MACROevolution vs MICROevolution - what is it?

Here's the question you need to ask... How closely related are those 12 individuals? Say they are all siblings, ie. they come from the same parent. That would not be random mating, regardless of who mated with who, that would be inbreeding - a form of non-random mating.Inbreeding occurs when individuals are more likely to mate with close relatives, or in genetic terms, are more likely to unite gametes that are identical by descent, ie. inherited from the same parent. The result is a tendency towards homozygosity.So you could have random mating in a population of 12 individuals, but they would have all had to come from different parents. Sometimes, yes, changes in allele frequency is sufficient to explain differences in morphology. But in general, it's just not enough. Something else is needed to produce new species, especially those that are genetically incompatible with the parent population.HBDEdited by herebedragons, : clarity in last paragraph

Most of the time using the term inbreeding is fine, but when discussing population genetics and changing allele frequencies and such, the term has important implications to the discussion. "Interbreeding" would be a more appropriate term for general breeding within a population.Still, the point is that in small populations, inbreeding will affect the genetics of the population. Inbreeding, along with drift, are the main factors that cause small populations to become increasingly homozygous and lead to the fixation of a disproportionate number of alleles. Randomly mating populations tend toward Hardy-Weinberg equilibrium. They may or may not be... it depends on the mutation. Besides, one single mutation is unlikely to cause genetic incompatibility. It is the accumulation of mutations that would lead to incompatibility. Not necessarily. There are several ways of developing reproductive incompatibility. For example, the main characteristic that causes reproductive isolation in Greenish Warblers is mating song recognition. If you took gametes from individuals on opposite ends of the ring and combined them in the lab, they may produce viable offspring (I don't know if they for sure if they can actually produce viable hybrids or not) but in the wild, they don't recognize each other as potential mates and so are reproductively isolated, even though their ranges overlap. How many mutations did that take? Plumage, nesting behavior, and genital incompatibility can also play a role in reproductive isolation. It is not limited to the failure of gametes to form viable hybrids.HBD

Funny... when I first glanced at the image in your post, I thought "That green block is not a clade! Why are they depicting it as a clade?" Then I read the caption... HBD

Exactly, and a major point of my example of RIL populations. The effects that you are expecting in daughter populations cannot happen any faster than they can in a population derived from a single parental line, isolated individually and self fertilized for several generations. That breeding strategy operates at the MAXIMUM potential for fixation of alleles and homogenization.If a system that operates at maximum potential for fixation of alleles and homogenization cannot produce new species in 10 generations (98+% homogeneous populations), how could a wild population do it... that is if isolation and changing allele frequencies are enough? Nonsense. The initial parental cross distributes the alleles to the offspring as predicted by Mendelian genetics. Each RIL begins with a single individual or breeding pair which would have an allele frequency for each gene. In the case of an individual, allele frequency would be 0%, 50% or 100%. In the case of a breeding pair, allele frequency would be 0%, 25%, 50%, 75% or 100%. So each RIL starts with an allele frequency that may or may not be different than the parents at each gene loci. For sure the combination of alleles across all genes will be different in every single RIL individual. What is important is taking those alleles to fixation. How would having a different allele frequency produce different phenotypes? What needs to happen is one population needs to be fixed for allele 'A' and the other fixed for allele 'a'. You have mentioned this yourself, that the other traits, the other alleles need to be eliminated from the population in order to have differentiation. So fixation of alleles is what is important to differentiating populations. RIL is the most efficient method for doing that across many loci.BTW, I already mentioned that this system is used for animals... it is how laboratory mice and rats are produced. They use sibling crosses rather than self crosses, but otherwise it works using the same principles. Sibling crosses would actually result in a slower rate of homogenization and fixation than selfing, but still would operate much faster than a wild population.And don't forget, as a wild population grows, the effect of inbreeding will be reduced and the process will slow even further.And... you yourself have recognized this system in breeding programs. Isolate and breed within a small population until desired trait is fixed. The main differences in a RIL population and a standard breeding program are:1. The RIL program produces homozygotes and fixed alleles much faster than traditional breeding approaches2. The RIL population is not selected for any specific trait (ie. there is no directional selection)3. The RIL population consists of numerous (hundreds) or lines, each with its own unique set of traitsYour objection to this being done with plants is unfounded. For one, it can and is done with animals. Secondly, genetics of plants and animals operate in the same way. They undergo meiosis and mitosis; they reproduce sexually; they undergo recombination; they respond to inbreeding, outcrossing, bottlenecks, selection, drift, etc. the same way animals do. If fact, most of what we know about population genetics and breeding comes from plant systems. Plants are easy models to work with that don't have the same ethical implications that animal models do.RIL populations demonstrate, beyond a reasonable doubt, that isolation and changing allele frequencies alone are not enough to produce new species.HBD

Another example of a reproductive barrier would be the timing of mating season. Let's say we have two populations of foxes. One in the north and one in the south. Litters in the south are born in late February to early March, but in the north conditions in late February may not be suitable for giving birth. The population in the north adapts to the conditions by mating later so that litters are born late March to early April. If these populations then come together for some reason, they may not be able to interbreed because their reproductive cycles are not syncronized.How many mutations would that take to shift the mating season to 3 or 4 weeks later?What allele frequencies would each population need to have in order to have different mating seasons?Why would you think allele frequency is a good explanation for that type of adaptation?HBD

And so begins the insults... I assume that means you have no answer to my critique other than you can't understand it, it seems irrelevant and I am being pedantic.Got it. I'll stop now.Anyone else have a relevent response?HBD

Look, I get it that you don't understand basic population genetics concepts. However, I have no doubt that you could if you were only willing to give up your misconceptions about how population genetics work and actually learn about the concepts. But alas, you are only willing to dip your toes in and not go any deeper than that. The problem is that by dipping your toes in, you think you know what the whole ocean is like. I bring what I want to the discussion. I already explained that this same thing works for animals such as laboratory mice and rats and is routinely used for that. Also some plants are not self-fertile and so are done using the sibling-cross method. Same thing...Your objection regarding plants is unfounded dismissal. I study population genetics, not as my main subject, but as a specialty within my main subject. Why shouldn't I be confident? You're a Trump supporter aren't you? Good DayHBD

Odd... nothing you have said thus far has given me any indication that you have training in the biological sciences. Granted. I also accept creation. I believe that the God of the Universe created all that is and all that will be.I also accept evolution as the best explanation for the diversity of life we have on earth.Not incompatible. Only incompatible with certain interpretations of the Bible. Science and creation and not incompatible with one another. If, for example, we share a common ancestor with chimps... so what? It doesn't make me any less human nor does it change the relationship between God and myself. If you insist on a particular interpretation of that relationship, then yes, it could be incompatible.HBD

Everywhere I used the word "plant" substitute the word "mouse." And everywhere I mention "selfing" substitute the word "sibling cross." No one does Faith, it's stuff that is made up in your own head. Maybe if you could provide a mathematical model or diagram the process so we could see where we are going wrong as far as understanding what you are saying.HBDEdited by herebedragons, : grammar

Forget about mutation for now... that doesn't have to be part of the discussion yet. If all you are arguing for is two populations that look different, it is a very trivial point. But we have much more than a collection of populations that "look different." Even if we limit our idea of speciation to "within a kind" there is a lot more going on than populations that "look different." Example: Felidae, the "cat kind" Focus on this part for now. Describe, using allele frequencies, how this would play out. Maybe do this for 10 genes or whatever you think necessary to make your point. Describe allele frequencies of the parent population and daughter population. I don't think so, it is just now happening (2:30 EST) where I live, so you should have a couple more hours before it peaks there.HBD

The point is... if I do it, it will prove you wrong... and then you will accuse me of not understanding your argument.If you don't know how to do it... then I don't see how you can be so confident in your conclusions. The point you are trying to make now and the one PaulK probably "admitted" to is trivial. We have always agreed that selection would reduce genetic diversity; and that new phenotypes come about with selection. That's trivially true. It is how breeding works.And if that was the entirety of your point, there would be no argument. But it's not, is it?You claim that this process, of which we trivially agree is true, is how evolution occurs and is how the diversity of species is explained. And that is what we (PaulK included, I'm sure) would disagree on and is the larger point of my argument.HBD

Yea, I found an automation of how the eclipse traveled across the country and I didn't realize that's how it went. Hmmm. It only got a little dim here for about 20 minutes, like a hazy day. Hardly noticeable.

Show me the data... or the math...You show me HOW your process works, not just tell me it does. I could show you how it really works, but that would be "irrelevant and pedantic."Once I see how the math works I will be able to see where I "misunderstood" your process.I contend that removal of alleles or "loss of genetic stuff" is insufficient to produce a new species. I went to significant lengths to demonstrate that with my example of how RIL populations are made. They maximize genetic loss and allele fixation, and yet... no speciation. There is something missing in your process.Show me how it works.HBD

Uhmmm.... The development of breeds, varieties and species by loss of genetic diversity is EXACTLY what you are arguing.If all you are trying to do is convince us of how a breeding program works, then you are wasting your time. But you're not... you are trying to extrapolate how you think a breeding program works to natural systems - and you're wrong to do that. You have obviously NOT proven that. That is the claim. Evolution has NOT come to a halt... how can you even claim that when you are supposedly not even arguing that speciation requires a loss of genetic diversity? If you allow that speciation can occur without loss of genetic diversity, then you have no claim as to the "end of evolution."If you are not claiming that loss of genetic diversity is required for speciation, then that leaves it open that it might require a GAIN in genetic diversity to cause speciation. Would you agree that a gain is required? No, you have vehemently opposed that idea. In fact, you claim that genetic diversity CANNOT possibly increase.With my example of RIL populations, I have demonstrated beyond a reasonable doubt that loss of genetic diversity does not cause speciation. So if loss does not cause speciation and gain cannot be the culprit, what could? Staying the same?It is obvious that your claim is that speciation requires a loss of genetic diversity, but that is demonstrably false. Are you willing to concede that genetic loss does not and cannot lead to speciation? But you cannot demonstrate this... mathematically or otherwise. All you have is what you THINK happens. But you should be convinced by now that there is more to the story of genetic diversity, selection, and speciation than you originally thought.HBD

You are not considering divergence. The parent and daughter populations diverge and develop along separate evolutionary paths. Think about it.HBD