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Author Topic:   Molecular Population Genetics and Diversity through Mutation
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


Message 23 of 455 (784873)
05-24-2016 11:08 PM
Reply to: Message 8 by Faith
05-24-2016 4:29 PM


Re: Fitness graphic
There are conditions in which populations are stable, that is, NOT EVOLVING, which is what Hardy-Weinberg is describing. It is actually described AS not evolving.
Hardy-Weinberg is based on idealized conditions 1) infinite population size 2) completely random mating 3) no mutation 4) no selection pressure and 5) no migration (gene flow). It is not intended to describe any real populations as there is no populations that would fully meet these 5 conditions. The equation is used to identify what forces are acting upon a population since any of these conditions not being met would cause deviations from HW equilibrium.
Geographic isolation prevents or limits gene flow, but by itself, isolation does not bring about genetic change. All combinations of alleles present in the daughter population are also present in the parent population. Below is an example of a subpopulaton derived from a parental population complete with the loss of 2 alleles in the subpopulation due to sampling error (ie., those alleles were not represented in the founding population that established the subpopulation or perhaps they were lost to drift shortly after establishment).
Parent: {90% a1, 10% a2, 60% b1, 40% b2, 40% c1, 60% c2, 10% d1, 90% d2}
Subpopulation: {60% a1, 40% a2, 100% b2, 60% c1, 40% c2, 100% d1}
What genotypes exist in the subpopulation that don't exist in the parental population?
Again, what I am focusing on is what happens when you are getting the active production of new phenotypes in reproductive isolation, because that is the clearest expression of evolution,
I think we have all agreed that isolation of a population, especially a small one, will likely result in the loss of genetic diversity. I think we would all agree that selection removes undesirable alleles and so reduces genetic diversity within a population (except in a few special cases where selection can increase or maintain diversity). I think we all agree that drift can bring alleles to fixation and therefore reduce genetic diversity.
But the fact is that this leads ultimately to genetic depletion, yes even with all the additions you can throw at it -- as long as new phenotypes are being produced you are getting a loss of genetic diversity.
But this "genetic depletion" is not something we observe, it is not a thing. There is not this massive lack of genetic diversity in natural systems. Sure there are examples of species where genetic diversity has been depleted (such as the cheetah) but those are the exception not the rule. Your "hypothesis" predicts that we should detect "genetic depletion" in species where there has been rapid speciation or that there are large numbers of species that probably originated from an original population (or common ancestor).
Orchids - 80,000 +/- species... no sign of genetic depletion
Dogs - 100s of breeds... no sign of genetic depletion
Fruit flies (Drosophilidae) - 4,000 species... no signs of genetic depletion
Cats (Felidae) - 41 species... cheetahs have severe genetic depletion, but not domestic cats
So how have these species maintained genetic diversity according to your hypothesis?
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 8 by Faith, posted 05-24-2016 4:29 PM Faith has replied

Replies to this message:
 Message 46 by Faith, posted 05-26-2016 2:38 PM herebedragons has replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


Message 35 of 455 (784896)
05-25-2016 9:38 AM
Reply to: Message 30 by Faith
05-25-2016 4:33 AM


Allele frequency alone is insufficient
If all the alleles in a parent population except one come over to a reproductively isolated daughter population, that will be a reduction in genetic diversity. If the daughter population is significantly smaller than the parent there should be a decrease of more than one allele. Then as higher frequency alleles bring out new phenotypes in the population over some number of generations,
Allele frequency alone is not sufficient to explain evolution (or even microevolution if you wish).
Parent: {90% a1, 10% a2, 60% b1, 40% b2, 40% c1, 60% c2, 10% d1, 90% d2}
Subpopulation: {60% a1, 40% a2, 100% b2, 60% c1, 40% c2, 100% d1}
What genotypes exist in the subpopulation that don't exist in the parental population?
How is this sufficient to explain observed genotypes of species or subspecies?
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 30 by Faith, posted 05-25-2016 4:33 AM Faith has not replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


Message 41 of 455 (784942)
05-26-2016 10:33 AM
Reply to: Message 40 by PaulK
05-26-2016 8:07 AM


Re: Why neutral and deleterious mutations count
Another thing to point out as to why neutral (and slightly deleterious) mutations count...
When we refer to a mutation being neutral, we are specifically referring to the effect of selection. In reality all mutations have an effect on the dynamics of the genome, even if the effect is imperceptible. I got into a discussion several years ago about how stream energy changes when restrictions are introduced (starting here Message 1411). Even a small stone thrown into a river changes the dynamics of the river even though the change may be imperceptible. Keep adding stones and eventually the change will be noticeable. Throw in a large barrier and the change may be immediately noticeable.
Mutations work the same way on a molecular level. Even a single base pair mutation causes a different dynamic - even if that change is imperceptible - and that effect may be independent of its effect on fitness. For example, a G-C pair has 3 hydrogen bonds while an A-T pair has only 2 hydrogen bonds. So a point mutation from an A to a G would increase genomic stability slightly even though it may have no effect on fitness. But add up enough of these neutral point mutations and you can have a noticeably different genome.
Now consider a large mutation such as a duplication. The duplication may be completely invisible to selection, and therefore neutral, but it significantly changes the dynamics of the genome. For one thing, there are more bases to duplicate, so more energy and resources are consumed in replication. This may seem insignificant at first but consider the amount of repetitive regions in genomes and it can really add up. In addition, since the duplication is invisible to selection, it can freely accumulate mutations until it does have some type of fitness effect.
So, while mutations may be neutral in regard to fitness, there are not neutral in regard to the genome. Mutations count whether they are neutral or not.
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 40 by PaulK, posted 05-26-2016 8:07 AM PaulK has not replied

Replies to this message:
 Message 43 by Faith, posted 05-26-2016 2:04 PM herebedragons has not replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


Message 52 of 455 (784972)
05-26-2016 4:03 PM
Reply to: Message 46 by Faith
05-26-2016 2:38 PM


Re: You are looking at the wrong part of the system
When you have a population of over a million individuals, say of black wildebeests, you are probably getting something like Hardy-Weinberg equilibrium in reality.
Yes, "probably" "something like" HW, if all the conditions meet the HW assumptions; 1 million individuals is pretty much an infinite population size, and if all other assumptions were met then geneotypic frequencies would be very close to HW equilibrium. Also keep in mind that HW is calculated for a single locus. The gene for coat color may be in equilibrium while the gene for horn length may be under selection and so the genotype frequency may be out of equilibrium.
And even Genomicus agrees, which is why I prefer to debate her rather than anyone else here:
First off, I have agreed with you on occasion as well such as in the very post you are responding to.
HBD writes:
I think we have all agreed that isolation of a population, especially a small one, will likely result in the loss of genetic diversity. I think we would all agree that selection removes undesirable alleles and so reduces genetic diversity within a population (except in a few special cases where selection can increase or maintain diversity). I think we all agree that drift can bring alleles to fixation and therefore reduce genetic diversity.
But your claim goes beyond those things, and when I address them, you say they are irrelevant. If your whole argument is that a population split can (and usually does) reduce genetic diversity, then the debate is over and we all agree.
A change in gene frequencies does indeed bring about genetic change, it's even given as a definition of evolution. Put Evolution as a change in gene frequency into Google. The first line of the Berkeley page on the subject says Microevolution is a change in gene frequency in a population.
And even Genomicus agrees, which is why I prefer to debate her rather than anyone else here:
Genomicus in message 22 writes:
... I should also add that new phenotypes can arise through novel allele combinations in a diploid organism, so this wouldn't technically be a mutation.
A couple things are being conflated here.
1) The Berkeley page refers to microevolution, which means evolution WITHIN a population. Changes in allele frequency causes the phenotypic composition of a population to change over time. This could even apply to sub-populations, as you are doing, which may be considered a subspecies, a variety, a morph, etc.
2) Genomicus said that "new phenotypes can arise from novel allele combinations" not that new genotypes could arise. And I agree with that, novel phenotypes can arise and become more prevalent as allele frequencies change. But new genotypes do not arise from changing allele frequencies. What new genotypes exist in the daughter population that don't exist in the parent population for the following example?
Parent: {90% a1, 10% a2, 60% b1, 40% b2, 40% c1, 60% c2, 10% d1, 90% d2}
Subpopulation: {60% a1, 40% a2, 100% b2, 60% c1, 40% c2, 100% d1}
Changing allele frequencies and eliminating alleles does not create new genotypes.
You insist on talking about the ENTIRE population of a species, which I'm NEVER talking about. Sure you can have lots of genetic diversity in the whole population
No, I am talking about speciation. Although you keep referring to "sub-populations" and avoid calling them separate species, that is what your hypothesis is attempting to explain right? How we went from a single mating pair to all the species (or sub-species) that we have today. Your hypothesis requires that when new species are formed, genetic diversity is removed until evolution comes to an ultimate standstill because it is utterly depleted of genetic diversity. The examples I gave are meant to show that is not what we observe in natural populations. There is not "genetic depletion" despite thousands of population splits.
What you are failing to get is that I'm only talking about EVOLVING populations, that is, populations where you are getting new phenotypes due to new gene frequencies, which requires losing alleles for competing phenotypes.
I get it, Faith, I get it. But that's not the whole story, is it? How does your "genetic depletion" hypothesis explain how we got from an ancestral population (parental) to the species of the genus Canis ( the grey wolf, coyote, red wolf, and several species of jackals). Or how about the species within the genus Drosophila? Or any other genus of plants, animals or fungi that you care to address. How does shuffling alleles around create those different genomes?? (in less than 4000 years, no less)
the processes of EVOLUTION, meaning the production of new species or subspecies from whatever genetic diversity is present, MUST reduce genetic diversity. Evolution itself must bring evolution to a stop.
You must be missing something because this "bringing to a stop" bit is not observed in natural populations.
(Windows 10 doesn't let me copy links or I haven't figure out how to yet)
You updated to Windows 10, huh? I remember when you were debating about upgrading and I meant to advise against it, but didn't get the chance. How is it working out so far? I would guess you will probably want to upgrade your memory to the maximum your setup will allow in order to keep it from bogging down really bad.
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 46 by Faith, posted 05-26-2016 2:38 PM Faith has replied

Replies to this message:
 Message 54 by Faith, posted 05-27-2016 4:31 AM herebedragons has replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


(1)
Message 63 of 455 (785059)
05-27-2016 1:32 PM
Reply to: Message 54 by Faith
05-27-2016 4:31 AM


Re: You are looking at the wrong part of the system
This quote from the Wikipedia article on Genotype Frequency doesn't treat the H-W equilibrium as an ideal but as a reality.
My statement about Hardy-Weinberg is correct regardless of what you think Wikipedia seems to be saying.
Another point... a population, such as your wildebeests, could be a stable population (not undergoing evolution) and still not be in HW equilibrium, but to show how that would work I would need to use maths... so, you'll just have to take my word for it.
Microevolution means "evolution within a population???" I have NO idea what you are saying. Microevolution IS evolution, it's what is happening wherever new varieties or subspecies are being formed from new gene frequencies.
You quoted a statement from Berkeley but don't even understand how they use the terms they are using?
Defining microevolution
quote:
Biologists who study evolution at this level [microevolution] define evolution as a change in gene frequency within a population.
You have absolutely lost me. You are talking gobbledygook as far as I can tell, making unimportant distinctions as far as my argument is concerned. It is "gene frequency" not "genotype frequency" that is defined as evolution, and it's evolution I'm talking about.
Ok, first of all, I said "genotypes" not "genotype frequency." I am asking what genotypes exist in the daughter population that do not exist in the parental population. Answer: none. In my example (of a loss of alleles due to a sub-population split), all the genotypes in the daughter population exist in the parental population. I am asking you to account for how daughter populations could have unique genotypes (genotypes that do not exist in the parent population). In order for this to occur, there would need to be new alleles introduced, no?
And secondly, this is an example of why I think you are being intentionally obtuse. You claim to understand topics like Hardy-Weinberg better than I, or at the very least you call my points about the subject "gobbledygook" and yet you claim that you don't get the connection between allele frequency, Hardy-Weinberg and genotypic frequency. If you talk about allele frequency and Hardy-Weinberg, you ARE talking about genotypic frequency. Since you obviously know that, your failure to comprehend my point is evidently feigned.
What IS the problem? Extrapolating back from the loss of genetic diversity brought about by selection, random or artificial or natural (it's all the same effect), I add back the genetic diversity lost down the generations and arrive at LOTS of genetic diversity at the starting point from which all the types and breeds descended. A lot more heterozygosity I've many times suggested. WHAT'S THE PROBLEM?
WHAT'S THE PROBLEM? You don't recognize that there is a lot more differences between the genomes of Drosophila melanogaster and Drosophila erecta or between Canis lupus and Canis aureus than a just reduction in heterozygosity. I am asking you to explain how your hypothesis of genetic depletion explains those differences.
It would be if you understood what I'm talking about and looked in the right place for the right evidence.
Of course... that's the problem.
It's obvious that your responses to me are designed to end the discussion between you and I. If you don't wish to further our discussion, then just don't respond to me. Pretending to not understand so that you don't have to address my points is just silly nonsense.
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 54 by Faith, posted 05-27-2016 4:31 AM Faith has replied

Replies to this message:
 Message 65 by Faith, posted 05-27-2016 1:48 PM herebedragons has replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


Message 78 of 455 (785140)
05-28-2016 9:20 AM
Reply to: Message 65 by Faith
05-27-2016 1:48 PM


Re: You are looking at the wrong part of the system
You aren't going to get "new" genotypes, just a new frequency of genotypes.
Precisely! That is exactly my point. But we need to explain new genotypes... how do new genotypes arise? So, back to my example of cytochrome C (cytC). This is a coding gene that is widely used for species identification, aka. a bar coding gene. (Note: unfortunately it is not a universal bar code meaning it doesn't work with all types of organisms. We don't use it for fungi, for example, but it is widely used for plants and animals). Every species has a unique cytC sequence(s) that can be used to identify an organism as a member of a species. Say you discover an organism that you are not quite sure what species it is, maybe it has a unique morphology or form that makes it difficult to place it with a particular group. Or maybe the distinction between species requires the analysis of very obscure characteristics. You could sequence the cytC and compare that sequence to a database in order to identify what species the organism is.
OK, let's start with a single mating pair with maximum number of alleles at the cytC locus - a, b, c, d. These alleles could segregate into sub-populations so that 4 species, subspecies, varieties, breeds, whatever you want to call them have a unique cytC identifier.
THE PROBLEM. There are many, many more species than 4 that would have come from a single ark pair. Even working from the genus level in Canis or Drosophila, there are dozens of species with unique cytC sequences. Even being generous and considering there to be 10 actual unique species within each of those genus, that would mean there needs to be 6 alleles of cytC that have arisen since the ark kind.
Yes, your hypothesis would only involve shuffling alleles around and altering allele frequency, which is sufficient to explain evolution within a population, that is, how a population with brown fur becomes a population with white fur. But it is a small part of the big picture and it doesn't explain how we have the actual genetic diversity that we observe today.
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 65 by Faith, posted 05-27-2016 1:48 PM Faith has replied

Replies to this message:
 Message 84 by NoNukes, posted 05-28-2016 9:56 PM herebedragons has not replied
 Message 124 by Faith, posted 06-03-2016 1:52 AM herebedragons has replied
 Message 136 by Faith, posted 06-03-2016 7:38 PM herebedragons has not replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


(3)
Message 140 of 455 (785416)
06-04-2016 11:42 AM
Reply to: Message 124 by Faith
06-03-2016 1:52 AM


Trying to clarify cytochrome C
Ok, first off I made a mistake in describing the situation with cytochrome C. CytC is a mitochondrial gene which means it is haploid, so there would not be two copies in each organism, but only 1. It is also inherited primarily through the maternal line, so there is no recombination with the male counterpart. So in reality we would expect only 1 haplotype to exist in the original ark pair - although I could be open to the idea that multiple sequences existed in the same organism.
This explains, in part, why the study Genomicus cited showed increasing genetic diversity while other reports suggest that the population has not recovered from their genetic bottleneck. Elephant seals are highly polygamous, meaning that a single dominant male will fertilize between 30 and 100 females. This greatly reduces the effective population which in a population with only a few dominant males getting all the action, the effective population could be as low as 1/10th the actual population. In addition, the dominant male would be breeding with his own daughters and granddaughters further increasing homozygosity. Mitochondrial DNA does not have these problems. So it should be clear why the discrepancy between the two systems.
But I digress...
So back to cytC.
So each separate breed of dog has its own unique cytC sequence? You can identify, say, a spaniel from a wolfhound from a poodle by their own unique sequence?
Yes and No. Theoretically you should be able to trace a lineage through the maternal line, so in that way, yes, each breed or more precisely, each breeding population should have its own identifying sequence. However, the amount of differentiation between sequences is probably not sufficient to identify a specific breed. The other complication is that contrary to what you are suggesting, the main way that new breeding lines are developed is by the introgression of desirable traits into a preferred genetic background and then selecting for those desirable traits (think 'gene flow'). Rather than 'muddying the waters', gene flow provides variation for which further evolution can operate. How this complicates the cytC situation with dogs, or other breeding programs, is that if a trait was introduced from a male parent, there would be no mitochondrial record of that introgression. So mtDNA (mitochondrial DNA) has its uses in breeding programs, but it is not used for ID.
Or a Persian cat from Siamese? Or from a lion, or a lion from a tiger?
A grizzly from a polar bear?
Persian from Siamese - Probably not. Same deal as with dogs above - although I don't think cat breeding history is as complicated as dogs.
House cat from a lion - Yes
Lion from a tiger - Yes
Grizzly from a polar bear -Yes
Rat from a mouse - Yes
Below is an alignment of a rat sequence and a mouse sequence. Where there are not vertical bars between the sequences indicates a difference in sequences - ie. a mutation.
IIRC, the sequences had 95% or 96% identity. So if I had a sequence and wasn't sure what it was, I could compare it to a database and I might find that it matched 99% with a mouse sequence and 95% with a rat sequence and I could conclude the sequence was from a mouse.
If I did the same thing with a dog sequence, I would probably return dozens of sequences from many different breeds that had 99% identity, so while they may be different and even unique, it would not be conclusive enough to assign the sequence to a specific breed. However, it may be different enough from a wolf and certainly would be from a coyote or a fox.
*******Side topic alert*********
You can eliminate drosophila from the list because God didn't command Noah to save insects or bacteria, or even plants for that matter, although I'm willing to think about plants.
This is what puzzles me about literalists.
quote:
Gen 7:21 - 23
And all flesh died that moved upon the earth, both of fowl, and of cattle, and of beast, and of every creeping thing that creepeth upon the earth, and every man: All in whose nostrils was the breath of life, of all that was in the dry land, died. And every living substance was destroyed which was upon the face of the ground, both man, and cattle, and the creeping things, and the fowl of the heaven; and they were destroyed from the earth: and Noah only remained alive, and they that were with him in the ark.
*Literally* "every living substance was destroyed" and "all that was in the dry land, died." which includes "every creeping thing that creepeth on the earth,". I guess I understand plants not being on the list, but insects? It is abundantly clear that ALL animal life was completely wiped off the face of the earth, yet literalists want to interpret this in some other manner than a simple, straightforward, literal reading.
******end of side topic******
The more I think about this the less sense it makes.
The problem is that rather then looking at the evidence at determining what it tells you, you are trying to get it to fit the narrative you have created. I can understand why it would not make much sense.
1) These alleles are species identifiers, you say, so how is it that two individuals of the same Kind/Species would have four different species-identification alleles among them?
They wouldn't. I was trying to fit these observations into an imaginary scenario (and by imaginary here I simply mean that rather than being able to go somewhere and learn about this hypothesis of yours, I have to imagine what it means. Whether it is imaginary in the sense of being not real is what we are discussing).
2) When that pair mates, say they are dogs, they aren't going to have four new species or even one new species, they are going to have a litter of puppies. Which should all have the same cytC identifier since they are all of the same Kind/Species, shouldn't they?
3) After they grow in numbers to a sizeable population then they might split off into subpopulations and eventually become new subspecies of dogs. But they'd all still have the cytC identifier for Dogs, wouldn't they?
What are you saying? That when a new subspecies emerges, at some point it gets a new cytC identifier? What would bring that about? At what point would you expect it to emerge in the process of its evolution?
Just to be clear, cytC does not determine the species, it identifies it. Meaning there is nothing about the sequence that gives an organism its unique phenotype. cytC sequence changes occur independently of what is happening in the nuclear genome.
Mutations in the cytC gene accumulate in step-wise fashion. Within a breeding population, there will be some variations in sequence; not all members will have identical sequences. Perhaps a sub-population splits off from the main population. This sub-population will continue to accumulate changes, but these accumulated changes will be different from the parent population. Over time the sequences of the two populations will be recognizably different. During this same time, changes are also occurring in the nuclear genome. When these changes in nuclear genes are sufficient to prevent (or minimize) interbreeding with the parent population, the changes in cytC have diverged sufficiently to be used to be identified with that new species or subspecies.
Another thing to clarify, there is nothing specific about a cytC sequence that allows one to identify the species, it is comparison to known samples from a database that provides identity. If no representatives from a species has ever been sequenced, a search may present no close matches. It this case, you may be able to say that it is closely related to some other species, but not a close enough match to identify it as a specific species.
This can be a powerful tool in understanding the history of a species and what has driven its evolution. If a pattern and pace of nucleotide changes have occurred in the cytC gene since a population diverged, one would expect similar changes to have occurred in similar nuclear regions. If they haven't, if the pattern and pace is significantly different that expectation, it is an indication of one of the evolutionary forces at work. Often a gene tree will be developed based on a region such as cytC (the standard now is 4 or more independent regions) and other traits will be overlaid on the tree to study how they have changed or how they vary in different species.
I know you probably think this is completely irrelevant to your argument, but its is relevant. The patterns we observe require an explanation. Here's where that comes in...
All I can think is that if it is a species-identifier then it is a Dog identifier, not a dog-breed identifier, in other words it is an identifier of the Biblical Kind or Species. If that's the case then it would make a wonderful way of defining what a Kind is.
Yes, that would be the expectation, wouldn't it. Based on what I have said about the system in this post (hopefully it is a bit clearer) how would you predict that one could distinguish between "kinds" using this method? Saying that the sequence of a dog should be more similar to another member of the dog kind than it would be to a cat kind is not enough, since that is also what the ToE would predict. How would you predict that there would be disparity between the kinds? How would you recognize different kinds?
I think if nothing else, this should make it clear that mutations do occur and accumulate. I know you have allowed for "some kind of mutation" meaning... I don't know what. Yes, the mutations in cytC are essentially neutral, which is maybe the "some kind" that you allow for. But, the bigger point is that we see this same pattern at play in nuclear coding genes. But we'll have to cover that later, once you understand the point about cytC and how it is used.
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 124 by Faith, posted 06-03-2016 1:52 AM Faith has replied

Replies to this message:
 Message 143 by Faith, posted 06-04-2016 3:01 PM herebedragons has replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


(1)
Message 145 of 455 (785432)
06-04-2016 7:46 PM
Reply to: Message 143 by Faith
06-04-2016 3:01 PM


Re: Trying to clarify cytochrome C
Then how could it possibly be a species identifier?
Maybe you could try reading the whole post before you begin replying?
Fine, you've explained the discrepancy but not solved the problem of whether there is increased genetic diversity or not. Seems to me that the mitochondrial DNA measure in fact says nothing about the true situation,
mtDNA is also a "true situation." The inheritance patterns for cytC don't have the same problems as nuclear genes do, that is, they aren't affected by the same evolutionary forces as nuclear genes are - they are pretty much only affected by mutation.
Obviously the mitochrondrial DNA method is useless as a measure of genetic diversity so why is it used at all?
Did you read the paper that Genomicus cited? What did they use it for? What sort of things did they detect from their study.
Maybe that study wasn't the best example to show an increase in genetic diversity because of the confounding factors, but it does nicely show an increase in genetic diversity that is due to ONLY mutations.
How are you getting any "differentiation between sequences" at all in the first place?
Mutation. If you would have read the entire post before replying it would have been clear.
That entire paragraph is absolute gobbledygook to me.
Standard go to response. I am still convinced you are being deliberately obtuse.
What I've described of breeding practices is so well known, not only is this statement undecipherable, but insofar as it aims to contradict what is well known it's ridiculous.
I take it you have experience with a breeding program, since breeding is "so well known" to you? If so, then you should know what introgress and genetic background means. But... introgress means to introduce a trait from a different species, breed, or a wild relative and then backcrossing until it is a fixed part of the target genome. Genetic modification is an example of this where a specific gene (and only a specified gene) is introduced into a breeding line. If you have a line that say has high yield and high protein content, this would be the genetic background. These are the traits you want to maintain in your new variety.
But say this line is susceptible to a disease that is becoming an increasing problem. And say there is another variety that does not have the desirable yields or has some other undesirable characteristics but is resistant to the disease in question. A breeder will breed the two varieties together and do several backcrosses until that desirable trait (disease resistance) has 'introgressed' into the desirable genetic background. Then they will use selection to develop the new variety.
Not only does it not tell me anything about why I'm wrong about breeding practices, it doesn't tell me anything at all about breeding methods, period.
You only focus on the selection part, but where does the variation come from? You claim the variation is always there, built in, but you have NO support for that idea other than your narrative that it must be so. You have also claimed that gene flow "muddies" the breed, but in fact that is not the case. A breeder will introduce new variation into a breeding line so that new traits can be selected. The creation of new breeds or varieties requires new variation not reduced genetic variation. Breeders introduce this variation artificially while in nature variation is introduced via mutations (although mutation does play some role in breeding and crossbreeding does play some role in nature).
But you've said absolutely nothing about how these different species get or don't get a particular species identifier. Ordinary reproduction should pass on the same identifier indefinitely, so in related species how do they get different identifiers?
Mutations that are passed on to the offspring which then accumulate new mutations which are passed down to their offspring which then accumulate more mutations which are passed on to their offspring, etc... over many generations the sequences are distinguishable from the original parental sequences. I already said this...
That is a completely gratuitous unfair accusation.
I didn't mean it as an insult, I can see why this would not make sense to you... it doesn't fit you idea of how genetics work.
I'm doing my best to understand your completely garbled presentation of these things.
No you're not. You are trying to find reasons to dismiss it, to ignore it. Claiming it is completely undecipherable is the only thing you can come up with at this point.
Maybe you should just try explaining what you know instead of making up straw men.
Make up your mind.
Faith writes:
Perhaps you could try thinking like a YEC for a moment, maybe you'd come up with the explanation.
But then when we do...
Faith writes:
Maybe you should just try explaining what you know instead of making up straw men.
Ok. Here's what I know... Your idea about how genetics works is totally crap and has absolutely no explanatory power. It matches nothing we observe in population genetics and doesn't even work mathematically.
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 143 by Faith, posted 06-04-2016 3:01 PM Faith has replied

Replies to this message:
 Message 146 by Faith, posted 06-05-2016 5:18 AM herebedragons has replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


Message 147 of 455 (785438)
06-05-2016 7:19 AM
Reply to: Message 146 by Faith
06-05-2016 5:18 AM


Re: Trying to clarify cytochrome C
Rage????
I realized long ago that one of your strategies for replying to me was to try and elicit an emotional response and I don't allow you to goad me into that kind of response. The most emotion you should get from my response is annoyance. I'm in a rage, really? That's the best response you got????
HBD
Edited by herebedragons, : typo

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 146 by Faith, posted 06-05-2016 5:18 AM Faith has replied

Replies to this message:
 Message 148 by Faith, posted 06-05-2016 7:22 AM herebedragons has replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


Message 149 of 455 (785441)
06-05-2016 8:04 AM
Reply to: Message 148 by Faith
06-05-2016 7:22 AM


Re: Trying to clarify cytochrome C
Right. I am bad at explaining things. I have a bad personality. I am a bad psychologist. I am a bad Christian. What else did I miss?
How about responding to the arguments rather than attacking my character. I find it hard to believe you don't have a clue what I am talking about.
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 148 by Faith, posted 06-05-2016 7:22 AM Faith has replied

Replies to this message:
 Message 152 by Faith, posted 06-05-2016 12:08 PM herebedragons has not replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


Message 158 of 455 (785484)
06-05-2016 11:02 PM
Reply to: Message 157 by Faith
06-05-2016 9:54 PM


Re: You are looking at the wrong part of the system
The way added mutations could mess up a breed is by changing major characteristics. If you've been working for decades to get a perfect purebred Whozit you don't want a mutation to pop up for a Whatzit. You DO NOT WANT this new trait in your breed.
Easy solution. Don't use your newly mutated Whatzit to breed your next generation of Whozits. It happens. Breeders have good breeding stock and stock that they don't breed because it has a Whatzit look to it.
ABE:
And this is after the Whozit breed has been pretty well established, so that it's ALREADY lost genetic diversity in its formation, which is NECESSARY to its formation. What you've got is a LARGE net decrease in genetic diversity with respect to former populations from which it was derived.
What if I had a Whozit breed and I wanted develop a new breed from that called a Howzit? What would I do to go from a Whozit to a Howzit?
HBD
Edited by herebedragons, : No reason given.

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 157 by Faith, posted 06-05-2016 9:54 PM Faith has replied

Replies to this message:
 Message 162 by Faith, posted 06-06-2016 7:37 AM herebedragons has not replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


(2)
Message 182 of 455 (785569)
06-07-2016 8:41 AM
Reply to: Message 180 by Faith
06-07-2016 3:07 AM


Re: Mt DNA and microsatellites as measures of genetic diversity
I appreciate your previous reply to me and I plan to go back and answer some of those questions, but I am at a conference this week and don't think I will have time to do so until the weekend. But I wanted to touch on a couple things in this post real quick (I hope)
Pretty standard definition here. Polymorphic loci, many alleles per locus I take into account as a matter of fact as where most loss of genetic diversity occurs; Heterozygosity, alleles per locus, exactly what I've been talking about.
True genetic diversity would need to be measured over the entire genome, not at just a few loci. Currently this is just not possible to do. So we need a measure - a proxy of genetic diversity. Heterozygosity is one proxy that is used for overall genetic diversity, but it needs to specify what loci it is measuring and then all it can really say is the amount of heterogeneity at those loci. If those loci are chosen properly, then it can represent the genetic diversity of the entire genome, but it is not the actual, true diversity.
Think about it... let's say an organism has 20,000 gene loci and 100 of them are fixed (homogeneous) while the remaining 19,900 are polymorphic (heterogeneous) - that's the true situation (but you don't really know this - it is what you are testing for). Now you choose 4 nDNA (nuclear DNA) loci that determine key characteristic traits of said organism and find that they are all monomorphic (homogeneous). What does that say about the genetic diversity of the organism?
Interesting that there's no mention here of MtDNA or microsatellites either.
Wikipedia is fine for general information or as a general reference, but it doesn't trump actual scientific articles. The journal article cited used mtDNA as a measure of genetic diversity, the fact that Wikipedia fails to mention that as a suitable measure does not make the use of mtDNA questionable. Can you cited a scientific article that questions the utility of using mtDNA as a proxy, or a measure, of genetic diversity?
These different measure of diversity tell us different things - they are not all measures of exactly the same thing. As my example above shows, even using nDNA can give misleading results. Understanding what the different measures tell you is key to understanding the results. I will try to come back to this point later (when this conference is over) and respond to your last reply to me.
Then it must agree with the normal ways of measuring genetic diversity or it's of no use anyway, and assuming it does agree I'll stick with heterozygosity and number of alleles per locus.
OK, you know what this sounds like? "I will stick with what agrees with me." Rather than that, you should try to understand how researchers use these different measures and what they mean.
Your reference on the elephant seals found high genetic diversity, which has to be some kind of delusion
Wrong. They did not find "high" genetic diversity. They found increasing genetic diversity. Big difference. The point of that citation was to illustrate that genetic diversity could increase despite isolation. Just because you don't accept mtDNA as valid is irrelevant. As I already pointed out, mtDNA diversity increasing while nDNA is not tells a story about what is going on with the population. The researchers were NOT suggesting that the population was not at risk because of low genetic diversity (however, northern elephant seals are not endangered they are on the 'Least Concern' list). Rather, they were studying the effects of a severe bottleneck and subsequent recovery. This same approach could be used to study the "flood bottleneck" right?
Or there's something wrong with the study
You don't make a case for that except to cite some facts that raise questions about it. Do you know or understand the data they analysed in order to come to that conclusion? Have you raised concerns about there methodology? No, you only doubt the study because the conclusions don't match what you think the conclusion should be. That is an insufficient reason to conclude "there's something wrong with the study."
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 180 by Faith, posted 06-07-2016 3:07 AM Faith has replied

Replies to this message:
 Message 183 by Faith, posted 06-07-2016 11:40 AM herebedragons has not replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


(5)
Message 275 of 455 (785784)
06-10-2016 11:37 PM
Reply to: Message 246 by Faith
06-09-2016 10:18 AM


Re: Situation
Any changes needed by the organism are already available through the built-in genetic possibilities, while the changes being added are either neutral or deleterious. I don't know why this isn't obvious.
Well it's not obvious because it's not true. I came across this study thanks to caffeine's reference to the Runx-2 locus in dogs in Message 252.
Here is the full paper Molecular origins of rapid and continuous morphological evolution
And here is a short article about the paper that may be a bit more accessible Tandem Repeats and Morphological Variation
First, let's talk about microsatellites. Microsatellites are tandem repeats of short sequences of nucleotides, such as ACTACTACTACT which can also be written as [ACT]4 which means that the sequence ACT is repeated 4 times. The interesting thing about these tandem repeats is they can vary greatly in length from one individual to another. They are subject to high rates of mutation because of strand slippage mispairing. Since the same sequence is repeated over and over, when the strands pair up, a repeat on one strand can align with the wrong repeat on the other strand. In other words, say we have 4 repeats - # 1, 2, 3, 4. These should pair up with repeats 1, 2, 3, 4 on the opposite strand. However, mispairing can occur so that 1 pairs with 1; 2 pairs with 3 and 3 pairs with 4. Depending on whether the slippage is on the template strand or the replicate strand, the replication machinery will either insert an extra repeat or delete one. A figure illustrating this is shown below
It turns out that in the gene Runx-2, as well as 16 other genes studied in this paper, the lengths of the microsatellite regions in these genes affect the traits associated with the gene. Runx-2 affects cranio-facial length. Runx-2 is a transcription factor, which means it regulates transcription. Small changes in sequence can affect binding affinity for the target region which would up-regulate or down-regulate transcription.
The image below shows a series of dogs skulls that have considerable variation in cranio-facial features.
quote:
Rapid and sustained evolution of breeds. (A) Purebred St. Bernard skulls from 1850 (Top), 1921 (Middle), and 1967 (Bottom). (B) Purebred bull terrier skulls from 1931 (Top), 1950 (Middle), and 1976 (Bottom) (24). (C) Purebred Newfoundland skulls from 1926 (Top), 1964 (Middle), and 1971 (Bottom). Despite the lack of genetic diversity caused by population structure and history, these breeds are able to continually create new and more extreme morphological variations at a rapid and sustained pace. Analysis of the Runx-2 repeats in the 1931 bull terrier reveals a more intermediate allele (Q19A14) than is present in the modern bull terrier (Q19A13). - bold mine
This alone should be sufficient to frustrate your argument, but I suppose you may still think it is just built in alleles that are being brought out by interbreeding.
So... the researchers sequenced 37 repeat loci of 17 genes in 142 dogs representing 92 dog breeds. What they found was that 10 of the genes had 5 or more alleles and 5 had 12 or more alleles! In addition, they sequenced 3 of these genes in 12 other mammals including the gray wolf, coyote and the red fox. Results of the number of alleles per gene for each species is shown in the table below:
speciesRunx-2Dlx-2Twist-1
dog12512
gray wolf5516
coyote7517
red fox411
Here we have multiple alleles in coding regions that have an effect on morphological characteristics in a series of dogs. Everything your hypothesis says couldn't happen.
Here is the evidence this paper presents that refutes your hypothesis:
> Multiple alleles in a coding gene. Maximum alleles in any single gene within a "kind" should be 4.
> Morphological and genetic changes in fixed breeds over 45+ years. You have claimed that genetic diversity would be depleted limiting further phenotypic change.
> A proven, simple mechanism for a rather large scale mutation. How mutations happen are not a huge mystery.
> Demonstrated mutations that are not deleterious. Most mutations that cause phenotypic change are in regulatory regions. This study provides another way mutations can create phenotypic changes.
> These variations in repeat length are recent alterations as evidenced by purity of the repeats.
Now I can't wait to find out more about the deception of how mutations in MtDNA and microsatellites increase genetic diversity. Just can't wait.
Well, I've shown how microsatellites increase genetic diversity. We can talk about mtDNA later, but this should give you something for you to consider for a while.
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 246 by Faith, posted 06-09-2016 10:18 AM Faith has replied

Replies to this message:
 Message 276 by Faith, posted 06-11-2016 8:50 AM herebedragons has replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


(2)
Message 278 of 455 (785794)
06-11-2016 11:08 AM
Reply to: Message 276 by Faith
06-11-2016 8:50 AM


Re: Situation
I’ve agreed many times that multiple alleles need an explanation, some kind of mutation, so I’m certainly not saying that can’t happen.
So... "some kind of mutation" can increase number of alleles per locus but it does not increase genetic diversity? If you accept that "some kind of mutation" occurs, then what you must really be wondering is how and why these mutations occur and what kind of effect they have on the organism. The paper cited provides a very good example of this and shows very clearly that mutations can provide new variation even within a purebred dog. I guess you agree that mutation can add diversity.
Also, as long as there is any genetic diversity in a breed you can get changes. What I’ve said is that after you have an established breed you don’t WANT any more changes because they mess up the breed.
But you have stated that to get a pure breed you have to eliminate all the alleles for other breeds. So now you are implying that these variations for other breeds actually remain in the pure breed. What this paper showed was a clear mechanism for how variation can arise in an incremental fashion and be selected for in subsequent breeding programs. This was not variation that existed in the earliest breeds that was just recently brought out.
No, what I’ve said is that there is a TREND to genetic REDUCTION down any evolving line, and dogs in particular seem to have so much genetic diversity they might never reach the point of depletion. You've said these breeds are "fixed" but without giving specific information about their level of genetic diversity, homozygosity etc. Perhaps you think that's explained somewhere in this post, so perhaps I'll figure it out if so, but my impression is that you haven't effectively discounted continuing genetic diversity.
Faith, there is only so much genetic diversity to go around. Dogs have been split into so many subpopulations that there is just no way the original mating pair had the amount of diversity that exists within the entire population of modern breeds. But then since you accept "some kind of mutation," you don't need all that diversity in the original pair because some of that diversity is generated by "some kind of mutation." If you originally had 'x' amount of diversity in the original pair and you now have '2x' in the "kind" then you have doubled the amount of genetic diversity, even if individual populations have '0.5x' diversity.
Also, one idea I’ve been pondering and mentioned a few times is that when it comes to intensification of traits this can be the result of strong repetition of the same genotype generation after generation. I think I even read about this somewhere at some time or other. I brought this up in relation to the big-headed lizards and Darwin’s pigeons with exaggerated breasts: neither of those characteristics is in the original population, but seem to be the result of many generations of strong selection of the same genotype. This would not require mutation, and could even occur at fixed loci.
Why would the same genotype provide a more intense phenotype? If a loci is fixed how could selection cause "trait intensification?"
Also, I do still have to cope with your tendency to use jargon: I think I know what "tandem repeats" means but it's jargon and would be a lot clearer in descriptive English.
Oy vey... I figured you knew what 'tandem' meant and what 'repeat' meant and since I explained that microsatellites are repeats that are attached one after another, I didn't really think "tandem repeats" required a definition.
Tandem repeats are repeats that are connected in tandem, such as ACTACTACTACTACT with ACT as the repeat unit.
Faith, what you are trying to argue is evolution that is not evolution, which is a very confusing argument, especially since you are not arguing from data or literature, but from a vague image that you have in your mind about what is happening. It is really hard to wrap my head around this imaginary and often contradictory proposal.
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 276 by Faith, posted 06-11-2016 8:50 AM Faith has replied

Replies to this message:
 Message 279 by Faith, posted 06-11-2016 12:33 PM herebedragons has not replied
 Message 281 by Faith, posted 06-11-2016 1:04 PM herebedragons has not replied

  
herebedragons
Member (Idle past 857 days)
Posts: 1517
From: Michigan
Joined: 11-22-2009


(3)
Message 296 of 455 (785821)
06-11-2016 4:15 PM
Reply to: Message 290 by Faith
06-11-2016 2:43 PM


Re: An allele by any other name
"Allele" implies USEFUL CODING FUNCTIONAL form of a gene, not "neutral" unfunctioning mutations or deleterious mutations. However, I can try to remember to put in some kind of qualifier since evo thinking is nutty enough to confuse the two.
Because you don't understand how the terminology works nor how scientists use terms to describe known phenomenon doesn't make it "nutty." That you trying to come up with new ways of interpreting how new species arise is fine, but using terminology in odd ways is very confusing.
Allele refers to alternate forms of a gene at a given locus. We don't usually refer to genes with mutations in introns as different alleles; we would refer to them as different haplotypes. We also don't refer to different forms of a gene in different species as 'alleles'; we refer to them as homologous. But I haven't really wanted to introduce this terminology because it is somewhat confusing and this topic is already confusing enough. So I have been using a loose definition of allele to mean simply "a variant form of a gene" and including the concepts of haplotype and homology in the term.
But, yes, 'allele' implies mutations or variations in coding regions and more specifically, in the gene product. But as to your assertion that it implies "useful coding functional" not "neutral unfunctioning mutations or deleterious mutations" is nonsense. In the old days an allele referred to the phenotypic effects of different genes, but we are in the molecular age now. We can detect different gene alleles regardless of their phenotypic effects.
You complain that Dr. A is referring to phenotype while you are referring to genotype and then you insist that to be different alleles have to have "useful" phenotypic effects? So what is it, phenotype or genotype? If we are talking about genotype, then the resulting phenotype is not the issue.
Yes I know what tandem means. But you have to know what is being repeated in the first place and I still say "repeat" should suffice without adding "tandem."
Well, the use of the word 'tandem' would be so as to distinguish 'tandem repeats' from other types of repeats such as 'interspersed repeats'. I know scientists have a bad habit of given things odd names, believe me, I have had to learn them. But as caffeine said, they are intended to express a clear and well-defined concept. Often one or two words can convey an entire concept. As I confessed to NosyNed, sometimes I don't even recognize these terms as "jargon." they are just the words that are used to convey a particular concept. If you want to have serious discussions about genetics, it would do you well to learn the terminology.
HBD

Whoever calls me ignorant shares my own opinion. Sorrowfully and tacitly I recognize my ignorance, when I consider how much I lack of what my mind in its craving for knowledge is sighing for... I console myself with the consideration that this belongs to our common nature. - Francesco Petrarca
"Nothing is easier than to persuade people who want to be persuaded and already believe." - another Petrarca gem.
Ignorance is a most formidable opponent rivaled only by arrogance; but when the two join forces, one is all but invincible.

This message is a reply to:
 Message 290 by Faith, posted 06-11-2016 2:43 PM Faith has replied

Replies to this message:
 Message 299 by Faith, posted 06-11-2016 6:36 PM herebedragons has replied
 Message 301 by Faith, posted 06-11-2016 7:08 PM herebedragons has replied

  
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