Why Darwinism is wrong

No one knows anything !! ??
You should speak only to your own level of understanding.
Ever heard of experimentation and direct observations ?
They help you 'know' things.Scientists 'know' plenty, and what we do know all fits very nicely with evolutionary theory. There is not one concrete observation, or set of observations, that directly contradicts evolutionary theory, nor is there any living phenomenon or organism that cannot be accounted for within the framework of evolutionary theory, and without any need to 'trim' anything to make it fit.It is rather creationists that repeatedly try to 'shoe-horn' snippets of biological evidence into a predetermined model dicatated by the bible.And you shouldn't ever say 'don't reply to this' in a forum.
That's like saying "I'm going to have the last word now and I don't care to hear your response".It's a FORUM !

I agree Mick.
The large effective population size of humanity is enough to prevent speciation.High dispersal frequency of individuals among subpopulations facilitated by modern technology generates the high gene flow you mention.
And we know it only takes very little gene flow to prevent speciation.Also, we are far too 'K-selected' to evolve quickly in the genetic sense. Cultural evolution is another matter entirely, and here is where we can see rapid changes within the span of one lifetime.One of the key factors determining the rate of *genetic* evolution (and hence also speciation) is the generation time of the species.
Assuming a median age at first reproduction of around 20 (I know its less in many underdeveloped countries) you can have only about 50 human generations per millenium, which isn't much. Just to put your theoretical extrapolation of 32 billion generations into some context, which I assume is derived from N (effective population size).This message has been edited by EZscience, 05-09-2005 11:01 AM

Yes. Good point.
I notice many threads where titles should have been altered much earlier.
I appologize for my laziness.EZ

I agree. Publications count for something.
Just being a doctor, MD or otherwise, doesn't mean much.There are a lot of PhD's that aren't worth the paper they are written on.
Unfortunately, I have witnessed quite a few of them successfully defended at major land grant universities in my own discipline.An argument should rest on its own merits, not on the qualifications of the debater.
Otherwise the debate just becomes a pissing contest.Edited to add title.This message has been edited by EZscience, 05-11-2005 08:44 AM

Endocytosis of a bacteria by a primitive eukarotic cell that led to a symbiotic relationship and continued co-existence of the two.Go to message 36 of this thread to read more.

Well, the actual event would probably have occurred a few billion times and resulted in consumption of the bacteria before a unique event led to the symbiosis becoming established. I have no problem with this.
NS can only work on what already exists and has some mechanism of heritability.This message has been edited by EZscience, 05-11-2005 01:03 PM

OK now we have a problem.
I am familiar with gradualism versus punctuated equilibria etc when it comes to phylogenies, and allopatric and sympatric models of speciation,
but instantaneous speciation ?Do you mean like a polyploidy event that makes for instantaneous reproductive isolation?That's about as close to instantaneous speciation as I can conceive.

Loss of sexuality is an interesting evolutionary scenario that appears to have occurred more than once in some lineages.
But I would not call it a common event.
What kind of animals were you thinking of here ? I am interested.
What other phenomena are you refering to ?
Any references ?

Of course. I have worked with aphids for almost 20 years.
I am also quite familiar with the distribution of parthenogenesis and apomixis among animal taxa.
Incidentally, when I said 'not a common event' I was referring specifically to the 'loss' of sexual reproduction within a phylogenetic lineage.I would also agree that asexual lineages can *potentially* diverge more quickly than sexual ones.But how does that relate to mechanisms of speciation for obligately sexual (amphimictic) populations that make up the majority of higher animals?I looked at the four parts of your theory as explained on the website, and I immediately see at least one problem for applying it to higher animals.
What about inbreeding depression and detrimental homozygosity among siblings?
Most higher animlals have many behavioral mechanisms (dispersal etc.) that evolved specificall to reduce or prevent inbreeding.
The only organisms truly adapted to inbreeding are those that routinely mate only with siblings, like gregarious hymenopterous parasitoids.
Your model might work for them, but not for organisms adapted for outbreeding.
The first few generations of your new species would have very low fitness compared to their progenitors, and yet presumably they would still be trying to occupy the same niche.

Yes, and don't hold your breath but Lamarkian inheritance might be making a comeback.Recent evidence suggests that the genetics of host plants can effect changes in the genetics of infecting viruses that are henceforth heritable for the virus, i.e. the virus is changed by passage through a particular host plant. (Not all host plants do this to the virus.)Likewise, infection by the virus can (sometimes) permanently and heritably alter the geneome of the host plant in various, apparently random ways.
(yes - germ cell lines !)When this is experimentally tested with crop plants, some of the progeny of infected parents express completely novel traits, some of which are potentially desirable for the crop.Is that Lamarkian enough for you - environmental influences having a heritable effect?This message has been edited by EZscience, 05-11-2005 10:45 PM

Well I have to agree they are not on a level of the characteristics that Lamarck had in mind. And I admit I was being a bit playful with this.And you are right about the virus of course. But the plant situation is a bit more interesting.
If you can accept a viral infection as a form of 'environmental influence' (and again, I know I'm stretching this a bit), then you have some heritable changes resulting from this influence.But of course the resulting characters are not expressed in the parent, so again, you could fairly use this as grounds for saying it is not as Lamarck had imagined.But it appears to be a bit more than the virus inserting some sequences in the plant genome.
There appears to be a re-arrangement of the plant genome in some cases, and permanently altered expression of certain plant genes without evidence of any incorporation of viral DNA (although I am not sure how this could be ruled out).
In these cases, you can generate an amazingly diverse array of plant morphologies among the progeny of the infected plant, many of which seem to 'breed true'.This is part of a colleagues' work on sorghum, not mine.
I am an ecologist, not a molecular biologist, so I am probably not doing his work justice either.

Yes, I think what we are now beginning to 'see' (with all the new techniques), and therefore appreciate more, just how many forms of 'mutation' there really are.And I mean mutation in a larger sense than merely substitutions/additions/deletions. Various sorts of epigenetic modifications.Working with aphids for many years, I have always been amazed at how quickly a single clone can diverge in charcteristics from the parental line from which it was derived. You collect a single aphid from one plant, establish a colony on another plant (say, because its more suitable for lab culture), and 15-20 asexual generations later the damn thing won't even feed on the ancestral host anymore.Bottom line is, I don't think we have yet identified all possible sources of 'mutation', nor all possible causes of heritable genetic modifications, whether you want to term them mutations or something else.Opportunities there for an ambitious grad student in molecular biology to maybe make a name for him/herself

Well I won't deny that heritable genetic and epigenetic changes can happen abruptly in populations.I did raise the challenge about inbreeding depression in the progeny of your 'clustered mutants' as applied to higher animals that you haven't really addressed.And, I also do not see how novel sources of heritable variation can negate the validity of natural selection in any way, whether they happen to sometimes generate new species or not.
The products will all be subjects of natural selection.What you are really delineating with your theory (it would seem to me) are just some genetic mechanisms that may have the *potential* to cause sympatric speciation in some cases.And I don't think you should extrapolate too much generality of applicability for your mechanisms yet.
I think they are unlikely to be important in higher animals that are obligately outcrossing.

Which I would contend is > 90 % of outcrossing species.
The only animal species that benefit from inbreeding are those with Hamiltonian, as opposed to Fisherian, sex ratios.
That is to say, species such as gregarious parasitoids that have evolved in circumstances where sib-mating is the norm, rather than the exception. In these cases, female parasitoids search for rare hosts that, once encountered, are used to produce a large clutch / litter of offspring. Upon emergence, opportunities to mate with anyone other than a sib are slim to none.The interesting thing is, the sex ratio becomes distorted drastically in favor of females in these situations.Thus, conventional evolutionary theory would predict that 'if' sib-mating were in any way a significant contributor to population structure in a species, one would observe female-biased sex ratios.This occurs because, as Hamilton pointed out in the 1980's (I can produce the exact reference if you insist), once sib-mating is without significant physiological cost (i.e. inbreeding depression), then females are favored who produce predominantly daughters, since these provide the biggest fitness 'payoff' to mothers - they are the ones that go out and parasitize hosts (or otherwise 'produce offspring') as opposed to sons, whose fitness is only determined by their mating success, which is much more of a 'crap shoot'.Males are expendable. If they are only going to mate their sisters of the same clutch with any probability, their mother is better off (evolutionarily) producing one or two sons to mate 30-40 daughters, or the absolute minimum required to ensure all her daughters get mated. This leads to the strongly female-biased sex ratios observed in hymenopterous (wasp) parasitoids that are gregarious (large clutches of offspring emerge from a single parasitized host).However, this strategy is not impervious to invasion by 'Fisherian Females'The only way this strategy 'pays off' for the mother is IF her sons are the only ones mating her daughters.If the sons of other females make a timely appearance, her skewed-offspring-sex-ratio strategy will fail because unrelated males will mate her daughters, and their mothers will exceed her in fitness. Under these situations, the sex ratio rapidly reverts to a Fisherian one, i.e. one-to-one.In summary, it would be very difficult to demonstrate a significant role for inbreeding in the evolution of higher organisms without accounting for distorted sex ratios.Now Zhang might argue that these 'super twinning events' are of low probability, but with huge contingent consequences when they do occasionally happen, and we could not rule that possibility offhand. However, I think that WK and I would both agree that old Zhang here bears the burden of evidence, evidence he has yet to produce.