Register | Sign In


Understanding through Discussion


EvC Forum active members: 65 (9162 total)
3 online now:
Newest Member: popoi
Post Volume: Total: 915,821 Year: 3,078/9,624 Month: 923/1,588 Week: 106/223 Day: 4/13 Hour: 0/2


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   Why Darwinism is wrong
Jianyi Zhang
Inactive Member


Message 1 of 305 (202587)
04-26-2005 11:57 AM


Why Darwins theory of speciation or biodiversity by random mutation and natural selection (RMNS) is wrong?
1. Different species has different chromosomal karyotypes
Different species in sexual animals almost all have karyotic changes, which means chromosomal differences detected under microscope. They are deletion, amplification, duplication, insertion, and inversion, even chromosomal number changes. Neo-Darwinism is based on change of allele frequencies, which cannot provide explanation how allele change lead to addition, deletion of pieces of chromosome, or change of chromosomal numbers.
2. Against all scientific evidences so far available
For example, lateral transfer in bacteria, polyploids in plants, generation of asexuals from sexual animals (virgin births), generation of SARS or HIV and many virus, incorporation of mitochondria by symbiosis, etc. they all fall into instantaneous biodiversity, not gradual one by RMNS mechanism.
Can anybody give me an example of speciation by RMNS? (do not just tell difference allele frequencies in different groups of same species).
3. Lack of explanatory power
Beside lack of transitional fossils, there are more examples, such as chicken-egg paradox, atavisms, innovative organ, bottleneck effect, mosaic evolution, Cambrian explosion, rate of evolutionary change, few speciation in big mammals, RMNS mechanism poorly explains these phenomena.
4. Un-falsification
Because RMNS model has no predictory power, there is no way falsifying it, and you cannot prove it wrong by scientific methods. In other words, it stands in any outcomes. By Popperian criteria, Neo-Darwinism is a pseudo-science.
5. Too complicated
According Neo-Darwinists, there are several mechanisms of speciation (biodiversity): genetic drifting, natural selection, geographical isolation, sexual selection and instantaneous speciation. Among geographical isolation, there is vicariant speciation, peripatric speciation, also parapatric speciation. Each mechanism has own myths and assumptions. Worse than that, nobody can tell which organisms come into beings by which mechanism; they are just intensive exercise of your imagination.
This message has been edited by Jianyi Zhang, 04-26-2005 12:17 PM
This message has been edited by Jianyi Zhang, 04-26-2005 12:18 PM

Replies to this message:
 Message 3 by JonF, posted 04-26-2005 3:16 PM Jianyi Zhang has not replied
 Message 5 by coffee_addict, posted 04-26-2005 3:50 PM Jianyi Zhang has not replied
 Message 8 by arachnophilia, posted 04-26-2005 5:25 PM Jianyi Zhang has not replied
 Message 10 by mick, posted 04-26-2005 8:37 PM Jianyi Zhang has replied
 Message 12 by Wounded King, posted 04-27-2005 6:51 AM Jianyi Zhang has replied
 Message 19 by cmanteuf, posted 04-27-2005 3:24 PM Jianyi Zhang has not replied
 Message 79 by Brad McFall, posted 05-04-2005 2:58 PM Jianyi Zhang has replied
 Message 216 by Ben!, posted 05-13-2005 2:31 AM Jianyi Zhang has replied
 Message 221 by wnope, posted 05-17-2005 10:46 PM Jianyi Zhang has not replied

Jianyi Zhang
Inactive Member


Message 6 of 305 (202745)
04-26-2005 5:09 PM
Reply to: Message 4 by Brad McFall
04-26-2005 3:47 PM


read my website
If you read my website, http://chickensfirst.net and you will get better ideas.
Darwin's RMNS is wrong from many scientific perspectives. The correct answer of mechanism for speciation in any sexaul organism is twins mutation and inbreeding.

Jianyi Zhang

This message is a reply to:
 Message 4 by Brad McFall, posted 04-26-2005 3:47 PM Brad McFall has replied

Replies to this message:
 Message 7 by arachnophilia, posted 04-26-2005 5:14 PM Jianyi Zhang has not replied
 Message 9 by Brad McFall, posted 04-26-2005 6:03 PM Jianyi Zhang has replied

Jianyi Zhang
Inactive Member


Message 11 of 305 (202893)
04-27-2005 1:18 AM
Reply to: Message 9 by Brad McFall
04-26-2005 6:03 PM


Re: read my website
Could/would you please Sir indicate how this vision is any shorter, different, or better than
I went in other sites and just come back.
The idea in the website is very simple:
I propose a new model that suggests twins mutation and inbreeding, only one step assumed. For speciation of a sexual organism (viviparous), there are only four steps in whole process.
1. Formation of fraternal twins zygotes (male and female).
2. Similar gross mutations on these zygotes by a certain probability (even very low).
3. Self-splitting of zygotes into two groups of identical zygotes in both genders.
4. Development of zygotes with birth of babies and inbreeding when they mature
For oviparous animals and asexual organism, these principles will be same, i.e. gross changes in genetic material, instantaneous biodiversity, and inbreeding (if sexual organism). Only step 2 is assumed, the rest 3 steps are natural phenomena.
Many unsolved myths have answers under the proposed mechanism, which are discussed in the website. Also I list several falsifiable mechanisms to the model.
I had some discussions in talk.origins, I answer major critiques in FAQ section of a website.
I see no mathematical incorporation of the two different kinds of 1-D symmetry Weyl distinguised in SYMMETRY(book). The two eves idea no matter about the initial diversity of genetic variance across the line a progeniture motion crosses seems to give SHAPE to the dashed line. I had not seen your proposal before because *this* is not supported by anymath or any metric application I am aware of.
I never thought any metric application necessary, and I do not know them anyway.
How would you get 1:3 traits in the generations rather than the simple bifurcation your work seems to ply again.
Why do I have to get 1:3 traits? With similar gross mutations at both zygotes (female and male), inbreeding among them would generate a new species with new genomic struture.
i continue to read it you could theoretically get two identical mutations by TWO different physical chemical paths
Why two different physical chemical paths? Same type virus can infect both twin zygotes easily with same gross mutation.

Jianyi Zhang

This message is a reply to:
 Message 9 by Brad McFall, posted 04-26-2005 6:03 PM Brad McFall has replied

Replies to this message:
 Message 13 by Brad McFall, posted 04-27-2005 9:43 AM Jianyi Zhang has not replied

Jianyi Zhang
Inactive Member


Message 15 of 305 (203003)
04-27-2005 12:36 PM
Reply to: Message 12 by Wounded King
04-27-2005 6:51 AM


Original post by Wounded King
Changes in allele frequencies do not explain these karyoptypic changes because many of these changes are themeselves changes in allelic frequency. Duplications, deletions, inversions, amplifications and insertion may all lead to a change in allele frequency in a population, although they do not neccessarily do so.
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.
It is also by no means a given that differences in karyotype are the be all and end all of speciation.
Yes, not all differences in karyotypes leads to speciation, but different species almost have different karyotic patterns, some gross mutations can not be seen by karyotypic study, as they are not big enough to be seen.
None of these are evidences against the operation of RMNS, all they show is that there are many more sources of variation than had been supposed when the 'modern synthesis' was being developed. As has been pointed out they are by no means 'instantaneous' biodiversity any more than a point mutation is.
All of these evidences are against RMNS as the mechanism of speciation. Can you tell me how polyploids in plants occur by RMNS?
If you still think polyploids consistent with RMNS, you should read some books by E. Mayr, top Darwinists. How about virgin birth of shark in zoo? How do you apply RMNS to it?
http://news.nationalgeographic.com/...20925_virginshark.html
In the case of the chicken and egg the answer is obviously egg. Reptiles and various species of bird had been laying eggs long before chickens turned up.
Do you mean eggs give a birth to a new species?
I don't see how RMNS makes no predictions. there are many papers investigating the theoretical exploration of fitness landscapes providing testable models of how organisms adapt to selective pressures and a number of experimental approaches, especially in bacterial cell culture, to test such hypotheses.
There is no way to predict anything with RMNS. BWT, does a new bacteria a new species? Almost all antibiotics bacterai are generated from lateral transfer, which is an instantaneous process, regardless of existence of antibiotics, they were there, ones have no way to find out them.

Jianyi Zhang

This message is a reply to:
 Message 12 by Wounded King, posted 04-27-2005 6:51 AM Wounded King has not replied

Replies to this message:
 Message 16 by mick, posted 04-27-2005 1:17 PM Jianyi Zhang has replied

Jianyi Zhang
Inactive Member


Message 17 of 305 (203022)
04-27-2005 1:33 PM
Reply to: Message 14 by Admin
04-27-2005 10:19 AM


Originlly posted by Percy EvC Forum Director
If you decide to participate in this thread, be sure you set your frustration tolerance level to maximum.
You get frustrated, as you do not know evolution and mechanism of evolution two totally different things.

Jianyi Zhang

This message is a reply to:
 Message 14 by Admin, posted 04-27-2005 10:19 AM Admin has not replied

Jianyi Zhang
Inactive Member


Message 18 of 305 (203031)
04-27-2005 2:14 PM
Reply to: Message 14 by Admin
04-27-2005 10:19 AM


Originally post by Percy EvC Forum Director
If you decide to participate in this thread, be sure you set your frustration tolerance level to maximum.
You get frustrated, as you do not know evolution and evolution mechanism totally different issues.

Jianyi Zhang

This message is a reply to:
 Message 14 by Admin, posted 04-27-2005 10:19 AM Admin has not replied

Jianyi Zhang
Inactive Member


Message 20 of 305 (203066)
04-27-2005 4:11 PM
Reply to: Message 10 by mick
04-26-2005 8:37 PM


Originally posted by Mick:
The theory of evolution does not claim that changes in allele frequency result in karyotype changes. Changes in karyotype may, however, affect allele frequency (i.e. if an allele is deleted or duplicated). You will need to explain how the existence of various karyotypes is meant to be a challenge to the theory.
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.
This is no challenge to neo darwinism. It just means that our population genetics models have to be modified when we study bacteria. The existence of HGT challenges neither the existence of mutations nor the existence of natural selection.
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.
I fail to understand how abnormal cell division, resulting in duplication of the genome, is meant to challenge evolutionary theory. A polyploid cell resulting from whole genome duplication isn't "instantaneous biodiversity". It's just a normal individual with twice the amount of genetic material.
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.
it's clear that human HIV evolved from SIV and didn't appear instantaneously.
Of course, they did not come from dirt.
The molecular evolution of HIV is explained well by neoDarwinism, showing purifying selection on some regions of the viral genome and diversifying selection on others. Are you really suggesting that HIV didn't evolve from SIV?
I agree HIV derived from SIV. However, the very first HIV probably generated by combining several viruses including SIV.
Visna sequences
I 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.
They could well have arisen by multiple endosymbiotic events, not just one spontaneous event. Just compare a chloroplast or a mitochondrion to a bacterium, and look at the diversity of chloroplast structure in plants, to see that this wasn't just an instantaneous transition that has been frozen over the millenia.
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.

Jianyi Zhang

This message is a reply to:
 Message 10 by mick, posted 04-26-2005 8:37 PM mick has replied

Replies to this message:
 Message 21 by mick, posted 04-27-2005 4:26 PM Jianyi Zhang has replied
 Message 22 by Ooook!, posted 04-27-2005 6:30 PM Jianyi Zhang has replied

Jianyi Zhang
Inactive Member


Message 23 of 305 (203137)
04-27-2005 7:14 PM
Reply to: Message 16 by mick
04-27-2005 1:17 PM


Originally posted by Mick:
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.
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.
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?
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.
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
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.
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?
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.
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.
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.
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.
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.
Your assertion the karyotype changes are necessary for speciation is wrong.
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

Jianyi Zhang

This message is a reply to:
 Message 16 by mick, posted 04-27-2005 1:17 PM mick has replied

Replies to this message:
 Message 27 by mick, posted 04-28-2005 12:47 PM Jianyi Zhang has replied

Jianyi Zhang
Inactive Member


Message 24 of 305 (203198)
04-27-2005 10:55 PM
Reply to: Message 21 by mick
04-27-2005 4:26 PM


Originally posted by mick:
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".
Agree.
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?
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.

Jianyi Zhang

This message is a reply to:
 Message 21 by mick, posted 04-27-2005 4:26 PM mick has not replied

Jianyi Zhang
Inactive Member


Message 25 of 305 (203217)
04-28-2005 12:17 AM
Reply to: Message 22 by Ooook!
04-27-2005 6:30 PM


Originally posted by ooook:
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.
"Plasmids containing mitochondria could infect bacteria and stayed inside"
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?
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.
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?
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.
If so, how can you reconcile the fact that mitochondrial eve never met (let alone mated with) Y chromosomal Adam?
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

Jianyi Zhang

This message is a reply to:
 Message 22 by Ooook!, posted 04-27-2005 6:30 PM Ooook! has replied

Replies to this message:
 Message 26 by Wounded King, posted 04-28-2005 5:49 AM Jianyi Zhang has replied
 Message 36 by Ooook!, posted 04-29-2005 12:53 PM Jianyi Zhang has replied

Jianyi Zhang
Inactive Member


Message 28 of 305 (203395)
04-28-2005 2:18 PM
Reply to: Message 27 by mick
04-28-2005 12:47 PM


Originally posted by mick:
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.
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.
Next, the two individuals have to meet each other and mate successfully with each other.
As the supertwins or twins live together, it is very easy for them meet and mat.
All of these events are vansihingly unlikely, and the multiplication of their likelihoods has to be pretty small.
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?
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.
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?

Jianyi Zhang

This message is a reply to:
 Message 27 by mick, posted 04-28-2005 12:47 PM mick has replied

Replies to this message:
 Message 29 by mick, posted 04-28-2005 7:33 PM Jianyi Zhang has replied
 Message 30 by mick, posted 04-28-2005 7:39 PM Jianyi Zhang has not replied

Jianyi Zhang
Inactive Member


Message 31 of 305 (203487)
04-28-2005 8:46 PM
Reply to: Message 29 by mick
04-28-2005 7:33 PM


Originally posted by mick:
Rather than denying my challenge, you have now added "twinning" to the mix.
Do I add anything? I published the book in 2003 and setup the website one year ago. The idea was there by then. Why does I need anything?
Read post 11 and 3. and see what I said there. You are just so careless.
Do not project your confusion to others.

Jianyi Zhang

This message is a reply to:
 Message 29 by mick, posted 04-28-2005 7:33 PM mick has replied

Replies to this message:
 Message 32 by mick, posted 04-28-2005 9:32 PM Jianyi Zhang has replied

Jianyi Zhang
Inactive Member


Message 33 of 305 (203527)
04-28-2005 11:11 PM
Reply to: Message 32 by mick
04-28-2005 9:32 PM


Originally posted by mick:
I will await your explanation of speciation in birds, reptiles and insects.
This is very simple. Birds, reptiles and insects (I assume they are oviparous organism). There are supertwins zygotes in mothers body, which are subject to various gross mutations. Identical gross mutation can be from viral infection as they are grouped together (both male and female), or develeped by splitting of mutated zygotes in both genders.
Multiple fertilized eggs in shells are layed and hatched, with a birth of group of animal in two genders. Key is whether an organism
has two or more zygotes at the same time. Almost all sexual animals do.
I would want an explanation that is general to archaeosauria plus insects, but also generalisable to other animals, including bacteria and viruses, in the same way that NS is universally applicable.
Archaeosauria, bacteria and viruses are asexual organisms, biodiversity(not speciation) occur even much simpler; just gross mutation, no inbreeding. Gross mutation includes errors in self-replication, also lateral transfer, recombination, etc. NS only works after new group organisms were born. I discuss it in HIV case.
This message has been edited by Jianyi Zhang, 04-29-2005 10:27 AM

Jianyi Zhang

This message is a reply to:
 Message 32 by mick, posted 04-28-2005 9:32 PM mick has not replied

Jianyi Zhang
Inactive Member


Message 34 of 305 (203640)
04-29-2005 11:23 AM
Reply to: Message 26 by Wounded King
04-28-2005 5:49 AM


Originally posted by Wounded King:
No it doesn't, it means that RM&NS can give rise to biodiversity, not that they are the only concievable mechanisms,
If RM&NS can give rise to biodiversity, but nobody knows which organism work by the rule, and it is unfalsifiable. It is a faith or pseudo-science claim.
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.
My point is without NS biodiversity occur, as they are very few members. It takes a long time for us to find out them, NS works after they were born.
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.
It is not important whether plasmid, or virus, or bacteria, or something else involved with endosymbiotic origin of mitochondria, since nobody knows, they are all hypothesis. What I say is that it an tantaneous process.
Using early bacteria in a discussion of speciation is totally pointless.
So, I did not say it speciation, I just say it biodiversity, which you might have different definition.
Any shred of evidence for that?
The cheetah is one of the most amazing animals in the cat family. As the worlds fastest animal, it has been clocked at 110 kilometers per hour for short distances. In 1900, estimated 100,000 cheetahs were estimate worldwide and had, fallen to 30,000 by 1975. In 1997, only 9,000 C 12,000 cheetahs remained in Africa.
Blood samples taken from 50 cheetahs for genetic testing revealed they were genetically identical to each other. Electrophoretic studies have shown that cheetahs are monomorphic and homozygous at many loci, thereby lacking the 10-60% polymorphisms found in other species. Furthermore, skin graft experiments in cheetahs indicated a significant lack of variability at the major histocompatibility complex.
In another similar case, the pocket gopher lives in tunnels in the American west. Researchers at the University of California, Santa Cruz found out each Humboldt gopher accepted grafts of small skin patches from other members within its own species, whereas the Carmel Valley gophers did not. To test immune function of Humboldt gophers, the researchers grafted skin from Carmel Valley gophers onto Humboldt gophers that rejected the grafts. This result suggests a uniformity of the Humboldt gopher genome.
In biology textbooks, the bottleneck effect or genetic bottlenecks are considered as the result of environmental fluctuations. According to the theory, sudden reductions in population size can alter the resulting gene pools. In the recent past, with change in environmental condition, many individuals in these animals were killed and only a small number have survived. With the drastic reduction in their population, close relatives were forced to breed, and the cheetah became genetically inbred, meaning all cheetahs are closely related. Oddly, no explanation is available to elucidate why and how such kind events only selectively kill cheetahs and leave every other big cats alive to develop its expected genetic variation.
The proposed GMCMI provides an alternative explanation: in stead of mysterious events which only selectively killed only a few types of these animals, some of the animals might be new-evolved species, the plasticity of genetic structures in the animals are very poor, they are still identical and very close to the initial stage when they were created by Nature.
The other lessen is that regardless of how they were generated, they are genetically identical and survived. If they can, why not others in the similar situation?
These cases are just accidental findings.
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.
The estimated number depends on sample in the study, the female and male were from different samples. The study did not show only one Adam or Eve at that time, just says these man or women from one person at that time, the timing might be different, and there might be others then.

Jianyi Zhang

This message is a reply to:
 Message 26 by Wounded King, posted 04-28-2005 5:49 AM Wounded King has replied

Replies to this message:
 Message 35 by Wounded King, posted 04-29-2005 11:46 AM Jianyi Zhang has replied

Jianyi Zhang
Inactive Member


Message 43 of 305 (203834)
04-29-2005 8:36 PM
Reply to: Message 36 by Ooook!
04-29-2005 12:53 PM


Originally posted by Ooook!
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.
Mitochondrial ‘Eve’ doesn’t have to be alone. There is nothing to suggest that any ‘Eve’ is the only female in her species.
Mitochondrial study suggests there might be alone Eve, even not the Eve in the study.
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.
The estimated number depends on sample in the study, the female and male were from different samples. The study did not show only one Adam or Eve at that time, just says these man or women from one person at that time, the timing might be different, and there might be others then.
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 did not say the model has been tested. I said "every species has two Eves", I use Human Mitochondria study as my support. This is the my prediction, which can be falsified with future study.
How exactly would you really test this?
Sequence a few individuals from branch new species
There certainly have been genetic bottlenecks — but how can you tie them specifically to your ‘super-twin’ speciation events?
Sequences from super-twins are much more homogenous than ones from otherwise.
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?
Ones can not confirm something in the past, if there are many missing links. However, one can look for the future. By definition of prediction, it is about future.
This is another example of a misunderstanding on your part. Your model requires common ancestry just as much as the current ToE does.
Yes, my model suggests common ancestry, how does that show my misunderstanding?
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.
Super-twining is needed for sexual animals, it has nothing to do with asexual ones.
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?
Over 90% sexual animals have distinct karyotic patterns under microscope, the rest of them might have karyotic changes invisible under microscope, as to be seen under microscope, one needs 1-2 million base pair difference. The definition of gross mutation in sexual animals is at FAQ section of my website.
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.
I do not know what you mean.
This message has been edited by Jianyi Zhang, 04-30-2005 10:50 PM

Jianyi Zhang

This message is a reply to:
 Message 36 by Ooook!, posted 04-29-2005 12:53 PM Ooook! has replied

Replies to this message:
 Message 80 by Ooook!, posted 05-04-2005 5:58 PM Jianyi Zhang has replied

Newer Topic | Older Topic
Jump to:


Copyright 2001-2023 by EvC Forum, All Rights Reserved

™ Version 4.2
Innovative software from Qwixotic © 2024