Examples of beneficial mutations?

[Mallon]

I think the difficulty with identifying "beneficial" gross morphological mutations in real-time is simply a function of the fact that not many labs out there are trying to do this. It is hard to get funding for a project description that consists simply of, "We just want to play with animal genes and see what good things pop up."
Most work being done on hox genes, for example, centre on testing specific evolutionary questions: What controls the development of limbs? How are vertebral elements differentiated? How does the hox code work? In answering these questions, scientists have stumbled across a whole slew of neat mutations, producing extra limbs, giving birds teeth, creating extra fingers, etc. I've even seen a study that resulted in molars that developed in the lining of the uterus. It is easy to think that some of these mutations might be beneficial in some way or another, but the animals that exhibit them aren't normally bred to produce offspring since these aren't the questions being asked. Such studies do provide a mechanism as to how such evolutionary novelties might come about, though, which is a step in the right direction as far as evolutionary theory is concerned.

 

[laptoppop]

Since "bad" examples abound and even false positive "good" examples are at best rare, possibly non-existent...

Have there been any studies of ratios of mutations -- good v. bad as defined within a particular critter and a particular environment? Seems like that could be a pretty basic part of any robust mathematical analysis.

 

[Mallon]

Fair enough -- although we do see missing a muscle type of mutations fairly often.

I don't think anyone here would disagree with you. Deleterious and neutral mutations occur far more often that beneficial ones -- that much is obvious. This has little impact on whether "radical", new bauplans might be occasionally beneficial, though.

 

[laptoppop]

Right - but the ratio of good versus bad (with all the problems in defining) mutations combined with mutational rates in a given population could be very very interesting.

 

[Mallon]

Right - but the ratio of good versus bad (with all the problems in defining) mutations combined with mutational rates in a given population could be very very interesting.

I suppose. What would be your definition of "good" and "bad", though? How would you control for mutation rate?

 

[Xaero]

http://www.ncbi.nlm.nih.gov/entrez/..._uids=17148371&query_hl=1&itool=pubmed_docsum

The fixation of a beneficial mutation represents the first step in adaptation, and the average effect of such mutations is therefore a fundamental property of evolving populations. It is nevertheless poorly characterized ibecause the rarity of beneficial mutations makes t difficult to obtain reliable estimates of fitness. We obtained 68 genotypes each containing a single fixed beneficial mutation from experimental populations of Pseudomonas fluorescens, evolving in medium with serine as the sole carbon source and estimated the selective advantage of each by competition with the ancestor.

... also don't forget the Vadoma tribe: http://en.wikipedia.org/wiki/Vadoma

A substantial minority of this tribe has a condition known as ectrodactyly in which the middle three toes are absent and the two outer ones are turned in, resulting in the tribe being known as the "two toed" or "ostrich footed" tribe. This is an autosomal dominant condition resulting from a single mutation on chromosome number seven. It is reported that those with the condition are not handicapped and well integrated into the tribe. Indeed it may help in tree climbing. The Kalanga of the Kalahari desert also have a number of members with ectrodactyly, and may be related.

 

[Assyrian]

Oh boy...

Since "bad" examples abound and even false positive "good" examples are at best rare, possibly non-existent...

Don't forget that bad mutations come with parents desperately looking to a medical specialists to find what went wrong with their baby. There are doctors and professors immortalised by having their name attached to some syndrome, and with the advent of modern genetic, vast amounts of research dedicated to finding the genetic basis for the syndoms.

On the other hand, a lot less effort is invested into seeing why things go better than usual, and the concept of gm atheletes raises all sorts of ethical questions.

 

[Deamiter]

Indeed, I remember reading about an athlete who was disqualified from some European sporting association because of his naturally high red blood-cell count. There are drugs that are designed to do this but are utterly undetectable except for their effects (Lance Armstrong was on this type of medication during his cancer treatment which is the reason many people questioned some of his successes).

He later was reinstated when he was able to convince some committee that he was not, in fact, taking this kind of medication.

No, it isn't a gross structural change, but would you call it beneficial? The mutation might allow a person to better compete in a race, but it also requires a higher intake of nutrients.

Same goes for families in Europe that resist high cholesterol or that have larger than normal hearts and lungs. It sure seems beneficial by our standards, but then again there's really very little selection going on since the vast majority of humans can pass on their genes WELL before they die of cancer or heart attacks.

 

[The Barbarian]

No geneticist doubts the many documented cases of useful mutations. Nor does anyone who understands the field, doubt that most mutations are neutral, a few harmful, and a very few useful. (most of us have a few neutral ones)

This, in itself would not be sufficient for the observed degree of variation in living things, unless there was a way to sort them out.

That was Darwin's great discovery.

 

[grimbly]

Actually Lance Armstrong might be just what you're looking for as far as a beneficial mutation. Here's a guy with phenomenal lung capacity that gave him an edge over other competitors. Yea sure he trained hard, very hard, and I am not trying to minimize his accomplishments but a lot of other competitors also trained hard. Yet he stood head and shoulders above the rest of the field. One of the reasons Lance was so successful was due to his innate ability to more efficiently utilize his oxygen intake.

Great cyclists generally have an extraordinary heart capacity. The average resting heart rate is 66 to 72 beats per minute (bpm). A well-trained endurance athlete has a resting heart rate of 40 bpm. Miguel Indurain, a five-time Tour de France winner and Olympic gold medalist in 1996, recorded a resting heart rate of 28 bpm. In the mountain stages of the Tour de France, Indurain could take his pulse rate up to 190 beats per minute and drop it back to 60 on the descent within half a minute. To varying degree, these traits are all hereditary. As the renowned Swedish exercise physiologist Per-Olof Åstrand once said, "The most important thing an aspiring athlete can do is to choose the right parents."

http://news.nationalgeographic.com/news/2004/08/0820_040820_olympics_athletes.html

Not a very scientific source but the best I could find on short notice.

Now in todays society, this trait would not be strongly selected for but imagine living in Africa 100,000 years ago where being able to outrun some big predators would probably be a really neat idea. Actually you don't have to out run a predator, you just need to be faster than most of the other people in you group. Seems to me that that trait would certainly minimize your chances of ending up as a pile of lion poop which would definitely increase the probabilities of your genes being spread through out the population.

 

[laptoppop]

No geneticist doubts the many documented cases of useful mutations.

PLEASE name a few.

 

[Xaero]

Taken from:http://creationismunleashed.blogspot.com/2005/07/evolution-disproven-hypothesis.html

Obvious examples of beneficial mutations are those giving rise to genes or parts of genes that now serve a useful pupose but have a clear mutational origin (such as retrotransposition or viral elements) examples include:

Utp14b in mice a gene that clearly evolved by a retrotransposition mutation from a normal gene (1) as did:
PGAM3,
Pgk2,
PMCHL1,
PMCHL2,
Sphinx (3)
and 24 genes on the drosophila X chromosome (5)
and Many G-protein-coupled receptors (7)
Gin-1 a gene that evolved from parts of a transposon (2) the insertion of which is a mutation.
HLA-DR-1,
human DAF,
lungerkine mRNA,
mNSC1 mRNA arose in a similar way (3)
fucosyltransferase
jingwei
Tre2 arose by exon shuffling mutations (3)
CGβ
Cid
RNASE1B arose by gene duplication mutations (3)
human beta 1,3-galactosyltransferase 5 colon promoter is derived the mutational insertion of a retrovirus (4)
as have promoters of:
Endothelin B Receptor
Apolipoprotein C-I Genes (6)
and:
CYP19
TMPRSS3
HYAL-4
ENTPD1
CASPR4
MKKS
CA1
SPAM1
KLK11
MSLN
BAAT
MAD1L1
CLDN14
SIAT1
FUT5
ILT2 (8) In fact about 25% of human regulatory elements are derived from transposable element insertion mutations (9)
Syncytin derives from a retroviral protein (10)

All these genes and parts of gene serve a useful and beneficial purpose and the origin of them all invloved commpnly observed types of mutation.

Refs:
(1) An X-to-autosome retrogene is required for spermatogenesis in mice. Julie Bradley1,4, Andrew Baltus1,4, Helen Skaletsky1, Morgan Royce-Tolland1, Ken Dewar2,3 & David C Page. VOLUME 36 | NUMBER 8 | AUGUST 2004 NATURE GENETICS.

(2) A Mammalian Gene Evolved from the Integrase Domain of an LTR Retrotransposon. Carlos Llorens and Ignacio Marın. Mol. Biol. Evol. 18(8):1597–1600. 2001

(3) THE ORIGIN OF NEW GENES: GLIMPSES FROM THE YOUNG AND OLD. Manyuan Long*‡, Esther Betrán§, Kevin Thornton‡ and Wen Wang. NATURE REVIEWS | GENETICS VOLUME 4 | NOVEMBER 2003 | 865.

(4) An endogenous retroviral long terminal repeat is the dominant promoter for human beat 1,3-galactosyltransferase 5 in the colon. Catherine A. Dunn*†, Patrik Medstrand‡, and Dixie L. Mager*. www.pnas.org/cgi/doi/10.1073/pnas.2134464100

(5) Retroposed New Genes Out of the X in Drosophila Esther Betran,1 Kevin Thornton,2 and Manyuan Long. http://www.genome.org/cgi/doi/10.1101/gr.6049.

(6) Long Terminal Repeats Are Used as Alternative Promoters for the Endothelin B Receptor and Apolipoprotein C-I Genes in Humans. Patrik Medstrand‡, Josette-Rene´e Landry§, and Dixie L. Mager. THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 276, No. 3, Issue of January 19, pp. 1896–1903, 2001.

(7) Many G-protein-coupled receptors are encoded by retrogenes. Jürgen Brosius. Trends in Genetics August 1999, volume 15, No. 8.

(8) Transposable elements in mammals promote regulatory variation and diversification of genes with specialized functions. Louie N. van de Lagemaat1, Josette-Rene´e Landry1, Dixie L. Mager1,* and Patrik Medstrand. TRENDS in Genetics Vol.19 No.10 October 2003.

(9) Origin of a substantial fraction of human regulatory sequences from transposable elements. I. King Jordan1, Igor B. Rogozin1, Galina V. Glazko2 and Eugene V. Koonin. TRENDS in Genetics Vol.19 No.2 February 2003.

(10) Direct Involvement of HERV-W Env Glycoprotein in Human. Trophoblast Cell Fusion and Differentiation. Jean-Louis Frendo,et al.MOLECULAR AND CELLULAR BIOLOGY, May 2003, p. 3566–3574.

Also we had the example of Flavobacterium with a beneficial-gain-of-information gene duplication and frameshift mutation.

You can also search Nature,Sciam,PLoS or whatever, there are tons of them ... but you won't except them since they are only "microevolution"

 

[Mallon]

PLEASE name a few.

Is this a joke?
Is that not what we've been doing in this thread the whole time?
The ectrodactyly mutation was a good example you never responded to. Nor did you respond to the study by Barrett et al. And you outright snubbed my examples of nylon- and lactose-digestion in bacteria.
We've given you what you've asked for. Why do you continue to act as though we have not?

 

[Deamiter]

Yeah, just notice that you just changed what you asked for. Before you were requiring observed major structural change -- that's hard to observe in just a couple hundred years. But when you ask for any beneficial mutation... there's an abundance of evidence there.

 

[laptoppop]

Right - I gave up on gross morphological changes. Although I just want to clearly point out that we have PLENTY of negative gross morphological examples -- isn't it logical that we'd have a few positive ones? It seems to me that the negative/positive ratio must be HUGE -- but nobody has numbers. Of course, the skeptic in me says that no one has numbers because numbers end up disproving the possibilities of evolution itself.

For example, if all we can ever find is tiny changes that can be classified as beneficial, how can we prove that those are outside the normal variation range of the critter? Gross morphological changes make it easy -- you look and see it. There are huge gross morphological differences between the various animals -- if they came from teeny tiny changes, why doesn't the fossil record reflect that?

It seems like instead, we have a system that allows for minor variations, but becomes self correcting beyond hard to define boundaries.

 

[laptoppop]

I do want to clearly say - thank you for the examples of tiny beneficial variations. I'll be looking at them in more depth to understand them better.

What its looking like is that we have small beneficial changes/variations, a fossil record which shows large morphological differences, and a thought that lots of small variations can add up over time, without any direct evidence.

 

[gluadys]

Right - I gave up on gross morphological changes. Although I just want to clearly point out that we have PLENTY of negative gross morphological examples -- isn't it logical that we'd have a few positive ones?

It is logical that there will be many more negative examples of gross morphological changes because when these occur, they are the most disruptive of the species norm and therefore the most likely to be very harmful. Beneficial changes are much more likely to be smaller and less noticeable.

For example, if all we can ever find is tiny changes that can be classified as beneficial, how can we prove that those are outside the normal variation range of the critter?

Changes within the "normal variation range" of the critter are caused by mutations too. All variations originated as mutational differences. All variations were once outside the normal variation range. The mutations which survive generate the variation range. The more mutations that survive, the greater the range of variability.

Gross morphological changes make it easy -- you look and see it. There are huge gross morphological differences between the various animals -- if they came from teeny tiny changes, why doesn't the fossil record reflect that?

Because the fossil record is incomplete. There are often many millennia between the nearest related fossils in a lineage. Lots of time for those many small variations to accumulate in different directions in different populations.

Where we do have fairly complete records (mostly in shelled invertebrates) we do see fairly smooth transitions as different populations branch off from ancestral species.

http://www.don-lindsay-archive.org/creation/fossil_series.html

It seems like instead, we have a system that allows for minor variations, but becomes self correcting beyond hard to define boundaries.

Hard to define because they do not exist. The current boundaries between different groups are a post facto consequence of the extinction of intermediate forms. You would get exactly this sort of break in continuity if you wiped out a section of a ring species.

 

[Deamiter]

It's hard to imagine that you'll ever find the evidence you're looking for when you define anything we've seen as "tiny" and what we have seen as "gross."

For example, many fossilized species differ in length and size of bone structures. Mark Kennedy brought up recently (IIRC -- it was a creationist anyway) that Beagles have developed longer snouts in observed history due to an added copy of some gene. Every species of dog has a number of these identical genes and apparently there's a strong correlation between number and length of the snout.

Of course, you'd probably consider this "tiny" but doesn't that suggest that many observed morphological differences in the fossil records are a result of such 'tiny' mutations?

Now if you're looking for development of whole organs, are you honestly looking for observed new organs within just a couple hundred generations? Organisms that reproduce extremely quickly like bacteria have undergone millions of generations under observation and have developed entirely new structures (i.e. the oft-cited nylon-digesting enzyme).

Another problem is your acknowledgement of "small variation" and your insistance on a boundary. Evolutionary biologists have published many theoretical evolutionary paths that account for observed differences via a large number of subsequent small mutations. I've never seen anybody ATTEMPT to define your "barrier" beyond the utterly undefined creationist "kind." If it's just hard to define, shouldn't it be easy to define a range in which the self-correcting barrier kicks in? Yet this has never been done.

Any mutation has a chance to 'beat' the correction mechanisms and if it happens to be neutral or beneficial it will then persist in the population. ANY mutation -- there is no limit to type or number (though some have a higher chance of beating the correction mechanisms as has been discussed in Mark Kennedy's current thread). Let the system go for enough generations and the resulting organism will be very different from the original organism.

 

[Mallon]

Right - I gave up on gross morphological changes.

Ectrodactyly is a gross morphological change, pop. Still, you continue to ignore it...

There are huge gross morphological differences between the various animals -- if they came from teeny tiny changes, why doesn't the fossil record reflect that?

It does, in many cases (though not always, as pointed out by gluadys, given the incomplete nature of the record). I just don't think you are being honest in examining the evidence. Look at the reptile/mammal jaw system for example: two very different masticating arrangements that can be linked via small, chronologic evolutionary changes in the fossil record:

This is exactly the kind of thing you are looking for, but I suspect you will continue to ignore it. Most creationists look at this kind of evidence and just wave their hands, using the ad hoc argument that it's just evidence for a "common designer" (or a "creative designer", depending on whether they're trying to downplay the similarities or the differences).

 

[laptoppop]

Ectrodactyly is a gross morphological change, pop. Still, you continue to ignore it...

That's because this appears to me to be more of a malformity rather than something that we look at as clearly beneficial. Negative or neutral examples abound. This one is "iffy" at best.

It does, in many cases (though not always, as pointed out by gluadys, given the incomplete nature of the record). I just don't think you are being honest in examining the evidence. Look at the reptile/mammal jaw system for example: two very different masticating arrangements that can be linked via small, chronologic evolutionary changes in the fossil record:

This is exactly the kind of thing you are looking for, but I suspect you will continue to ignore it. Most creationists look at this kind of evidence and just wave their hands, using the ad hoc argument that it's just evidence for a "common designer" (or a "creative designer", depending on whether they're trying to downplay the similarities or the differences).

IF the fossil record was covering as long of a period as postulated, including as many areas as it covers, it strains credibility that it never captures the essence of the changes.

Are there ANY clear examples of the kinds of beneficial postulated morphological changes represented in each of these steps?