Experimental evidence for evolution

[StevePush]

On the matter of speciation it is Lenski himself who brings up this point. And my direct quote from the paper shows this.

It is admirable that the authors showed restraint and did not immediately declare the Cit+ population to be a "distinct" species. But it probably is a new species. Since E. coli reproduces asexually, the two populations are effectively isolated. (Even if they weren't, the Cit+ population is isolated from the other 11 cultures.) Unless the entire Cit+ population reverts back to the Cit- genotype, it is a new species. In other words, we now have two kinds of bacteria that differ in both genotype and phenotype and descended from a common ancestor.

It is also clear that historical contingency is a theory that provides the drive towards speciation. So this experiment is about the mechanism of speciation. After all Darwinian theory is about speciation.

I'm not sure what point you are trying to make here. Historical contingency is a proposed mechanism of Darwinian evolution. The LTEE study supports the hypothesis that historical contingency was important in this particular evolutionary change. It does not, however, establish that historical contingency plays an important role in evolution generally. But even if the importance of historical contingency does become established, that would not falsify Darwinian theory; it would reveal in greater detail how Darwinian evolution works.

Therefore the Darwinian mechanism is not a proven theory and I simply argue that it should not be presented as a fact as it so often is.

I would not use the term "proven." Darwinian theory (or more precisely, neo-Darwinian theory) is one of the most well-confirmed theories in science and thus ought ot be taught in science classes. Evolution, on the other hand, is a fact. Even before Darwin, scientists recognized that organisms change over time. They just didn't know how it occurred.

Just to also clarify we are not talking about 30,000 generations. Please remember that there are 12 populations and the experiment has now proceeded past 50,000 generations for each population. That makes 600,000 generations so far.

My take on these numbers is just the opposite of yours. The first bacteria on Earth that could exploit an abundant energy source would have undergone explosive growth, since there would have been no competitors. Within a short time, the numbers of these bacteria would have dwarfed the number in the LTEE's 12 small cultures. If the LTEE shows evolutionary change in 30,000 or 50,000 generations, I would expect such changes to have occurred much more rapidly in the much larger population that probably existed billions of years ago -- or for that matter in the larger natural populations that exist today.

It is also a mistake to generalize from the mutation rate in the LTEE, because mutation rates vary greatly. My evolution textbook has a table showing various mutation rates per 100,000 cells or gametes. These range from 0.00004 for streptomycin resistence in E. coli to 12 for yellow body in fruit flies and 4.2-14.3 for achondroplasia in humans. (Source: Evolution by Douglas J. Futuyma, 2005, Sinauer Associates, p. 171)

Steve

[jevg]

Patrick

I wouldn't argue with you regarding the exchange of genetic information in real life. You have the real life experience, I don't.
I can only refer to the papers by biologists themselves.

Why Lenski has not sought out a real life environment, only he can answer. I expect it has to do with control of the process.

My experience has shown me that peoples' views are most often sincerely held. So although they may not be in accord with the facts I feel that the people holding them should be treated with respect. It can sometimes be very frustrating though.

Joss

[StevePush]

Joss,

But before that Dobzhansky and Pavan state very clearly that they are dealing with at least 5 races within the species Drosophila pcrulistorum. This experiment was about determining the cause of sterility in one of the strains during hybridization, as I understand it. They could not establish the actual cause, however they hypothesize that it may be the result of some symbiotic relationship between Drosophilia and a virus or other microorganism.

The main objective of the cited article is indeed an investigation of hybrid sterility among subspecies of Drosophila paulistorum. This topic is interesting because it elucidates an important aspect of speciation: Sexually reproducing species must be reproductively isolated.

The evidence you seek is mentioned only briefly in this paper. On page 152 the investigators wrote, "The Guianan [group of Drosophila paulistorum populations] is the most distinctive, and seems to deserve being regarded a species of its own." A year later the researchers published another paper documenting why the Guianan subspecies had evolved enough to be regarded as a separate species, which they called Drosophila pavlovskiana. I have not been able to find this paper free on the Web, but the first page, including the abstract, is available at http://www.jstor.org/pss/2423385

According to the Encyclopedia of Life (http://www.eol.org), Drosophila pavlovskiana is still recognized as a separate species.

Steve

[canalon]

Patrick

I wouldn't argue with you regarding the exchange of genetic information in real life. You have the real life experience, I don't.
I can only refer to the papers by biologists themselves.

Why Lenski has not sought out a real life environment, only he can answer. I expect it has to do with control of the process.

My experience has shown me that peoples' views are most often sincerely held. So although they may not be in accord with the facts I feel that the people holding them should be treated with respect. It can sometimes be very frustrating though.

Joss

There is quite a lot of data available on Horizontal genetic transfer (HGT), as it is known in bacteria. I encourage you to look at it. The evidence of genetic instability are there.
The main problem is that we know very little of the life of bacteria outside of the lab. take a gram of soils, and you will be able to identify 1000's of bacterial species. But bacteria can acquire DNA from dead cells (whatever they were) or from phages, which are estimated to be 10x more numerous than bacteria. Moreover the ability of bacteria to pick-up foreign DNA and to keep it is directly dependent of the environment. So the LTEE is a reductionistic view of what is happening in real life. Lenski has made the choice to observe what happens to isolated populations of E. coli if left for thousands of generation. It is a good way to estimate the importance of accumulation of point mutations. He is dong his analysis of his strains and point to the things that he finds interesting. As I have mentioned earlier, others have had a look at his strains and have demonstrated some interesting side effects, notably re speciation, something that Lenski seems not to have seen worth pursuing. But it is only a very tiny ray of light in the immensely complex unknown that bacterial communities are representing. Taking this experiment as a benchmark to estimate the rate of evolution in the real world is quite frankly foolish.

Maybe you could have a look at some of the work by (for example) Ivan Matic, François Taddei, Miroslav Radman and Erick Denamur on the mutator phenotype.

[jevg]

Patrick
You raise the real life scenario and quite rightly so, but what is this real life scenario demonstrating.
HGT is a major factor here. However what does it say about one of the central doctrines of Darwinism, Common Descent.

It took Carl Woese decades to have his views of a separate domain of Archaea accepted.
Why such resistance?
One of the reasons was that it contradicted the Darwinian view of common descent, a single tree of life, the simple illustration so often depicted in textbooks. This was one of the early things I was taught in biology class at college.

Ofcourse there is no single TOL. It’s now beginning to be regarded as more of a bush - I would argue as more of a forest. And you rightly point to the importance of HGT that is so prominent in this regard.

Also you quite rightly point out that the Lenski experiment is a good way to estimate the importance of accumulation of point mutations. But what has he discovered about these point mutations?
Well let him answer. ( Please note carefully)

Despite this potential, none of the 12 LTEE populations evolved the capacity to use the citrate that was present in their environment for over 30,000 generations. During that time, each population experienced billions of mutations (22), far more than the number of possible point mutations in the _4.6-million-bp genome. This ratio implies, to a first approximation, that each population tried every typical one-step mutation many times. It must be difficult, therefore, to evolve the Cit_ phenotype, despite the ecological opportunity.

“..each population tried every typical one-step mutation many times.”

So even in this most highly selective environment point mutations with or without historical contingency, the simple variation in a trait requires literally hundreds of thousands of generations. So as I asked previously how many generations would be required for a full digestive tract to be produced.

Now you rightly say to use this experiment, as a benchmark to estimate the rate of evolution is frankly foolish. I would say it is frankly ridiculous. There is no way to use this as a benchmark for something that isn’t happening.

Please bear in mind why this even modest change is so difficult - because of the rigid control the cell exercises during division. Clearly the cell legislates against random changes or biological noise as a communications engineer would describe it.

So in the wild we see the role of HGT (at the very least) compromising the idea of common descent.
In the lab we are getting direct evidence on the very weakness of point mutations to drive speciation.
That leaves natural selection, and Darwin himself acknowledged that NS is not the only mechanism to speciation. Natural selection can eliminate a species that is not adapted to it’s environment but it has no power to modify it’s form. It can only work on what is already there.

So of the three fundamental pillars of Darwinism , random variation/mutation, natural selection and common descent, I see only, possibly one third of one pillar that has potential.

In 1999 Ernst Mayr (one of the founding fathers of the modern synthesis) received the Crafoord Prize from the Royal Swedish Academy of Science and gave a lecture, and which in part he said

Darwin introduced historicity into science. Evolutionary biology, in contrast with physics and chemistry, is a historical science - the evolutionist attempts to explain events and processes that have already taken place. Laws and experiments are inappropriate techniques for the explication of such events and processes. Instead one constructs a historical narrative, consisting of a tentative reconstruction of the particular scenario that led to the events one is trying to explain.

He goes on

The discovery of natural selection, by Darwin and Alfred Russel Wallace, must itself be counted as an extraordinary philosophical advance.

And again

Another aspect of the new philosophy of biology concerns the role of laws. Laws give way to concepts in Darwinism. In the physical sciences, as a rule, theories are based on laws; for example, the laws of motion led to the theory of gravitation. In evolutionary biology, however theories are largely based on concepts such as competition, female choice, selection, succession and dominance. These biological concepts, and the theories based on them, cannot be reduced to the laws and theories of the physical sciences. Darwin himself never stated this idea plainly.

I am arguing against a philosophy, not science and I have no less an authority than Ernst Mayr himself promoting that view and with pride.

All I ask is not to confuse philosophy with empirical science. This confusion is all too apparent in, for instance Jerry Coyne’s book “Why evolution is true” that Steve referred to and I would be only too happy to discuss it, to demonstrate my point.

regards
Joss

[StevePush]

Joss,

HGT is a major factor here. However what does it say about one of the central doctrines of Darwinism, Common Descent.

It says that in addition to the genes of their immediate ancestors, organisms sometimes carry genes form other branches of the tree of life. Recent genetic analysis suggests that all life descended from a single ancestral gene pool.

It took Carl Woese decades to have his views of a separate domain of Archaea accepted.
Why such resistance?

It took more than a century for the Copernican model of the universe to be accepted. New discoveries sometimes take awhile to gain widespread acceptance. Usually this is for good reasons (e.g., not enough data yet).

One of the reasons was that it contradicted the Darwinian view of common descent, a single tree of life, the simple illustration so often depicted in textbooks.

Woese didn't challenge the tree; he rearranged it.

Ofcourse there is no single TOL. It’s now beginning to be regarded as more of a bush - I would argue as more of a forest.

None of those metaphors is perfect.

So even in this most highly selective environment point mutations with or without historical contingency, the simple variation in a trait requires literally hundreds of thousands of generations. So as I asked previously how many generations would be required for a full digestive tract to be produced.

What digestive tract? Human? Probably on the order of tens to hundreds of millions of generations. Along the way, more primitive digestive tracts evolved in fewer generations.

Now you rightly say to use this experiment, as a benchmark to estimate the rate of evolution is frankly foolish. I would say it is frankly ridiculous. There is no way to use this as a benchmark for something that isn’t happening.

If you believe evolution does not occur, what alternative do you support?

Please bear in mind why this even modest change is so difficult - because of the rigid control the cell exercises during division. Clearly the cell legislates against random changes or biological noise as a communications engineer would describe it.

Yes, cells repair DNA damage, deactivate viral genes, etc. Despite these mechanisms, genetic variation is an empirical fact.

I am arguing against a philosophy, not science and I have no less an authority than Ernst Mayr himself promoting that view and with pride.

You have misinterpreted the Mayr quote. He was speaking of the "philosophy of biology," that is the branch of phiosophy that studies how biology is done. He was not saying that biology is unscientific. It is, in fact, as rigorous as any other field of science.

Steve

[WDW]

My question is whether there have been any experiments conducted that provide empirical support for macroevolution. Has there been any experiments that show an organism changing to something different?

I'm unaware of an experiment that provides empirical support for macro-evolution above the species level. However, there are claims of new species produced from existing ones. With much debate over the meaning of the word "species" and over methods of species identification, its difficult to find consensus on the matter. Its possible that some of these "new species" may simply be variations within the species itself. In other cases, it appears the new species are a type of hybrid limited by reproductive postzygotic barriers.

[einfopedia]

i think that it is very informative for you and you also find the your answers in this paragraph..

Sperm competition, when sperm from different males compete to fertilize a female's ova, is a widespread and fundamental force in the evolution of animal reproduction. The earliest prediction of sperm competition theory was that sperm competition selected for the evolution of numerous, tiny sperm, and that this force maintained anisogamy . Here, we empirically test this prediction directly by using selective breeding to generate controlled and independent variance in sperm size and number traits in the cricket Gryllus bimaculatus. We find that sperm size and number are male specific and vary independently and significantly. We can therefore noninvasively screen individuals and then run sperm competition experiments between males that differ specifically in sperm size and number traits. Paternity success across 77 two-male sperm competitions (each running over 30-day oviposition periods) shows that males producing both relatively small sperm and relatively numerous sperm win competitions for fertilization. Decreased sperm size and increased sperm number both independently predicted sperm precedence. Our findings provide direct experimental support for the theory that sperm competition selects for maximal numbers of miniaturized sperm. However, our study does not explain why G. bimaculatus sperm length persists naturally at ∼1 mm; we discuss possibilities for this sperm size maintenance.