Mechanism to allow for evolution. How did this mechanism come to be?

[D H]

I don't think it is about what is better in all cases. For example blue eyes and blonde hair in northern climates I am not convinced is because of it being better for sunlight. Otherwise people in Greenland would be blonde with blue eyes since those people up there would choose partners with lighter skin and lighter eyes.

Blonde hair and blue eyes does not engender any significant biological advantage. Light skin does however, and the gene that makes Northern Europeans have lighter skin also happens to make them have blonde hair and blue eyes. Note very well: Just because their are some advantages for someone far from the equator to have lighter colored skin does not mean that having lighter colored skin is essential for life in the North. It is just biologically advantageous. This gene also happens to be a regressive gene.

In saying "Otherwise people in Greenland would be blonde with blue eyes since those people up there would choose partners with lighter skin and lighter eyes" you are implicitly making several assumptions

1. You are assuming that the gene is present, period. If it isn't present it will not express itself. This gene happens to be present to some extent throughout Caucasian populations. It is extremely rare among those of Asian descent.
2. You are assuming that the gene not only is present, but that its presence is statistically significant. This gene happens to be recessive. Genetic drift has a tendency to wipe out recessive genes, even advantageous ones. This tendency can be overcome if the gene is statistically dominant -- for example, by going through a population bottleneck.
3. You are assuming that life without this gene is impossible. Just because it is advantageous does not mean it is necessary.
4. You are ignoring that there are other ways to get Vitamin D. Fish, for example, is an excellent source of Vitamin D. Eskimos happen to have a diet very high in fish. Sans fish, various parts of animals such as the liver are fairly high in Vitamin D.

 

[alxm]

I have trouble accepting a 'chance-event' theory for the origin of life

It's not a 'chance-event' theory. Pick a random card from a deck. If it's not a king, put it back. Repeat that 1000 times. Is it a 'chance event' if you're left with four kings? It's not. If you apply a rule, such as a selection rule, to a random process, then the result is not random.

You should probably begin by reading up on common http://www.talkorigins.org/faqs/faq-misconceptions.html" about evolution.

the evolution of complex organs like eye

The idea that the eye would somehow be specifically difficult to explain is a myth perpetuated by creationists by http://www.talkorigins.org/indexcc/CA/CA113_1.html" .

 

[D H]

Galilean transformation was slightly refined by Lorentz's. But we have a new theory called SR bringing in lot of implications. I think a similar modification of a postulate of the theory of evolution will come in the future.

That's already happened twice since Darwin's time. The modern synthesis combined Darwin's ideas with the basic concepts of genetics. Then there was that twisty little chemical discovered by Crick, Franklin, Watson, and Wilkins.

 

[ViewsofMars]

I'd like to strickly address the subject "mechanism" as posed by the OP. I think this might be helpful.

Mechanisms: The Processes of Evolution

Evolution is the process by which modern organisms have descended from ancient ancestors. Evolution is responsible for both the remarkable similarities we see across all life and the amazing diversity of that life—but exactly how does it work?

Fundamental to the process is genetic variation upon which selective forces can act in order for evolution to occur. This section examines the mechanisms of evolution focusing on:

Descent and the genetic differences that are heritable and passed on to the next generation;

Mutation, migration (gene flow), genetic drift, and natural selection as mechanisms of change;

The importance of genetic variation;

The random nature of genetic drift and the effects of a reduction in genetic variation;

How variation, differential reproduction, and heredity result in evolution by natural selection; and

How different species can affect each other’s evolution through coevolution.
http://evolution.berkeley.edu/evosite/evo101/IIIMechanisms.shtml

 

[BigFairy]

Projection.

Where does it say the two are mutually exclusive?

 

[alxm]

In saying "Otherwise people in Greenland would be blonde with blue eyes since those people up there would choose partners with lighter skin and lighter eyes" you are implicitly making several assumptions [...]

Nice list. If I may I add one, more general observation:
People tend to have an extremely superficial view of human differences. Hardly a surprise since we can't see inside the body. Even today, we don't fully know what's going on. So in history we've had racial theories, and phrenology, and ideas that your eye color says something about your character, and all kinds of ideas that link superficial human traits to other ones.

Add to that, we also tend to think of things as independent traits when we have no real reason to do so.

Until one knows exactly what a gene codes for, and all the consequences of a mutation, we simply don't know. We don't know how things are actually connected 'under the hood', but they're often not at all connected the way we tend to think they'd be.

Example: East Asians tend to have dry, crumbly ear wax. What possible use is that?
Well, it turns out that is all due to a single point mutation. The same mutation causes people to sweat less. So there's a link between the amount you perspire and the consistency of your earwax. That's not obvious. (it has to do with cortisols IIRC).

The evolutionary reason here is believed to be that the ancestors of East Asians migrated from Siberia. Living in a harsh cold climate, sweating less is a survival advantage.

It's a common misconception. If genes only did exactly one thing, how could genetic diseases survive? Because they're ususally not connected to one thing.

Some people think that homosexuality can't be genetic -"they don't reproduce!" What those folks don't get is that until we actually know what the 'gay gene' does, we can't say. For all we know, it could be completely necessary for sexuality in general! It's superficial to think that the only biological options would be our anthropocentric view, that of gay-vs-straight. It could well be that the 'genetic choice' wasn't between gay and straight, but between a gene that made 5% of people gay and one that made people dramatically less interested in sex. Obviously the former would propagate better.

 

[BoomBoom]

Until one knows exactly what a gene codes for, and all the consequences of a mutation, we simply don't know. We don't know how things are actually connected 'under the hood', but they're often not at all connected the way we tend to think they'd be.

Good point, in fact, there is probably no such thing as a single gene that is responsible for any phenotypical trait. An expressed gene can have hundreds, if not thousands, of interactions that result in different outcomes.

I think when many (lay)people think of evolution, they tend to really over-simplify and gloss over the complexity of the intricate biological processes involved and only see the "big picture" while neglecting the details of what is really going on.

 

[ViewsofMars]

Earlier on there was a discussion about the *eye*. This article is helpful.

Squid Pax-6 and eye  development

Stanislav I. Tomarev * , †, Patrick Callaerts ‡, Lidia Kos §, Rina Zinovieva , Georg Halder ‡, Walter Gehring ‡, and Joram Piatigorsky *
*Laboratory of Molecular and Developmental Biology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892-2730; ‡Department of Cell Biology, Biozentrum, University of Basel, Switzerland, Klingelbergstrasse 70, CH-4056 Basel, Switzerland; and §Laboratory of Genetic Disease Research, National Center for Human Genome Research, Bethesda, MD 20892-2730

Abstract:
"Pax-6 in vertebrates and its homolog eyeless in Drosophila are known to be essential for eye development. Here we investigate the role of Pax-6 in eye development in another major systematic group, molluscs. We demonstrate that alternatively spliced RNAs derived from a single Pax-6 gene in the squid (Loligo opalescens) are expressed in the embryonic eye, olfactory organ, brain, and arms. Despite significant sequence differences between squid Pax-6 and Drosophila eyeless in the region outside the paired- and homeodomains, squid Pax-6 is able to induce the formation of ectopic eyes in Drosophila. Our results support the idea that Pax-6 related genes are necessary for eye and olfactory system formation throughout the animal kingdom."

You can read the entire article from the Proceedings of the National Academy of Sciences of the United States of America (PNAS).
http://www.pnas.org/content/94/6/2421.full?sid=496d4157-46f1-457f-825e-7aeca380c9dc
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Also, I hope newcomers will take the time to explore the link I provided on the previous page. There's a lot of valuable information. Thanks.

I hope everyone has a superb weekend. I'm off to the ocean for fun and relaxation.

 

[Monique]

Good point, in fact, there is probably no such thing as a single gene that is responsible for any phenotypical trait.

Well, there's an oversimplification. You can have an allele of a gene that causes a very specific phenotypical trait, just look at genetic disorders for many examples.

 

[BoomBoom]

You can have an allele of a gene that causes a very specific phenotypical trait, just look at genetic disorders for many examples.

Most genetic markers as they relate to disease association involve statistical probablilities (if you have such and such allele, you have such and such probablility of contracting such and such disorder). But that said, sure you could have a certain mutation, duplication, or deletion that may result in some disorder, but that gene is most likely just a part of a larger interaction with other genes and probably has multiple functions and forms.

 

[Monique]

Most genetic markers as they relate to disease association involve statistical probablilities (if you have such and such allele, you have such and such probablility of contracting such and such disorder). But that said, sure you could have a certain mutation, duplication, or deletion that may result in some disorder, but that gene is most likely just a part of a larger interaction with other genes and probably has multiple functions and forms.

Sure there are multifactorial or polygenic disorders, but there are also mendelian disorders where a single gene is responsible for a specific disease (or trait). Look at Mendel's work on peas or Brenner's work on nematodes for examples of mendelian genetics.

 

[BigFairy]

Thanks for clearing that up.

 

[ViewsofMars]

Here’s something worthy to note from the Journal of Evolutionary Biology, Volume 22 Issue 1, Pages 192 – 200, Nov 11, 2008.

The evolution of sex-determining mechanisms: lessons from temperature-sensitive mutations in sex determination genes in Caenorhabditis elegans

C. H. CHANDLER*, P. C. PHILLIPS† & F. J. JANZEN*
*Department of Ecology, Evolution, and Organismal Biology, Iowa State University, Ames, IA, USA
†Center for Ecology and Evolutionary Biology, University of Oregon, Eugene, OR, USA
Abstract:"Sexual reproduction is one of the most taxonomically conserved traits, yet sex-determining mechanisms (SDMs) are quite diverse. For instance, there are numerous forms of environmental sex determination (ESD), in which an organism's sex is determined not by genotype, but by environmental factors during development. Important questions remain regarding transitions between SDMs, in part because the organisms exhibiting unique mechanisms often make difficult study organisms. One potential solution is to utilize mutant strains in model organisms better suited to answering these questions. We have characterized two such strains of the model nematode Caenorhabditis elegans. These strains harbour temperature-sensitive mutations in key sex-determining genes. We show that they display a sex ratio reaction norm in response to rearing temperature similar to other organisms with ESD. Next, we show that these mutations also cause deleterious pleiotropic effects on overall fitness. Finally, we show that these mutations are fundamentally different at the genetic sequence level. These strains will be a useful complement to naturally occurring taxa with ESD in future research examining the molecular basis of and the selective forces driving evolutionary transitions between sex determination mechanisms.”
http://www3.interscience.wiley.com/journal/121510645/abstract?CRETRY=1&SRETRY=0

This also peeked my interest.

Title: Evolution and mechanisms of plant tolerance to flooding stress.
Author: Jackson, Michael B.
Ishizawa, Kimiharu
Ito, Osamu

Found In: Annals of botany. Oxford University Press 2009 Jan., v. 103, no. 2p. 137-142.

Abstract: "BACKGROUND: In recognition of the 200th anniversary of Charles Darwin’s birth, this short article on flooding stress acknowledges not only Darwin’s great contribution to the concept of evolution but also to the study of plant physiology. In modern biology, Darwin-inspired reductionist physiology continues to shed light on mechanisms that confer competitive advantage in many varied and challenging environments, including those where flooding is prevalent. SCOPE: Mild flooding is experienced by most land plants but as its severity increases, fewer species are able to grow and survive. At the extreme, a highly exclusive aquatic lifestyle appears to have evolved numerous times over the past 120 million years. Although only 1-2% of angiosperms are aquatics, some of their adaptive characteristics are also seen in those adopting an amphibious lifestyle where flooding is less frequent. Lowland rice, the staple cereal for much of tropical Asia falls into this category. But, even amongst dry-land dwellers, or certain of their sub-populations, modest tolerance to occasional flooding is to be found, for example in wheat. The collection of papers summarized in this article describes advances to the understanding of mechanisms that explain flooding tolerance in aquatic, amphibious and dry-land plants. Work to develop more tolerant crops or manage flood-prone environments more effectively is also included. The experimental approaches range from molecular analyses, through biochemistry and metabolomics to whole-plant physiology, plant breeding and ecology."
http://agricola.nal.usda.gov/cgi-bi...=20090923120352&SID=1&DB=local&STARTDB=AGRIDB

I'm in the process of comparing the last one to an antique book I picked up entitled AN EVOLUTIONARY SURVEY OF THE PLANT KINGDOM by Robert F. Scagel, Robert J. Bandoni, Glenn E. Rouse, W.B. Scholfield, Janet R. Stein, and T.M.C. Taylor, Wadswroth Publishing Company, Inc. , 1968.