogeny a rule, not an exception.

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This is another example of a misunderstanding on your part. Your model requires common ancestry just as much as the current ToE does.

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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?

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.

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Then I really fail to see why you have to invent ‘super-twinning’ at all. It has already been mentioned that you can view all changes in genetic content to be mutations. As HGT, duplication, deletion, insertion, single base change etc are all random in nature, and you’re not saying that N.S. doesn’t occur then there is no difference between your ideas and what is generally accepted anyway for asexual species.

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For sexual species: Do you have any evidence that only ‘gross’ mutation (something that you haven’t yet defined satisfactorily) leads to a new species, or is it just a feeling you have? If a beneficial mutation occurs in you super-twins what is the mechanism for stopping them mating with members of supermum’s species? Remember it has to cover all types of mutation, not just changes in chromosome number.

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This message has been edited by Ooook!, 29-04-2005 05:58 PM

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This message has been edited by Ooook!, 29-04-2005 06:05 PM

Hello again,Sorry about the delay in replying. I didn’t realise you had responded to my points because you added your reply by edit — I had already read the unedited post and was waiting for a second one. In future, if you are going to substantially change the content of your message then can you compose it in a separate post. I can then respond quicker .There are a couple of things I still don’t quite understand (apologies if this is a bit of a hatchet job, I'm feeling kind of tired). For example: I really don't know what you're trying to say here. Can you explain exactly who you think a mitochondrial ‘Eve’ is, in your own words and how you can trace the human mitochondrial line past this point without looking at chimpanzee mitochondria.and Likewise here. Are you suggesting that there is 80,000 years worth of error between the way 'Adam' and Eve' dates were estimated? Or are you agreeing with me that there is no way of distinguishing between a possible 'Super-twinning' event and one entirely due to neutral drift and natural selection? If you can't tell the difference then why present it as supporting evidence for your model? Well you did present a set of 'Predictions' made from your model followed by supporting evidence - this implies that you think it is being tested by the evidence to some degree. However, I think that you have made the wrong predictions in the first place or have used the wrong evidence as confirmation. For example: Well, if common ancestry is required then you would expect consistant molecular phylogenies, not (as you suggest) inconsistant ones. Luckily for you, they are consistant with common ancestry, unluckily this supports the current ToE as well. Among other things, there is a real practical problem with these tests. How do you suggest we go about finding these 'supertwins' in the first place before you sequence them? How do you determine whether past bottlenecks are supertwinning events? So in this case there is no difference between your ideas and those accepted as part of the current ToE! Why don't you state this plainly instead of trying to drag discussion of asexual organsims (evolution of mitochondria, antibiotic resistance) into the mix? Yep, sorry! I am guilty of not applying joined-up-thinking to my posts. I'll try and be more clear.Earlier, you admitted that both single point mutations and large scale mutation like HGT or duplication could be classed as 'gross' mutations. As you describe a gross mutation as one capable of causing speciation, what possible mechanisms are there for stopping twins with a such a small mutation from mating with their mother?I hope this makes sense.