What is the mechanism that prevents microevolution to become macroevolution?

The increase in diversity is observable at the level of the population in that it consists of a much greater range of genotypes than would be observed if it was all one gene pool.Diversity at the level of the population can arise in many ways other than simply an increase in the number of alleles occurring at specific loci.
For example, the linkage disequilibrium Quetzal refered to refers to a multi-locus effect.Lets assume 2 loci, A and B, with two alternative alleles at each, A/a and B/b. Assuming diploid sexual reproduction, meiosis yields four types of possible gametes:AB
ab
Ab
abThe first two are referred to as 'coupling' gametes and the second two as 'repulsion' gametes.Now, if there is no linklage between these alleles (or meiotic drive of any kind), we expect these gametes to be formed at equal rates and be present in equal proportions (.25) in the population.When there are statistical deviations from the .25 frequency (when coupling gametes outnumber repulsion gametes or vice versa), this can be considered evidence for selection favoring one type of gene combination over another. Thus AB and ab may be the most advantageous gametes to produce in one particular population, and aB and Ab the most advantageous in another population. These populations are then different, i.e. they are genetically 'diverse' relative to one another even though there is no increase in the number of alleles, or even any difference in the actual alleles possessed by them.Hope this helps,EZEdited by EZscience, : to change title...

Absolutely. Diversity at the level of organisms is what is meaningful and interesting. Allelic diversity is just one factor underlying organismal divsersity. Faith seems convinced that the loss of particular alleles on a statistical level is somehow indicative of a loss of 'diversity' when such is not the case. Organismal diversity is more a function of genetic organization patterns than it is simple allele frequencies, and virtually all alleles 'lost' in bottleneck events can potentially be re-created via mutation.

Actually, genotypes. Phenotypes have no heritability. The genotype is the set of heritable units in the organism, although it is not heritable as a unit itself. Fine. I am just pointing out that genotypic diversity is more than a simple function of numbers of available alleles. Actually, you can sometimes get a range of phenotypes from a single genotype, but the genotype is the set of genes underlying the organism so you are really talking about things affecting genotype. Genetic drift is a population-level phenomenon - the loss or fixation of some genes as opposed to others in particular populations purely be chance - so this can affect the range of genotypes observed in a population and their relative frequencies, but it doesn’t really ”produce new phenotypes’ or genotypes - that would require mutation. There are certainly cases where events reducing allelic diversity in a population can result in the subsequent appearance of novel genotypes, but to say that their emergence is invariably dependent on reductions in allelic diversity would be incorrect. Firstly, all genotypes (and the phenotypes they give rise to) in a population are novel (unless there is asexual reproduction) - they exist in one genration only and are never re-created - so population diversity is to some degree always a function of population size. Not at all. I am refering specifically to genotypes. I think you are failing to recognize that the ”diversity of genetic possibilities’ (in genotypes) is determined by more than simply allelic diversity. Remember chimps have > 97 % of genes (alleles) in common with humans, and yet the organization and coordinated expression of these alleles is very different in the two species. You wouldn’t say we are 97% the same as a chimp would you? Allelic frequencies are just one of the things we can measure to compare divergence between populations, but they are not the sole determinant of genetic diversity. Simply allele frequencies. Higher order structure on the genome is another important component of genotypic diversity that transcends simple allele frequencies. Non-transcribed regions may have unrecognized importance here. Allele frequencies are one thing that will change inevitably with population subdivision and the range of genotypes will be affected, but it is not the only way new genotypes emerge. Let’s not forget about mutation. Even if mutation rates are similar across the genome in disparate populations, different alternative alelles may become fixed in the two by chance. So we might have a number of loci in which a single allele is fixed in the 2 populations (no alternative alleles floating around), so their allelic diversity at those loci is quantitatively equivalent, and yet their genotypes are qualitatively very different. But it IS a known. Mutations are observed and have been proven to occur. Crash gave the example a way back of the bacterial experiment where only mutation in the culture could account for the results. Yes, we cannot observe directly or predict exactly where or when a mutation will occur, but the evidence for their occurrence is overwhelming and undeniable. I am not a molecular biologist, so someone like WK could probably provide you with better specifics, but there are recurrent mutations - changes between bases that tend to happen in particular sequences with higher probabilities than elsewhere on the genome. Alleles that are lost in a population can ocassionally reappear through recurrent mutation, although their fate in one population may be very different than their fate in another, even with similar rates of reversion. If we accept that errors during replication can occur, then they inevitably will occur - with some statistical probability. What is difficult to accept here? It seems to me that the alternative hypothesis - that all the chemical complexities of genetic replication must occur perfectly every time - is by far a more contrived and unlikely scenario. Your mistaken inference is that mutations are not occurring simply because so many loci are fixed for a single allele. There likely are occuring, but rates are very low because effective population size is very low, or the sequences of the alleles in question are highly conserved. Substituting ”genotype’ for phenotype, yes, you are correct. New genotypes can evolve without novel alleles, but that does not exclude the contribution of allelic diversity (created by mutation) to evolution. Novel alleles are required in order to produce novel proteins. There may be many situations where mutations are ”not needed’, but they happen anyway and they often contribute important changes to population structure. That changes in genotypic profiles in populations can occur without mutation is not evidence that mutations are not an important source of genetic diversity.

We may speak of 'selection pressure', but there is no such thing as 'mutation pressure'. Nor is mutation inherently essential for speciation to occur. I don't know where you learned your high school biology (Alabama ?), but you need to re-take it.Remember, 'beneficial' is always a loaded term because it is context-dependent. With that in mind, see if you can wrap your brain around this (hypothetical) example.The AIDS virus has a protein capsid that recognizes a particular protein structure specific to the surface of human T-cells. A mutation occurs in a single base pair that changes one amino acid in this protein leaving its function as a membrane protein unaffected, but rendering it un-recognizable to the AIDS virus.Would that comprise a beneficial mutation? Do you even know what a plasmid is? Because they don't occur naturally in the germ cells of higher organisms. And yes, there are regions of the genome subject to higher rates of mutation (base-substitution, deletion) than other areas. These are relative, not absolute terms. 'Highly conserved' just means there is a very low rate of alteration in sequence, so mutation is a low frequency event, but not impossible. We may also observe regions of a genome that are 'hot spots' for mutation in that many alternative sequences are observed in a population, but usually these are not transcribed regions. That would be difficult given that there is no such thing.
Mutation does not constitute a 'pressure' - it is merely a heritable molecular event with a range of possible consequences in an organism ranging from negative to neutral, to positive.

The problem is that phenotypes do not evolve, whereas genotypes do. Not within a population, because genetic drift is defined in terms of population divergence - it can’t happen within a population - only between them. It can be a factor in speciation, but it is not sufficient to account for speciation. But they aren’t. Speciation requires some form of reproductive isolation, be it spatial, temporal, behavioral or genetic. Then why can you not envisage any beneficial effect of a mutation, when the very term ”beneficial’ is so obviously context-dependent? Imagine a mutation that alters one amino acid in a critical developmental enzyme, lowering its thermal energy of activation without affecting other functions. Would you not expect this allele to be selected over its ancestral form in areas of the species’ range that were much colder, for ex. at higher altitudes? It would enable the organism to complete development at a lower temperature. Literally countless ”beneficial’ mutation scenarios are conceivable when you understand how biology works. Of course there is. There is a first time for everything. You have accepted that mutations can occur, how is it possible they would never produce anything novel when they simply comprise chance mistakes in transcription? That is a veiwpoint obviously arising from your pre-determined belief in YEC, but an interesting question, nevertheless.I would contend that no, there are not. This is because ecology and evironments continue to evolve and change, as they always have. Novel environments will select for novel alleles. There was no value to a gene for DDT resistance in mosquitos until we synthesized DDT and started spraying it everywhere. New niches will continue to evolve that provide new alleles opportunities to provide new advantages to their genotypes, just as new ecological niches will appear that represent evolutionary opportunities for species. This, to me, is the greatest conceptual failure of creationism - to provide any mechanism for change to occur a posteriori. If we accept that things are always changing in nature, a single creation event will never be sufficient to explain the ongoing diversification of life. You have all the answers to this question within your own words.
Your knowledge of population genetics is sufficient that you can easily appreciate how ”rare’ can easily become ”common’ after a few generations of selection. That mutations can *sometimes* be neutral simply allows them to hang around without affecting fitness under some sets of conditions. That they are potentially beneficial is not difficult to accept when you recognize that ”beneficial’ itself is a very context-dependent term, as I have explained above.

I had not heard the term used to imply asymmetry in forward/backward mutation rates. I was objecting to its use by Faith in the context of some sort of driving force in speciation.

Oops. Yes of course.
I had just finished my answer to Faith, hence my mistake.

The answer is that a mutation can occur in either conserved or unconserved regions - it's just a difference in the *probability* of mutation that distinguishes the two. By definiton, a conserved region is a region where mutations either rarely occur, or if they do, they are not tolerable and invariably result in an inviable genotype that fails to develop (or reproduce) successfully. Similarly, there are unconserved regions where the reverese is true, usually because these are sequences that are not transcribed and therefore do not code for proteins with exacting structural requirements.There seems to be a desire on your part to view 'beneficial mutations' as some sort of special case. A mutation is just a mutation. Whether it is deleterious, neutral, or beneficial is CONTEXT-DEPENDENT and depends on 1) the environmental context in which the individual lives, and sometimes 2) the genotype (genetic context) in which the mutation occurs. So the same mutation may be deleterious in one context, but beneficial in another. I can give you a nice example if you like. Of course it is a 'raw' mutation.
Check back in whatever biology text they gave you at Rockhurst.
Heritable mutations comprise additions, deletions and substitutions of bases in germ cell DNA. I posited a base substitution that generated a change in one amino acid following transcription...and viral gene pools are notoriously unconserved.
Viruses can evolve faster than almost any other living thing.
How do you think bird flu is starting to infect humans suddenly after being restricted to birds up till now?
It has to be a 'beneficial' mutation (beneficial for the virus, not for us).