Micro vs. Macro Evolution

Great Debates
21

Well, since this is Great Debates, and we are ostensibly debating, let me be the first to say it: you have no idea how evolution works.

I would like to point out that this debate is not about whether evolution is real or not, it is about the difference between micro- and macroevolution, and why some feel justified in accepting microevolution but not macroevolution. There are plenty of other threads where you can discuss belief in evolution in all its evil sinfulness.

And, I would also like to point out that your argument can very easily go the other way:

My apologies for this off-topic quasi-rant.

22

You can set your own standards for proof, but I have to wonder, are you setting these standards specifically to exclude evolution, geology, and astronomy, or for some other reason?

Are you saying that evolution has no value in biology? If so, there’s a real debate in that topic. The OP seems to have been answered pretty well.

23

OK, I work on development of the eye in fruit flies, so I am pretty confident that I can explain eye development in terms of evolution. Or at least give a plausible story. This is not to say how it did happen – it is to say that it could have happened, and it does not require divine intervention.

Here’s a shot:

In the first multicellular life, systems to handle stimuli from the environment evolve and link to the developing nervous system. The nervous system is built to organize these stimuli (Kandel’s Nobel Prize!). Eyes start slowly – a few chromatophore cells (even bacteria have rhodopsin and phototaxe). It is advantageous for the organism to be able to respond to light precisely – for orientation, for movement towards food, etc. etc.

So we have photosensitive proteins talking to the nervous system. No big deal here – recently in zebrafish, it is found that even individual organs can respond to light and dark cycles. Light/dark sensing is found everywhere in biology, and most nervous systems I can think of respond to it. Modifications of the photosensitive protein change the wavelength specificity. The protein is a membrane-bound protein, so in order to increase sensitivity, it is advantageous to increase the surface areas of the cell. After a while, in some organisms, this excess membrane can pinch off to form vesicles (mammals and such) filled with this photoreceptor pigment.

So we have created neurally linked photoresponsive tissue. Great. We are at flatworm stage now. In flatworms, we see the same genetic pathways that lead to eye development in all organisms with eyes – namely the eyeless pathway. This was first found in the fruit fly, and later linked to a mutation which causes small eyes in mice and aniridia (lack of an iris) in humans. Duplications and rearrangements of this pathway can happen very quickly evolutionarily, and so change, especially if the selection is strong, does not have to be so slow.

The next step is to refine these systems. We see this all through evolution – something works, and nature works to improve it. For some organisms, it becomes advantageous to respond to low light conditions. They get larger eyespots. In order to interpret new information, it becomes advantageous for the developing nervous system to devote more brain power to interpretation. Changes are associated with duplications, reshufflings, and modifications of the genetic pathway. In some organisms, the eye and the nervous system become one and the same system (vertebrates). In other organisms, they proceed through linked but separate pathways (flies).

At some point, eyesight becomes absolutely necessary for locating food sources (plants or seaweed growing near light) or escaping enemies. It becomes necessary for some kind of protection for the eyes. Animals develop clear overgrowths with the retinas underneath them. The thicker the tissue overgrowth, the better the protection but the more distortion of image you have. In order to adjust the image distortion created by coming through this curved piece of tissue, it becomes advantageous to have facial muscles evolve to move this developing lens and establish focus.

At some point, this system needs more protection, as the lens becomes crucial for vision. It is advantageous to evolve another clear skin overgrowth over the lens. This is called a cornea. As the transition is made to dry land, the cornea gets protection from the conjuctiva and eyelids and such.

The thing is, the genetic information supports this. We see this eyeless gene system in all animals with eyespots. In humans and in mice, the pathways are conserved, but are duplicated and in some cases these duplications are rearranged, reshuffled, and linked into other pathways. Just like the gross "macro"evolution has happened. Deleting one homolog of the eyeless ortholog family causes developmental failure of the iris in humans. Deleteing the only copy of eyeless in flies leads to flies with no eyes (this is a little simplified, but will work for our discussion). And, if you express eyeless in flies somewhere else, like the wings, eyes sprout on the wings. Very cute. Gives an example of rapid large scale change that is not beyond the realm of possibility.

Granted, this is just a possible mechanism. More liberal-minded creationists will argue that God could have directed all of these steps. I have no problem with this – in evolution science there is no argument against divine direction. It is something that can’t be measured, and therefore can’t be tested.

Sorry for being so long.

24

Kind of coincidental, but I was reading about how bacterial species are determined today. Since the vast majority of bacterial reproduction doesn’t include anything remotely resembling sex, the reproduction definition is useless.

Up until 30 or so years ago, the way to tell if two bacteria were the same species was to ask an expert, and he’d make an educated guess.

The current requirement is genetic. If two bacteria are identical at at least 70% of their nucleotides, and 97% in their 16S rRNA gene, they belong to the same species. Any more different and they’re different species. There are, of course, numerous exceptions. By this rule, most of the Enterobacter family, including E. coli and the Salmonella species, should be considered one species. They keep them separate purely for convenience.

Higher levels are even more vague. There’s a general rule that members of genera should share 20-30% of their nucleotide sequence, but it’s not hard or fast.

“But wait!” I hear you cry. “That’s completely arbitrary and stupid!”

My point exactly. How can you divide micro- and macroevolution when you don’t even have meaningful divisions among groups - or when no meaningful divisions even exist??

25

I would just like to thank edwino for that cogent, informative and educational (eyes on wings! I want some, too.) post.

26

Ditto on the thanks to edwino, and thanks also to Smeghead for reiterating what I’ve been trying to ask, specifically, how can micro and macro evolution be separated when the lines between species are not clearly defined.

Since the only comment form the micro only camp addressing this dilemma was along the lines of “I want to see and elephant give birth to a camel”, I think I understand the problem.

27

Asmodean wrote:

All right then, Asmodean, here’s a laboratory experiment that has been performed successfully several times. It shows unequivocably that new information can indeed be created by random mutation coupled with artificial selection.
[ul]
[li]Take a single pneumococcus bacterium. Check to make sure this bacterium is not producing penicillinase. (Penicillinase is an enzyme that breaks down penicillin molecules.)[/li][li]Put it in a nutrient dish and let it divide many many times, until you have a whole colony of pneumococci that all came from that same original pneumococcus. Note that bacteria do not reproduce sexually; a bacterium only has one parent that it received genetic information from.[/li][li]Divide this pneumococcus colony into two groups. Put one group into petri dish A, and the other group into petri dish B.[/li][li]In petri dish A, add a huge mega-dose of penicillin – call it 2000 penicillin units. You will notice, soon after you have done so, that every single bacterium in dish A is dead.[/li][li]In petri dish B, add only 1 unit of penicillin. Soon after you have done so, you will notice that most of the bacteria in dish B are dead, but a few of them will have survived.[/li][li]Add nutrients to dish B and let these surviving bateria multiply.[/li][li]Put 2 units of penicillin in dish B. Soon after, most of the pneumococci will be dead, but a few will have survived.[/li][li]Let these survivors flourish again, then hit dish B with 4 units of penicillin.[/li][li]Let the survivors of this last penicillin attack in dish B thrive, then hit them with 8 units of penicillin.[/li][li]Continue to feed the survivors in dish B, let them multiply, and then double the previous dose of penicillin, over and over again, until you’ve done it a total of 12 times.[/li][li]The pneumococcus population in dish B, when you are done, will be able to withstand the same 2000-unit megadose of penicillin which killed every single bacterium in dish A.[/li][li]Take one of these pneumococci and test it to see if it is producing the enzyme penicillinase. You will see that it is doing so.[/li][/ul]

Now where did the abililty for the bacteria in dish B to survive a megadose of penicillin come from? Where did the ability to produce penicillinase come from? The original pneumococcus bacterium you started with certainly didn’t have this ability. If it did, at least some of the bacteria in dish A would have survived.

The answer is, a random mutation in a few of the pneumococci caused it to produce a small quantity of a new enzyme which, quite by accident, happened to work kinds-sorta like penicillinase. The chances of such a freak mutation are not all that high, and in a population of thousands or millions of decendants, it is in fact likely that such a mutation would occur several times. This not-that-freakish mutation was not capable of handling the megadose of penicillin placed in dish A, but it was capable of handling that first teensy tinsy dose of penicillin placed in dish B. It was the key to the survival of the dish B population. Thus, when that small survivor population multiplied to produce the next colony in dish B, nearly all the members of the dish B population now had the ability to produce that vaguely-penicillinase-like enzyme. But a few of those newly-spawned bacteria happened to have another mutation which caused the vaguely-penicillinase-like enzyme they produced to resemble penicillinase a little more closely. It was the few bacteria that had this second mutation that survived the next incrementally-higher dose of penicillin, and carried that mutation forward into their offspring. Subsequent incrementally-higher doses of penicillin continued to weed out those pneumococci that didn’t have better and better mutations, until at the end you were left with pneumococci that pumped out oodles of perfect, shiny penicillinase.

The bacteria acquired new information by random mutation filtered through artificial selection. And if it can happen in a laboratory via artificial selection, why couldn’t it happen out in the wild via natural selection?

28

OK, here’s a meaningful definition:

A species is a diagnosable cluster of individuals within which there is a parental pattern of ancestry and descent, beyond which there is not, and which exhibits a pattern of phylogenetic ancestry and descent among units of like kind.
-“Phylogenetic Patterns and the Evolutionary Process: Method and Theory in Comparative Biology”, Niles Eldredge and Joel Cracraft (1980) [p. 92]

The species definitions commonly related (e.g., the various ‘biological species concepts’ and ones which involve interbreeding and nonsterile offspring and such) are not working definitions for the purposes of studying evolution; they are attempts at species recognition, which, while related to the concept of species in an evolutionary context, is not the same thing. They are also typically arbitrary (the one cited by Smeghead in Part I of my quotes above, for example, because it cannot be applied to obligate asexuals).

A working definition from a taxonomic perspective might be as follows:

We do see that there are discrete reproductive populations in nature. It is, therefore, possible to postulate that there also exist certain groupings of such populations which all share a common set of derived characteristics (synapomorphies, or shared-derived characters), and within which, no further hierarchical subdivision based upon these or other characters is possible.

In other words, a species is like a biological version of a mathematical set, in which the members of any subset are identical to the members of the set as a whole.
(no cite - this is my own rambling)

Assuming either (or both) of these definitions can be accepted, then we can proceed to the discussion of the merits (or lack thereof) of macroevolution :smiley:

29

It is at lease conceivable (though pretty ludicrous) that a gene for resistance to penicillin was present already (because there are natural sources of penicillin); but this experiment has also been carried out for totally synthetic antibiotics with the same result.

I love the related experiment by Hall; see A True Acid Test.