Why Darwinism is wrong

You still seem to fail to appreciate that all mutation is instantaneous and therefore the initial origin of all biodiversity is instantaneous.

All it shows is that there are significant events in the evolutionary history of life which are not simply a product of simple small scale genetic mutations, but no one ever claimed this was not the case.

It certainly provides no evidence that random mutation and natural selection can't give rise to reproductive isolation

The whole point in the debate is that I state initial origin of all biodiversity is instantaneous, no matter whether the mutation lead to change of allele frequency, or ones lead to speciation; where Darwinian claims mutation for speciation has occur by natural selection, not instantaneous one. You neither understand my position, nor Darwinian one.

The data shows all significant events in the evolutionary history of life not simply a product of simple small scale genetic mutations, no exception.

Data can only show what happens, and it can not rule out all possibilities for any event. ..... That is a faith, just like God created world at the beginning. If you want to say it scientific claim, I rather say it a pseudo-science.

I guess you don't understand the concept of creation.

The evidence supports neither evolution nor creation.

The existence of many species showing spectra of interfertility demonstrate that there is a variable range of interfertility.
Why do you feel there is some barrier to complete interfertility between 2 populations developing when there are so many populations in which this process is already underway?

Once again you claim that mutation occurs by natural selection

What are you using to define a significant event? Where is the scientific literature ranking the significance of all events in evolutionary history? How small is a small scale genetic mutation? Is it only point mutations? Insertions-deletions? inversions? Gene duplication? Chromosome duplication? Genome duplication? Where is the cut off?

All it shows is that there are significant events in the evolutionary history of life which are not simply a product of simple small scale genetic mutations

Where are your examples of supertwinning giving rise to a seperate reproductively isolated, or even just a less interfetrile, population?

Surely your proposal is considerably closer to pseudo-science since it suffers the exact same defects you highlighted but lacks the evidence suggesting that speciation can indeed develop via small scale genetic mutations.

It is you, Darwinist who claims mutation occur by natural selection.

You create another myth (a variable range of interfertility). If one species can mate with another with reproductive offspring, they are same species. It is wrong to think them as different species at the first place.

It is you, Darwinist who claims mutation occur by natural selection.

You should ask yourself, Sir. I copy your words from post 87:

I can not give you examples for electron, quark, entrapy, but they still exist.

Darwinists can not tell us how to falsify the theory, I do.

Don't blame me. Don't even blame Darwin. Taxonomical organisation was around long before modern evolutionary theory. It isn't my fault that a lot of modern day species are totally independent of any sort of verification as a truly distinct species from close relatives.

Is it also wrong to think of species which can successfully breed but produce sterile offspring as related?

My position is very clear and consistent: all mutation, no matter how small, how big, occur randomly. There is no causal relationship between them. NS has nothing to do with occurance, it only works after they occur.

It is you, Darwinist who claims mutation occur by natural selection

I asked you where you got the idea that anyone did make such a statement. Can you explain that?

Zhang writes:It is you, Darwinist who claims mutation occur by natural selection.

thenewguy03 writes:...the evidence is in, but it is trimmed and fitted into theory, simply because no one knows anything.

Jianyi Zhang writes:Can you tell me how speciation occur by RMNS, so I will start from there?

Wu and Ting writes: The molecular genetics of speciationTo understand the molecular basis of RI, three key questions need to be addressed. First, what genes contribute to RI? Second, what are the normal functions of those genes? Third, how did these normal functions diverge among different populations, leading to RI? The fact that the genes that underlie post-mating isolation must have normal functions that are distinct from their role in RI is an important point to keep in mind. After all, the function of RI genes could not possibly be to sterilize their carriers. In this way, the analysis of RI is not unlike the study of graft rejection in organ transplantation: the biology of the major histocompatability complex, which underlies graft rejection, certainly has much wider and more profound implications than the phenomenon of graft rejection itself. In modelling the evolution of RI, the practice has been to consider only the RI phenotype without addressing the underlying function (for example, see Box 2). The reason for such a glaring omission is clear the identities of speciation genes, and so, their normal functions, have not been known until very recently.Now, there are a handful of studies in which the identities of speciation genes have been shown: each of which we discuss. By definition, a speciation gene is one that can be shown to cause some degree of ecological, sexual or post-mating isolation between young, or even nascent, species. Although there have been other claims of speciation genes being identified, we consider the five that we discuss to be the only studies that have truly identified the molecules involved. There are many excellent studies that focus on genes that differ between species and the molecular interactions between them but that do not address their phenotypic effects on the whole organism (for example, see Ref. 23). Until these further studies have been done, such genes cannot be classified as speciation genes.Although the definition of speciation genes includes those with strong or weak effects on ecological, behavioural or physiological differences, most of these initial studies have concentrated on genes that have large effects on physiological characteristics. Four of these five examples focus on post-mating isolation. The final example, which concerns ecological adaptation between behavioural races, is therefore of considerable interest.Melanoma formation in Xiphophorus species hybrids (Xmrk-2). Many species in the fish genus Xiphophorus have spots on their skin that are composed of black pigment cells. In interspecific hybrids between X. maculatus (platyfish) and X. helleri (swordtail), these spots sometimes spontaneously develop malignant melanomas24-26. A two-locus Dobzhansky-Muller (DM)-type model (see Box 2) has been proposed to explain the formation of malignant melanomas. In this model, overexpression of the Tu gene causes these melanomas to form. The second locus involved, called the R gene, is a suppressor that negatively controls Tu. The platyfish contains both Tu and R genes, whereas the swordfish contains neither. In the backcross F2 hybrids, a quarter of the offspring produce melanomas owing to the presence of Tu but the absence of the R gene.The X-linked Tu locus was subsequently mapped to a candidate gene, Xmrk-2 (Refs 27—29). Xmrk-2 encodes a transmembrane growth factor of the RECEPTOR TYROSINE KINASE SUPERFAMILY that is important in signal transduction. Its closest homologue in humans is the epidermal growth factor receptor (EGFR)30. All the features of Xmrk-2 are consistent with those of the dominant ONCOGENE that causes the melanomas in the hybrid fish. In particular, mutations at the Xmrk-2 locus abolish the Tu phenotype and the overexpression of Xmrk-2 gives rise to a high frequency of tumour formation.In the adjacent genomic region, another EGFR homologue, Xmrk-1, was found in all Xiphophorus fish. Xmrk-1 and Xmrk-2 are therefore duplicated genes. However, Xmrk-1 transcripts can be found in all tissues, whereas Xmrk-2 transcripts are only abundant in the melanomas of the hybrids. Xmrk-2 apparently originated from non-homologous recombination between Xmrk-1 and an adjacent D locus31. So, this hybrid locus has the regulatory region from the D locus and most of the coding regions from Xmrk-1. The R gene represses Xmrk-2 as well as the D locus. Another important difference between Xmrk-1 and Xmrk-2 is the two amino-acid replacements in the extracellular domain, which shows ligand-independent activation32. So, divergence after gene duplication is important in the differentiation of these species and this might be a common feature of speciation genes (see also below).Xmrk-2 induces tumour formation only in the hybrids in which the R gene is absent, in accordance with the classical DM model of post-mating isolation. In other species, such as the medaka, overexpression of Xmrk-2 also causes embryonic lethality. The constitutively expressed Xmrk-2 activates a transcription factor, STAT5, and subsequently upregulates several downstream targets33. So, overall, there is strong circumstantial evidence that Xmrk-2 is a speciation gene. However, the multiple alleles at each locus in the natural populations of each species, all of which cause a different degree of hybrid phenotype, require further study. It is possible that some of these alleles are not becoming fixed but rather are simply deleterious mutations in the process of being removed by purifying selection. Those deleterious alleles that are destined to be removed would not contribute to species differentiation.Hybrid male sterility in Drosophila species (OdsH). The Odysseus (OdsH) gene from D. mauritiana causes complete male sterility when co-introgressed with the adjacent segment into D. simulans. Genetic mapping of the male sterility locus (Fig. 2a) allowed the initial identification of OdsH as this RI locus34. Recent transgenic studies have confirmed this identification35. OdsH is a homeobox gene from a family of transcription factor-encoding genes that are known to be slowly evolving. Curiously, OdsH has been evolving rapidly within the D. melanogaster subgroup even though its homologues from other species are extremely conservative.The most direct approach to assess the normal function and the phenotypic effect of a specific gene is to knock it out. Interestingly, the deletion of OdsH from D. melanogaster results in no obvious adverse phenotype35. So, at least at this crude level of observation, OdsH is dispensable. However, a more detailed examination showed a subtle effect: males missing OdsH suffer a 40% fertility reduction when they are two days old and mate repeatedly. This fertility reduction lessens to 20% and 8% in the next two days, also under sperm-exhaustion conditions. After five days, the role of OdsH in fertility enhancement vanishes. One interpretation of these findings is that the role of OdsH is to accelerate the maturation of sperm. So, only very young males under sperm-exhaustion conditions are affected.Comparative analyses indicate that OdsH was duplicated in the Drosophila lineage from a neuron-expressed gene, unc-4, after it diverged from the mosquito lineage. Whereas unc-4 in Drosophila has not diverged much in either sequence or expression from the ancestral state in the common ancestor it shares with mouse and C. elegans, OdsH has changed in both sequence and expression. Specifically, OdsH has been evolving away from the unc-4 pattern of embryonic and neuronal expressions to a testicular role35.Because OdsH is divergently regulated between D. simulans and D. mauritiana, its expression in the testis of the sterile hybrids is highly misregulated. OdsH transcripts accumulate in very young spermatocytes. The pattern is not observed in either parental species or in the fertile introgression line, which differs from the sterile line by a 3-kb segment of OdsH (Ref. 34). The expression of unc-4 in the sterile introgression line is also normal. Therefore, the divergence in the sequence and the expression of OdsH might both contribute to the hybrid sterility.Hybrid inviability in Drosophila species (Hmr). Another classical RI system in Drosophila is the hybrid incompatibility between D. melanogaster and D. simulans, two species that have been reproductively isolated more than 2.5 million years. Crosses between these species produce only inviable or sterile hybrids36-38. Five mutations that could rescue the inviable F1 hybrid progeny have been found and several were elegantly characterized for their MATERNAL or ZYGOTIC EFFECTS39-43. Given the multi-locus nature of hybrid incompatibility, it was surprising that such hybrid-rescue mutations could be identified.Among the hybrid-rescue mutations, the X-linked Hmr (hybrid male rescue) gene, which rescues the inviable hybrid males, was mapped and cloned44, 45. Hmr was identified as a transcription factor in the myeloblastosis family44. The primary amino-acid sequence of Hmr contains two DNA-binding protein motifs that indicate its role in transcription regulation. There were many amino-acid substitutions between the sibling species in the DNA-binding domains of Hmr. So, this pattern indicates that positive selection might drive the rapid evolution of Hmr. However, the Hmr mutation that rescued hybrid viability was a P-element insertion in its 5' region that resulted in a reduction in the amount of wild-type transcript. For Hmr to be considered a true 'speciation gene', it would be necessary to show that the D. simulans and D. melanogaster alleles are functionally divergent in their rescue effect of hybrid viability. A recent transgenic study indicates that this might indeed be the case (D. Barbash, personal communication).Hybrid inviability in Drosophila species (Nup96). Complementation mapping (Fig. 2b) has been used to analyse hybrid inviability between D. melanogaster and D. simulans. High-resolution mapping has allowed a speciation gene, Nup96, to be cloned and characterized22. The Nup96 allele from D. simulans causes inviability in the F1 hybrids if the copy from D. melanogaster is absent. Nup96, which has homologues in yeast, worm and human genomes, encodes a subunit of a nuclear-pore complex, which transports macromolecules between the nucleus and cytoplasm46 and is therefore essential for viability in flies.An excess of non-synonymous substitutions in Nup96 between D. melanogaster and D. simulans relative to non-synonymous polymorphisms within these species (calibrated against synonymous changes with the MCDONALD AND KREITMAN TEST) indicated that this gene is under positive selection. With the sequences from D. mauritiana and D. yakuba, it was possible to map putative adaptive changes onto an evolutionary tree. Presgraves et al.22 concluded that the adaptive changes occurred in the distant past, a suggestion that is corroborated by the analysis of the extant polymorphisms in D. melanogaster and D. simulans. Had some adaptive changes occurred recently, a reduction in the amount of neutral polymorphism, which might also be accompanied by a skew towards very low- and/or very high-frequency variants, would have been expected. Neither was observed in Nup96.Not only were Presgraves et al.22 able to map the Nup96 gene, but they were also able to locate the interacting locus in the DM model of hybrid incompatibility to the X chromosome. They did this by switching the source of the X chromosome in the hybrid males. One question to be addressed in the future is whether there are multiple loci on the X chromosome that interact with Nup96.Ecological/behavioural races in Drosophila melanogaster (desat-2). The final example of a proven speciation gene (under our broad definition; see Box 1) provides a glimpse of the molecular genetics of ecological, and possibly behavioural, isolation. D. melanogaster from central-southern Africa around Zimbabwe and those from the rest of the world (referred to as the Z and M types, respectively) have evolved to become different ecological/behavioural races. The females of African and cosmopolitan D. melanogaster carry different forms of a specific type of non-volatile CONTACT PHEROMONES. These two forms the 5,9-heptacosadiene and 7,11-heptacosadiene forms of the 27-carbon cuticular hydrocarbons (CH)47 differ in the position of a double-bond in a long chain of saturated hydrocarbons. Two independent studies have identified the gene that controls the (5,9)/(7,11) difference to be a desaturase gene, desat2 (Refs 48,49). Although CHs often act as contact pheromones between sexes, they have also been implicated in ecological adaptations, such as heat or starvation tolerance50.The desat2 gene apparently diverts the synthesis of 7,11-heptacosadiene into the 5,9-type. The loss of the promoter in the desat2 gene therefore results in the 7,11-type among the M flies. This observation raises the interesting possibility that loss of function of a gene has a role in this particular case of nascent speciation. The geographical distribution of the two desat2 variants (predominantly desat2+ in Africa and desat20 elsewhere) indicates that this strong differentiation must be maintained by differential selective pressure. An excess of high-frequency nucleotide mutations highlighted the influence of positive selection on the desat2 polymorphism49. Greenberg et al.17, 50 were able to show, by gene knock-out, that the loss of the desat2 gene (as in non-African M flies) results in an increase in cold tolerance and a decrease in starvation tolerance. It is plausible that, in the colder climate, a non-functional desat2 would spread through the cosmopolitan populations. So, this seems to be a case of ecological adaptation and differentiation.An interesting aspect of the Z—M differentiation is the unidirectional sexual isolation between these forms51. Zimbabwe females, in the presence of Z and M males, do not mate with M males. (Note that the observation by itself does not indicate male or female choice.) We know that at least seven or eight genes control female or male mating behaviour, respectively13, 14. So, the question is whether desat2 is one of the loci that governs Z females' mating characteristics (for example, reduced attractiveness to M males). CH differences have been known to govern females' attractiveness in interspecific crosses52. However, it was widely thought that desat2 was not involved in female attractiveness in the Z—M system because Caribbean flies, which carry the African desat2 allele, behave like M flies. Nevertheless, recent observations have shown that, within three African populations, the presence of the African desat2 allele correlates nearly perfectly with Z-femaleness53. One possible interpretation of this pattern is that desat2 governs female attractiveness to M males and that the Caribbean population is an anomaly that results from recent admixture between African and North American flies. Although this interpretation seems to contradict the widely-accepted view that D. melanogaster males might not be discriminatory when choosing a mate54, new work indicates that M males might not court Z females as ardently as they court M females, especially when the females are not highly receptive (C.-T.T. and C.-I W., unpublished observations). If this is the case, the desat2 gene might be playing a double role in this nascent speciation through differentiation in ecological adaptation and, secondarily, through mating preference.