Microevolution vs. Macroevolution

[Student Nurse]

Last semester I took Microbiology. Before then I was a Christian and believed in creation, but what I studied and what I saw undoubtedly proved evolution - hence the "switchover" or "atheistic conversion" or whatever you want to call it.

I hear a lot of Christians say "the microbiological world proves microevolution" (i.e. evolution on the small scale such as bacteria adapting to new hosts/environments and incorporating plasmids into their DNA in order to become resistant to antibiotics), "but that doesn't prove macroevolution" (ie human evolution)

If this isn't true, then what does it prove to you? How can something be true on the small scale and not on the large? (give examples please)

[Curious]

Not at all. The argument is concerning consistency. Eskimos were unable to interbreed with Africans in the past due to location. The advent of global travel has made these "different species" able to interbreed and so they are said to be the same species. Now let's use the same argument with previously isolated "species". It is now possible to mate these previously isolated "species" and produce viable, fertile offspring. Do these "different species" now become a single species for exactly the same reason?

Biologists define a species as as a group of animals which given the opportunity and willingness, any fertile female in the group could successfully breed with any fertile male member in the group. Inuit and Africans were never different species. The reason why Inuit and Africans did not interbreed for centuries was geographic separation (lack of opportunity and willingness) not genetic inability.
Evolution posits that isolated breeding groups within a species, if isolated for long enough, may evolve into a new species.

But it is also true that species have been defined, not by physical limitations to interbreed, but by geographical limitations. Fecundity varies enormously between individuals of the same species and between individuals of different species.
My objection in this case is to the assertion that 2 strains of a particular fly, which are eventually found to be unable to interbreed, should be said to be necessarily different species. Certain genes, in isolation, have no significant impact on an organism, but are particularly detrimental when combined with other genes. If 2 strains of fly are bred, for the sake of argument, let's say that a gene "deadly A" is present within population 1. In the 2nd strain, imagine that "deadly B" is present.
Due to the small number of parent organisms in either strain, it is likely that either gene could easily become widespread in a particular population. Strain A can quite happily breed with others of the same group with no problem. The same is true of strain B. When strain A attempts to breed with B however, the genetic incompatibility of "deadly A" and "deadly B" shows up. In strain A, the detrimental B was weeded out, and in strain B, the detrimental A was weeded out. In the original population, both were present but were controlled by the other. This genetic incompatibility is seen in individuals within the same species, so I don't see how the same incompatibility can be said to be proof of speciation.
It is entirely possible though, that individuals from either strain could interbreed with members of the original parent population which are not genetically incompatible.
I am not saying that this is always the case, but it does show that inability to breed between particular populations does not prove that speciation has occurred.

[Goat]

If the eskimo's were isolated for a couple hundred thousand more years, they could very well have become another species. However, they are not isolated. They swap genes with other people in north america.

It is you that brought up the 'eskimo' and 'african' example. Yes, it is a poor example, but that is what you came up with. It is known as a 'strawman' arguement.

Not at all. The argument is concerning consistency. Eskimos were unable to interbreed with Africans in the past due to location. The advent of global travel has made these "different species" able to interbreed and so they are said to be the same species. Now let's use the same argument with previously isolated "species". It is now possible to mate these previously isolated "species" and produce viable, fertile offspring. Do these "different species" now become a single species for exactly the same reason?

Isolation is just the first step. The eskimo's were not isolated through enough generations.. and now they are not isolated at all..since they occationally interbreed with other people in Canada and north america.

If you want to purposely misunderstand that, go right ahead.

[Curious]

Isolation is just the first step. The eskimo's were not isolated through enough generations.. and now they are not isolated at all..since they occationally interbreed with other people in Canada and north america.

If you want to purposely misunderstand that, go right ahead.

Please take the statement in context. I say that the definition of speciation changes. In this case, the definition of speciation is altered by logistics. Previously, Eskimos and Africans had no way to interbreed and so would be classed as different species. Now, they can interbreed easily and are classed as the same species.
By saying that I purposely misunderstand, you are calling me a liar. If that is the extent of your argument then perhaps you should look at the data. What exactly have I lied about and what data have I misrepresented? If you wish to cling to the present theory, then that is your prerogative, but don't call those who find fault with it liars just because you are afraid to admit that you might not necessarily have all the answers at your fingertips(ie. a google search).

[Furrowed Brow]

Hello Osteng,

You pointed Studentnurse to a website that outlines a stepping stone argument against evolution.

I'm sorry this post will be long. But I had to challenge the argument given on that post unless anyone gets mislead.

Meaningless or Meaningful
Of course, random mutations (or “letter changes”) to the codes of life do occur quite often in every living thing. These letter changes can result in the evolution of a new type or level of function or in no functional change at all. When no functional change is realized, this is called “neutral evolution.”1 For example, a change from the letter sequence grft to agrft via the addition of the letter a would be a neutral change with respect to meaning in the English language system since both letter sequences are equally meaningless.
The information systems that code for all the parts of living things often have such functionally neutral mutations. In fact, the large majority of all mutational changes are thought to be functionally neutral. What is especially interesting about these neutral mutations is that nature cannot tell the difference between them, since nature only recognizes differences in function, not “spelling.” However, on occasion, a mutation will actually change the meaning or function of a genetic word or phrase.
For example, if the spelling of vacation happened to get “mutated” to read vocation or even vucation, there would be a big change in meaning. Of course the word vucation has no meaning in the English language, but a loss of the meaning of the word vacation might be beneficial in certain circumstances, as would the gain of the meaning of the word vocation. Such meaningful changes, when they happen in the genetic codes of living things, can be detected by natural selection as either beneficial or detrimental. If they are deemed to be beneficial, they are kept for the next generation to use, but if detrimental, they are eliminated from the gene pool over the course of time.

Ok nothing too controversial here: But be aware. Don't let the English language metaphor mislead. The word Vucation has no meaning in English. Thus it might make seem like some permutations of the genetic code will always be neutral. But natural selection and changes in environmental pressures means that logically speaking all possibilities of code could in some circumstance be beneficial, neutral or detrimental. So no sequence of code is intrinsically neutral, benificial, or detrimental.

A Brutal Game
Nature plays a brutal game of competition, where the strongest survives to pass on genetic information while the weakest, along with the weaker genetic information, dies out. However brutal this game of survival is, it is a real game and it works very well as a preserving force that keeps the strong and gets rid of the weak. The question is, are there any examples of mindless evolutionary processes actually creating novel functions that were not there before?
The clear answer to this question is yes ; mindless evolutionary processes do actually create novel functions in creatures that were never there before. For example, antibiotic resistance is a famous case of evolution in action. As it turns out, all bacteria seem to be able to rapidly evolve de novo resistance to just about any antibiotic that comes their way. But how, exactly, do such novel functions evolve?

Ok I can go along with that.

Antibiotic Resistance
In the case of de novo antibiotic resistance, such rapid evolution is made possible because there are so many beneficial “steppingstones” so close together, right beside what the bacterial colony already has. Success is only one or two mutational steps away in many different directions since a multitude of different single mutations will result in a beneficial increase in resistance. How is this possible?

Ok here is a definition from wikipedia of de novo: In Medicine and genetics a de novo mutation is one which neither parent possessed or transmitted. It first appeared in the DNA of the affected individual.

continuing the last quote

In short, this is made possible because of the way in which antibiotics work. All antibiotics attack rather specific target sequences inside certain bacteria. Many times all the colony under attack has to do is alter the target sequence in just one bacterium by one or two genetic “characters” and resistance will be gained since the offspring of this resistant bacterium, being more fit than their peers, will take over the colony in short order. A simple “spelling change” made the target less recognizable to the antibiotic, and so the antibiotic became less effective. In other words, the pre-established antibiotic- target interaction was damaged or destroyed by one or two monkey-wrench mutations. As with Humpty Dumpty and all the king’s men, it is far easier to destroy or interfere with a pre-established function or interaction than it is to create a new one, since there are so many more ways to destroy than there are to create.

Ok. I'd go along with that.

So, do all functions within living things evolve as easily as the antibiotic resistance function? As it turns out, those independent functions that are not based on the destruction of or interference with other pre-established functions are much more difficult to evolve. For example, single protein enzymes catalyze many biochemical events within living things. They help to build and break down other molecules via their own independent abilities, which are not based on the gain or loss of any other system, function, or interaction.
Consider that several forms of antibiotic resistance are based on the production and activity of various enzymes. Perhaps the most famous anti-antibiotic enzyme is the penicillinase enzyme, which is produced by various bacteria having the proper penicillinase code in their DNA. What the penicillinase enzyme does is chop up part of the penicillin antibiotic so that it can no longer attack its target and kill the bacterium. Many people think that bacteria evolve this enzyme just like they can evolve other forms of antibiotic resistance. This is simply untrue.

All the King’s Horses
The information required to produce an enzyme which is specific enough to chop up penicillin is far greater than the information required to block the antibiotic-target interaction, since there are far fewer ways to make such a specific enzymatic function compared to the number of ways to block a specific antibiotic function. Creating a block to a previous function is like breaking Humpty Dumpty, while creating the function of an independent enzyme is like putting Humpty Dumpty back together again.

Ok. now we are getting into a whirlwind through a junkyard can't put a 747 together territory. Check out Dawkin's book The Blind Watchmaker.

But lets look at this closer:

The information required to produce an enzyme which is specific enough to chop up penicillin is far greater than the information required to block the antibiotic-target interaction, Either a penicillinase-producing colony already had this code before it was exposed to penicillin, or it gained this code by genetic transfer from some other bacterial population that already had the code.2 Simply put, the penicillinase enzyme does not evolve, or at least not often enough to have been observed in real time, while other forms of antibiotic resistance that are based on interference with or destruction of pre-established functions or interactions evolve all the time.

Ok. So what is the point here?

Premise A: The information required to produce an enzyme which is specific enough to chop up penicillin is far greater than the information required to block the antibiotic-target interaction,

Observation: The information required to produce an enzyme which is specific enough to chop up penicillin is far greater than the information required to block the antibiotic-target interaction,

Conclusion: Simply put, the penicillinase enzyme does not evolve, or at least not often enough to have been observed in real time,

But what is this term "real time" If the functionality of said enzyme is complicated then, the chances of a code able to produce that function is reduced. In this particular case "real time" might just = "long time".

Evolution in Action?
But what about other enzymes? Have any novel enzymatic functions ever been shown to evolve in real time? Interestingly enough, several enzymes with entirely new and beneficial functions have been shown to evolve in real time. For example, Kenneth Miller, in his book, Finding Darwin’s God, references a very interesting research study published by Barry Hall, an evolutionary biologist from the University of Rochester.3
In this study, Hall deleted the lactase genes in certain E. coli bacteria. These genes produced and regulated the production of a lactase enzyme called b-galactosidase. What this enzyme does is break apart a type of sugar molecule called lactose into two smaller sugar molecules called glucose and galactose — both of which E. coli can use for energy production. Obviously then, without the genes needed to make this lactase enzyme, the mutant E. coli were no longer able to use lactose for energy despite being placed in a lactose enriched environment, unless of course they evolved a new enzyme to replace the one that they lost. And sure enough, they did just that. In just one or two generations these E. coli successfully evolved a brand new gene that produced a new lactase enzyme. Aha! Evolution in action yet again!
Although most descriptions of Hall’s experiments stop right here, including the one found in Miller’s book, what Hall did next is most interesting. He deleted the newly evolved gene as well, to see if any other gene would evolve the lactase function . . . and nothing happened! Despite tens of thousands of generations with large population numbers and high mutation rates, no new lactase enzyme evolved. Hall himself noted in his paper that these double mutant bacteria seemed to have “limited evolutionary potential.”

And the point is? Only certain type of sequences can produce certain interactions I think. You remove a sequence you lose the interaction. so what is the difference between E.coli and penicillin? Well I guess the answer might be a bit complicated. But here is a stab at an answer. The de novo mutation found in E coli is just less difficult to form than that for penicillin.

Here is a counter view. The Hydrogen atom is simpler than the Helium atom. The hydrogen atom is made up of one proton and one electron, the Helium atom is made up of two protons, two neutrons and two electrons. Both atoms interact with their environments differently. Also one is more complicated than the other, by only a proton, 2 neutrons and an electron. The numbers aren't big but the difference is significant.

The consequence is that there is a lot less helium than hydrogen in the universe because it requires a more energy and a more complex set of events to produce. As one moves up the periodical table the heavier elements require second generation stars to form and are less and less represented. (You have to wait a long time to get a second generation star)

The point is you can have what looks like the same basic code, and you put it together differently and you find it is more difficult for some combinations to come together than others. There is nothing strange or anti evolution about this. In fact it would be stranger if E.coli and penicillin generated de novo mutations in exactly the same time frame. Like everything there is going to be degrees. Some mutation might occur quick, some slow.

Hey. And while I am at it. All genetic code is made of is a bunch of organised atoms.

Limited Potential
Other unfortunate bacteria seem to be just as limited in their evolutionary potential. Even though they would significantly benefit, many types of bacteria, after more than a million generations, have not been observed to evolve a relatively simple lactase enzyme.

Again. Maybe just maybe some combinations are less likely, or need more complex conditions for the molecule to be generated that fits the bill.

This is fewer generations than it supposedly took humans to evolve from ape-like creatures.

And that is an argument how? In fact does that mean we are quite closely related to some apes?

One should also note that these same bacteria, unable to evolve a lactase enzyme, are all able to evolve, in relatively short order, resistance to any antibiotic that comes their way. So what is it, exactly, that “limits” the evolutionary potential of living things, like bacteria, in their ability to evolve some functions but not others?
I propose that the answer can be found in the number and density of beneficial “stepping-stones” available (in the form of genetic sequences). For forms of antibiotic resistance that are gained by blocking the antibiotic-target function, there are lots of beneficial steppingstones very close together, but not so for the enzymatic functions of lactase or penicillinase.

Well you are going to have to Go back To Dawkins again. The argument goes something like 5% of an eye is better than no eye at all. So I guess that 5% of enzyme functionality is better than no enzyme at all.

The author of this page does not state what percentage of the total number of enzyme possibilities carry some fraction of Enzyme fucntionality. So when he then says...

For example, there are 676 potential two-letter words in the English language. Of these, 96 are defined as meaningful, creating a ratio of meaningful to meaning- less of 1 in 7. Now, there are 296 more meaningful three-letter words, totaling 972, but the total number of potential words increases 26 fold to 17,576. Since the number of meaningful words only increased by a fraction of this amount, the ratio of meaningful to meaningless dropped to 1 in 18.

...his point and his example mis the point of current evolutionary/Dawkin's argument. There may be relatively few well formed enzymes in the total, but what about the less functional sequences.

A Random Walk
Still, such ratios are relatively high, and random walk can get from any one-, two-, or three-letter words to any other via a path of meaningful words, as in the steppingstone sequence of cat – hat – bat – bad – bid – did – dig – dog. “Evolution” (changing meaning or “function”) at this level is rather simple because the stepping-stones are so close together. But, with each additional minimum letter requirement, the growth of the meaningless sequences quickly outpaces the growth of the total number of meaningful sequences, and the ratio of meaningful to meaningless gets smaller and smaller at an exponential rate.

Lets use the eye example. If you could do the math of all the possible genetic sequences over the specific sequences that produce perfectly functional eyes the the ratio is enormous. But what about all those accumulation of cells that give some light sensitivity. That is a much larger set. so the ratio comes down. Now all nature has to do is start with the simpler light sensitive bunch of cells, and time x natural selection does the rest.

Can we apply an argument of this form to enzymes. Why not?

For example, there are around 30,000 meaningful seven-letter words and combinations of smaller words totaling seven letters, but there are 8,031,810,176 potential seven-letter sequences. This produces a situation in which an average meaningful seven-letter sequence is surrounded by over 250,000 meaningless sequences. Obviously then, compared to three-letter steppingstones, it is much harder to “evolve” between meaningful seven-letter steppingstones without having to cross through a little ocean of meaningless sequences.

In this example of letters and seven letter words then I can agreet he conclusion. But in nature who is to say what benefit or or detriment any particular sequences is going to have. The analogy is simply false.

The same thing happens with the genetic codes in living things. The more genetic letters that are required to achieve a particular function, and the higher the level of the specificity of their arrangement, the more junk there is compared to the relatively few beneficial sequences at such a level of complexity.

Yes more junk, and more 1% functional, 2% functional, 3%, 4%,,,,,etc, arrangements there are going to be

For example, a simple BLAST 4 database search of known proteins will show that the shortest working lactase enzyme found in a living organism seems to require well over 400 amino acids at minimum with at least a fair degree of specificity.

So that is the shortest 100% functional enzyme. How about the 1%, 2%, 3%....etc.,

Some estimates suggest that the total number of beneficial sequences at the 400-amino-acid level of specified complexity totals less than 10^100 sequences.5,6 Now, considering that the total number of atoms in the entire known universe is around 1080, this 10100 number seems absolutely huge! 7 Huge, that is, until one considers that there are over 10520 possible sequences at this level of complexity, which creates a ratio of beneficial to non-beneficial sequences of 1 in 10^400 (which is like finding a single atom in zillions of universes).

Ok what the author has not done is divide 100^400 by all the number of sequences that produce partially functional enzymes. And then he has not consider the time period it took enzymes to appear on planet earth.

Real Life
Of course, since nature cannot tell the difference between two meaningless genetic sequences, it cannot select between them, making natural selection blind to such neutral changes. Since there are no recognizable “steppingstones” close by, all that nature has left, to find new beneficial sequences, is a blind random walk through enormous piles of junk sequences. Of course, this random, curvy walk takes a lot longer than a direct walk would take, and the time involved increases exponentially with each increase in the minimum sequence and specificity requirements for a particular function. This prediction is reflected in real life by an exponential decline in the ability of mindless evolutionary processes to evolve anything beyond the lowest levels of functional complexity.
Many simple functions, such as de novo antibiotic resistance, are easy to evolve for any bacterial colony in short order. Moving up a level of complexity, there are far fewer examples of single protein enzymes evolving where a few hundred amino acids at minimum are required to work together at the same time (and many types of bacteria cannot evolve even at this level). However, there are absolutely no examples in the scientific literature of any function requiring more than a thousand or so amino acids working at the same time (as in the simplest bacterial motility system) ever evolving — period.

How long did the science guys leave their test tubes. A billion years?

The beneficial “stepping-stones” are just too far apart due to all the junk that separates the few beneficial islands of function from every other island in the vast universe of junk sequences at such levels of informational complexity. The average time needed to randomly sort through enough junk sequences to find any other beneficial function at such a level of complexity quickly works its way into trillions upon trillions of years — even for an enormous population of bacteria with a high mutation rate.

No You only get a result of trillions of years if you don't divide the figure 100^400 by the partial possibilities.

At this point the mindless processes of evolution simply become untenable as any sort of viable explanation for the high levels of diverse complexity that we see within all living things.

Well it would if you don't follow through on the math.

The only process left that is known to give rise to functional systems at comparable levels of complexity involves human intelligence or beyond. No lesser intelligence, and certainly no other known mindless processes, have ever come close to producing something like the informational complexity found in the simplest bacterial motility system.8

Do the math. Do the math.

[McCulloch]

Please take the statement in context. I say that the definition of speciation changes. In this case, the definition of speciation is altered by logistics. Previously, Eskimos and Africans had no way to interbreed and so would be classed as different species. Now, they can interbreed easily and are classed as the same species.

Who exactly has said that Inuit and Africans are or were different species?

[Curious]

Please take the statement in context. I say that the definition of speciation changes. In this case, the definition of speciation is altered by logistics. Previously, Eskimos and Africans had no way to interbreed and so would be classed as different species. Now, they can interbreed easily and are classed as the same species.

Who exactly has said that Inuit and Africans are or were different species?

It is following on from the classification of species. If there are different phenotypic characteristics of particular groups, and these groups cannot interbreed due to location, then these groups are classed as different species, even if physically such groups could interbreed. It makes little sense, I admit.

[Goat]

Please take the statement in context. I say that the definition of speciation changes. In this case, the definition of speciation is altered by logistics. Previously, Eskimos and Africans had no way to interbreed and so would be classed as different species. Now, they can interbreed easily and are classed as the same species.

Who exactly has said that Inuit and Africans are or were different species?

No one. I made the comment that one factor in the production of new species is isolation so the two populations don't interbreed. Curious went on a strawman distraction.. and is being a bulldog about purposely misinderstanding by bringing that up.

[Curious]

Please take the statement in context. I say that the definition of speciation changes. In this case, the definition of speciation is altered by logistics. Previously, Eskimos and Africans had no way to interbreed and so would be classed as different species. Now, they can interbreed easily and are classed as the same species.

Who exactly has said that Inuit and Africans are or were different species?

No one. I made the comment that one factor in the production of new species is isolation so the two populations don't interbreed. Curious went on a strawman distraction.. and is being a bulldog about purposely misinderstanding by bringing that up.

I am not referencing you (goat) at all in this statement. I am pointing out that the classification of species is inconsistent. In human strains, there is no speciation claimed, but in non-human strains, speciation is said to be evident, even though the same type of differentiation can be seen in the apparently single species of human.

[McCulloch]

In human strains, there is no speciation claimed, but in non-human strains, speciation is said to be evident, even though the same type of differentiation can be seen in the apparently single species of human.

Can you cite an example of where there is a claim of speciation due to geographical separation but where interbreeding would still be possible?

[otseng]

But natural selection and changes in environmental pressures means that logically speaking all possibilities of code could in some circumstance be beneficial, neutral or detrimental. So no sequence of code is intrinsically neutral, benificial, or detrimental.

Of course natural selection is directly determined by the phenotype, rather than the genotype. So, it is indirectly that the genotype is considered neutral, beneficial, or harmful.

Ok here is a definition from wikipedia of de novo: In Medicine and genetics a de novo mutation is one which neither parent possessed or transmitted. It first appeared in the DNA of the affected individual.

I would think this would be the only way a novel phenotype could have arisen.

Check out Dawkin's book The Blind Watchmaker.

Actually, I have read the book cover to cover. And quite frankly, it was a disappointing book.

Lets use the eye example. If you could do the math of all the possible genetic sequences over the specific sequences that produce perfectly functional eyes the the ratio is enormous. But what about all those accumulation of cells that give some light sensitivity. That is a much larger set. so the ratio comes down. Now all nature has to do is start with the simpler light sensitive bunch of cells, and time x natural selection does the rest.

Can we apply an argument of this form to enzymes. Why not?

I think instead of arguing about hypotheticals (which Dawkins' book was chock full of), I think the best thing to do is to use real examples of evolution.

The main argument of the article is that as you go up in complexity, it gets much more difficult to achieve.

Galphanore has shown that evolution can produce Nylon eating bacteria.

I then asked the following:

Let's go up a step in complexity. Is there an example of a protein evolution where the new protein interacts with other proteins (instead of just a chemical)?

Let's explore this and then we can go even higher in complexity.