Convergent Evolution

[Jennifer]

See here (http://news.yahoo.com/s/hsn/20080229/hl_hsn/monkeygenethatblocksaidsvirusesevolvedmorethanonce ).

A gene in Asian monkeys that may have evolved as protection against a group of viruses that includes HIV has been identified by Harvard Medical School researchers, who add that their finding suggests the current AIDS epidemic is not a new kind of scourge.

....This is the second time a TRIM5-CypA hybrid gene has been identified in monkeys. The other one -- TRIMCyp -- was found in South American owl monkeys in 2004. But it's not likely that these two gene combinations arose from a single common ancestor, the Harvard researchers said...

This sort of thing is discussed all the time in the lab -- examples of convergent evolution, where a particular type of gene mutation is so beneficial that it arises (or very similar genes arise in separate unrelated species.

The eye is a similar process... where many eyes as we know them are wired in a backwards manner (the optic nerve runs into the eyeball on its way out, rather than just being affixed to the outside)... but a few unconnected marine species exist where the eye is wired in a "sensible way" -- suggesting that the eye structure evolved concurrently on parallel tracks, and the variation between attributable to the original random mutations.

Thoughts? Comments?

[Randomnity]

Yep, cool isn't it? :) It's remarkably common, actually...one of the many cool things about evolution.

That monkeys have already evolved some form of protection against AIDS though, that's pretty interesting. Although it sounds like it's more like protection against a whole family of less recent viruses (I don't remember exactly what lentiviruses are) that just happens to include AIDS.

[elfinchilde]

from the viewpoint of one who majored in microbiology:

convergent evolution is hardly a surprise. Because by Darwinian principle: Only the fittest survive, and adaptability is the key to survival. Hence, in all species, the genes that code for a specific trait that ensures survival will live on, whilst weaker members possessing 'undesirable traits' will die off. This ensures that the strongest live on to pass on their genes.

So if there was a virus that could target more than one species, for instance, then naturally, all the species which the virus targets will inevitably possess same/similar genes that confer protection against the virus. Because those species that did not, would have died out. Hence different species would posses the same/similar genes that confer a desirable trait.

Point of information: Monkeys developing genes against HIV. It has been postulated, but never proven, that AIDS (more specifically, the HIV virus) came about due to bestiality, originating from Africa, and transported throughout the world by sailors. The monkey equivalent is SIV--simian immunodeficiency virus. That has been around and acknowledged for decades, if not centuries.

HIV, however, only came into light in 1978, when a sailor was warded with a 'strange disease' in San Francisco. Subsequently, the cases exploded, and today, you have the AIDS pandemic.

So the possibility is that the virus simply mutated so as to be better virulent in humans, as compared to simians (ie, monkeys). Hence the parallel genes that protect against HIV--and SIV--exist in other species.

Additional information: (yes, a digression)
HIV is interesting in that it is a retrovirus--unique amongst the viruses in that it can survive both in DNA and RNA form: with the DNA form being a latent stage, explaining one of the reasons why HIV is so difficult to target in medical treatment.

Most living species possess only DNA, with RNA being a short phase when cells are reproducing. However, certain viruses genomes are made of RNA only. These are more rapidly mutating, as they lack what is known as a proof-reading function, which the DNA replicase enzyme possesses. Hence, there is less fidelity to the 'original script', which allows for greater species variation. Therein the second 'advantage' the HIV virus has: rapid RNA mutation.

[Jennifer]

from the viewpoint of one who majored in microbiology:

Neat, thanks!

convergent evolution is hardly a surprise. Because by Darwinian principle: Only the fittest survive, and adaptability is the key to survival. Hence, in all species, the genes that code for a specific trait that ensures survival long enough to reproduce will live on, whilst weaker members possessing 'undesirable traits' will die off before they can reproduce. This ensures that the strongest live on to pass on their genes.

Small tweak just to clarify it for others. (see bold)

I think one of the points where people get confused (and why I enjoyed this article) is that they are operating under the notion that almost all mutation will be bad mutations, therefore a "good change" doesn't seem believable to them.

Not only are good changes possible, but they are replicated in various species and actually do occur.

[elfinchilde]

Neat, thanks!



Small tweak just to clarify it for others. (see bold)

I think one of the points where people get confused (and why I enjoyed this article) is that they are operating under the notion that almost all mutation will be bad mutations, therefore a "good change" doesn't seem believable to them.

Not only are good changes possible, but they are replicated in various species and actually do occur.

No problem about the tweaking, thanks! I sometimes type stream-of-consciousness. So editing is much appreciated. :)

And yes. Mutations by themselves are never good or bad per se. It is what nature dictates for survival, that says if it is a good or bad mutation.

Using HIV again as the example (since it's quoted already), there are some people around who are naturally more resistant to the virus than others, due to some genes which they possess. In effect, this can be considered a good mutation, handed down from generations, and showing itself only when HIV surfaced in the human population.

H5N1 (bird flu) is the other example. There are some people, as well as birds, and other animal reservoirs, which have evolved/possessed immunity to this deadly disease. This is again due to genetic mutation--or more precisely, genetic variation. Sometimes it's rapid, sometimes it's not. All depends on the species, and the rate of the disease spreading.

note: because of the DNA/RNA thing---genetic mutation tends to occur much, much more slowly in animals, including humans, than in bacteria and viruses. In that sense, the microbes have one-up on us. Plus, one generation in humans is about 25 years, whilst for bacteria/viruses, it may be as short as a few hours. So generational mutation occurs much more swiftly in a same time frame for bugs than for us.

[Jasz]

thanks for the interesting discussion guys. now lunch is over.

[Nocapszy]

See here (http://news.yahoo.com/s/hsn/20080229/hl_hsn/monkeygenethatblocksaidsvirusesevolvedmorethanonce ).



This sort of thing is discussed all the time in the lab -- examples of convergent evolution, where a particular type of gene mutation is so beneficial that it arises (or very similar genes arise in separate unrelated species.

The eye is a similar process... where many eyes as we know them are wired in a backwards manner (the optic nerve runs into the eyeball on its way out, rather than just being affixed to the outside)... but a few unconnected marine species exist where the eye is wired in a "sensible way" -- suggesting that the eye structure evolved concurrently on parallel tracks, and the variation between attributable to the original random mutations.

Thoughts? Comments?
I'm not sure I understand: You're saying that the eye was two separate entities which eventually became one, to, presumably, serve a stronger or at least more important function? And that this is parallel (not timewise) to the way the anti-aids gene in those asian monkeys developed?

If that's the case then ears are largely the same way are they not?

[Jennifer]

I'm not sure I understand: You're saying that the eye was two separate entities which eventually became one, to, presumably, serve a stronger or at least more important function? And that this is parallel (not timewise) to the way the anti-aids gene in those asian monkeys developed?

If that's the case then ears are largely the same way are they not?

No. I'm saying the structure of the eye did not evolve just once. It looks like two separate strands of organisms separately developed it, as a response to environmental needs. But in the one strand, the optic nerve wired one way, and in the other, the strand wired backwards. Both work and are similar... but the specifics differ. (I think I read this in Dawkins' "The Blind Watchmaker.")

Just like with these monkeys, two different strands developed the same sort of useful protein separately.

[Nocapszy]

Of course :doh:

[Athenian200]

I'm afraid I didn't garner much from this. It seems like all I can infer is that similar environmental pressures can cause unrelated organisms to develop similar adaptations independently, and that seems fairly reasonable to me. What's strange about that?

Two scientists independently invented semiconductors around the same time, with the main difference being that one was produced with Germanium, and the other with Silicon... seems like a similar scenario in a way.

[Nocapszy]

No one said anything about strange. It's cool though.

Also, eyes are pretty complex. For them to be as similar as it sounds, without being an influence on one another is pretty phenomenal.

Maybe it implies that what they have in common are the only ways (or one of them) carbon life can use light energy for information.

Either that or, the groundwork was already mostly laid down, and eyes were inevitable (using the term loosely) thanks to what evolutionary steps came before them, but the two incarnations being shaped differently and such were the responses to the environment.

[ygolo]

For the biology majors here (and other knowledgeable individuals), I have a lot of questions about biological evolution in general. I think, it is still on-topic.

What is a "gene?" I have never quite gotten it's definition from it's usage. Is it a protien? Is it a small sequence of half a DNA-molecule that is known to be responsible for a certain function in an organism? What is it really? In specific/concrete terms?

What does it mean for a gene to be "expressed?" Is it that the through RNA (or whatever comparable mechanism there is in the organism), the identified "gene" creates the phenotype (or rather the little section of it) from the genotype (or rather the little section of it)?

Are there quantitative measures of "selection pressure"? IOW, are there somethings analogous to a "fitness functions (http://en.wikipedia.org/wiki/Fitness_function)" used by computer scientists in synthetic (computerized) genetic algorithms (http://en.wikipedia.org/wiki/Genetic_algorithm)? If so how does one determine such functions?

[Nocapszy]

For the biology majors here (and other knowledgeable individuals), I have a lot of questions about biological evolution in general. I think, it is still on-topic.

What is a "gene?" I have never quite gotten it's definition from it's usage. Is it a protien? Is it a small sequence of half a DNA-molecule that is known to be responsible for a certain function in an organism? What is it really? In specific/concrete terms? I'm not entirely sure (so someone who is should piggyback / correct me) but I think you're kind of right.

It's any combination of the segments of one's DNA that decides a characteristic. That is, the order of the chemistry provides groundwork for growth, which turns into distinctive attributes.

Again, I'm unsure if that's the full exact definition. I basically pieced that together from parts beginning physical anthropology class, so I could have easily left something out.

[Randomnity]

A gene is the DNA sequence that codes for a protein (or sometimes multiple proteins, or parts of proteins...but that's not important here). It is a blueprint, basically. Proteins are really what cause the eventual effects of the gene, for the most part.

A gene is said to be expressed when its protein is being produced...in other words, the gene is actually doing something.

I'm pretty sure there are quantitative measures of selection pressure, at least in models, but it's really not my area so I can't speculate.

HTH :)

[nightning]

And yes. Mutations by themselves are never good or bad per se. It is what nature dictates for survival, that says if it is a good or bad mutation.

Using HIV again as the example (since it's quoted already), there are some people around who are naturally more resistant to the virus than others, due to some genes which they possess. In effect, this can be considered a good mutation, handed down from generations, and showing itself only when HIV surfaced in the human population.

H5N1 (bird flu) is the other example. There are some people, as well as birds, and other animal reservoirs, which have evolved/possessed immunity to this deadly disease. This is again due to genetic mutation--or more precisely, genetic variation. Sometimes it's rapid, sometimes it's not. All depends on the species, and the rate of the disease spreading.

note: because of the DNA/RNA thing---genetic mutation tends to occur much, much more slowly in animals, including humans, than in bacteria and viruses. In that sense, the microbes have one-up on us. Plus, one generation in humans is about 25 years, whilst for bacteria/viruses, it may be as short as a few hours. So generational mutation occurs much more swiftly in a same time frame for bugs than for us.
Much agreed! :thumbup:

Stickle cell anemia can be deadly... so why do some many African Americans carry the gene? Because it's a beneficial mutation... For the heterogeneous carrier, 1 normal allele (copy of the gene) & 1 mutant allele, they are less susceptible of catching malaria. It's only when you have 2 copies of the mutant allele that you get the disease.

Mutation is just mutation... random changes. If you have a working system... there are more chances that random changes will impair the system rather than improve it. Perhaps that is why people associate mutation as being a bad thing. It really isn't... it's just RANDOM! Randomly good or bad.

Convergent evolution and evolution in general is always an interesting thing to see... The eye wiring is neat. :yes:

Another example would be the opposable "thumb" on the giant panda. They have 6 "fingers"... The ancestorial bears have evolved forward facing digits for running on the ground. The panda developed an appendage to help grip bamboo. Instead of relocating the first digit, the thumb is actually modified bone from their wrist. That's the power of random mutations for you.

There's always more than one way of solving a problem... convergent evolution nicely demonstrates that. :D


What is a "gene?" I have never quite gotten it's definition from it's usage. Is it a protien? Is it a small sequence of half a DNA-molecule that is known to be responsible for a certain function in an organism? What is it really? In specific/concrete terms?
A gene is a sequence of DNA. With the exception of viruses (they're technically not living) and bacteria, gene sequences are stored together in chromosomes, which are long long strands of DNA all coiled up together. Chromosomes are found within the nucleus (center) of every cell. As it's been said before, it's not a protein. It's the sequence of the DNA that allows for creating specific proteins. And it is the expression of these proteins that forms the phenotype of the individual (phenotype = what the individual looks like, eg hair color, eye color, height etc).

Technically one gene codes for one protein. This is known as the one gene/one enzyme hypothesis. Although multiple genes can produce multiple proteins that can influence a single attribute. Take hair color for example. Textbooks usually tell you that blond hair is recessive (needing 2 copies of blond) and dark color hair is dominant (1 copy of dark is sufficient). But what about the multitude of shades of blond or brunette... what about red heads? Hair color is controlled by multiple genes... However there's a main one that gives you the overall color. The interaction with the rest of them gives you the exact shade.


What does it mean for a gene to be "expressed?" Is it that the through RNA (or whatever comparable mechanism there is in the organism), the identified "gene" creates the phenotype (or rather the little section of it) from the genotype (or rather the little section of it)?
Gene is "expressed" into proteins (mostly enzymes). The exact process is like this:

DNA sequence (gene)-> translated (copied) to messanger RNA -> messanger RNA is processed and sent out of the nucleus -> mRNA is transcribed into (directs synthesis) proteins

Proteins are what makes up cells or acts as enzymes to influence parts of the cell.

Genotype = what gene alleles (copies) you have in your DNA
Phenotype = what is actually expressed... you can see it visibly


Are there quantitative measures of "selection pressure"? IOW, are there somethings analogous to a "fitness functions (http://en.wikipedia.org/wiki/Fitness_function)" used by computer scientists in synthetic (computerized) genetic algorithms (http://en.wikipedia.org/wiki/Genetic_algorithm)? If so how does one determine such functions?

I skimmed the wiki articles...
Genetic algorithm appears to be a computer model of evolution... taking factors like selection, chromosome crossover rate, mutation rate etc. The fitness function just tries to describe the selection forces. What might be beneficial for survival.

These parameters are difficult to pin point.

Take the rate of mutation... The rate is affected by the rate of cell division. Every time a cell divides into two, its genomic DNA needs to be replicated (copied). Mistake in the copying gives raise to mutations. So a fast dividing (in the case of bacteria) or fast reproducing (sexual reproduction) organism will have a higher rate of mutation than a slower dividing/reproducing one. Also the error rate of replication is not constant. A cell under stress will mutate faster (hence the use of UV radiation for mutation studies... or UV causing skin cancer). Different species also have different enzymes to copy DNA. Some enzymes have less "proof-reading" abilities than others. RNA retro viruses have an enzyme to copy RNA into DNA for insertion into the host. That enzyme is notoriously error prone and probably have been evolutionary selected to be that way. Afterall, the more mutations it makes... the more difficult it is for humans to come up with vaccines and drugs to stop them. ;)

Selection forces... it's something to keep in mind. Evolution happens far too slowly to be looked at much in real life (with the exception on bacteria, viruses, yeast). So evolutionary studies are based mostly on fossil records and on genomic and protein data we can extract from species that are still alive today. You can't say definitively what the environment thousands of years ago look like. Therefore there's no way to determine what factors are important for survival... Even for current times, you can only guess.

So they can't tell what exactly the selection forces are... but they can tell whether there are sudden changes in selection forces. Sudden change will be indicated in the fossil (DNA) record. With more changes in the DNA genome in the descendant species. (Age can be determined by carbon dating). It's also important to note that much of our genome (90 odd %) consists of non-coding DNA (what's known as junk DNA). Some sections might be necessary... but the sequence of these are not. The amount of random mutation arising in these segments can also be used to track time.

Uhhhh please excuse my rambliness. :blush:

[elfinchilde]

For the biology majors here (and other knowledgeable individuals), I have a lot of questions about biological evolution in general. I think, it is still on-topic.

What is a "gene?" I have never quite gotten it's definition from it's usage. Is it a protien? Is it a small sequence of half a DNA-molecule that is known to be responsible for a certain function in an organism? What is it really? In specific/concrete terms?

What does it mean for a gene to be "expressed?" Is it that the through RNA (or whatever comparable mechanism there is in the organism), the identified "gene" creates the phenotype (or rather the little section of it) from the genotype (or rather the little section of it)?

Are there quantitative measures of "selection pressure"? IOW, are there somethings analogous to a "fitness functions (http://en.wikipedia.org/wiki/Fitness_function)" used by computer scientists in synthetic (computerized) genetic algorithms (http://en.wikipedia.org/wiki/Genetic_algorithm)? If so how does one determine such functions?

*applause for the mousie*

i was going to answer your questions, ygolo, but then nightning and randomnity have said it all already. espcially nightning. :D hey, i perceive i have other bio people here! :holy:

was going to raise sickle cell anemia as an example, but thought better leave it out as it was late, and i didn't want to go into the details of sickle-cell shaped red blood cells vs regular shaped ones, and malaria. :nice: mousie.

just to give the poetic answer though, since what is life if it is only prose:

genes: from latin, genesis, meaning: creation.

that is why the standard defintion of DNA is "the blueprint of life". Because genes are essentially bases (A, T, C, G.) which code for all the functions of life.

In that sense, a singular gene can be defined as that particular sequence of DNA which codes for a sense function. i.e., a function that has utility and can potentially be expressed. (as opposed to non-sense DNA, which are bits of DNA that are all about a genome, which do not code for any function.)

note that a DNA 'molecule' is a complex structure. It is made of hundreds of thousands of bases linked together, then twisted together into a double-helix formation, which is THEN wound around what are known as histones. This is to compact the structure to save space in cells.

to get an idea of its complexity, here's a double helix image:

http://cache.eb.com/eb/image?id=73582&rendTypeId=35

2) when a gene is expressed, it means it produces a protein (via the DNA->RNA->protein process described by nightning) that is phenotypically seen in the person. Eg, if you talk about eye colour, then all people possess the alleles (different forms of the same gene) for every eye colour. But what is EXPRESSED, depends on which allele is dominant. (refer to mendelian genetics if you're interested in this). Hence an expressed gene is one whose function is seen in the person/animal. Be it for behaviour, or skin colour, hair colour, eye colour, etcetc. Even height, voice and all things.

3) quantitative measures of selection pressure. biostatistics. You use the chi-squared test, mainly.

hope this helps!

[ygolo]

I think it is clearer now what a gene and and what it means for it to be expressed. I don't think I was far off in my own conception.

However,...



3) quantitative measures of selection pressure. biostatistics. You use the chi-squared test, mainly.



Do you basically use chi-squared statistic to see if the relative frequecies of certain features/genes deviate significantly from expected (thereby indicating selection pressure for/against that feature/gene)?

[elfinchilde]

Do you basically use chi-squared statistic to see if the relative frequecies of certain features/genes deviate significantly from expected (thereby indicating selection pressure for/against that feature/gene)?

Chi-squared is just an example. THere are others you can use, as well. It depends a lot on your sample size, and all the other parameters that have to be fulfilled before hte results can be considered significant.

But yes, you use it to see for deviations as you said.

You can also use it to prove the links between genes and expressed phenotypes.

So versus a standard population, say testing to see if NPC (nasopharyngeal carcinoma, otherwise know as ear/nose cancer) and the EBV (epstein barr virus) are linked, you'd take populations with NPC+EBV, NPC alone, EBV alone, and another group without both.

Then apply whichever stats test is applicable, to see if there is significant deviation. the use of null hypothesis applies. So it all depends on the definition of hte criteria at the start.

need to note that for microbes, it's a lot easier to use biostats, as their lifespans are shorter, so you can get generations of information in a day/month. whereas for humans, it becomes pretty much an extrapolation process, since we've in essence not changed for at least 5,000 years. (the span of civilisation as we know it).

[ygolo]

Comming back to convergent evolution, doesn't convergent evolution indicate strong selection pressure (almost by definition--as defined by a chi-square comparisons using expected frequencies of all options)?

[elfinchilde]

Comming back to convergent evolution, doesn't convergent evolution indicate strong selection pressure (almost by definition--as defined by a chi-square comparisons using expected frequencies of all options)?


Yes. Athenian pointed out rightly. It shouldn't be a surprise at all. Life selects for the best; so the selection pressure will always be on the genes that confer survivability, across all species.

Hence convergent evolution.

Where you get divergent evolution, would be in a scenario of chaos. eg, different bugs specifically targetting different species, so that each species targetted needs to evolve different mechanisms for survival.

It's what is known as immunology: host-pathogen interactions. one of the most interesting of the bio-fields to study, because it is dynamic interactions we're talkign about; a constant process of evolution, as the bugs try to outsmart us, and we try to outsmart them in return. Cat and mouse game.

Alternatively, if there are more than one ways of beating the microbe, such that different paths evolve in different species (ie, different genes expressed, but all for the same function of beating the microbe, just in different ways). However, the end is the same: continued survival of the species. Selection pressure will always be for the best possible combination that best confers the ability to survive.

[Zergling]

It's also important to note that much of our genome (90 odd %) consists of non-coding DNA (what's known as junk DNA). Some sections might be necessary... but the sequence of these are not. The amount of random mutation arising in these segments can also be used to track time.

As a side note, figuring out what, if anything, "junk DNA" does is something being researched at the moment, since it otherwise seems strange that so much of DNA would not be being used. the amount of junk DNA also tends to increase with organism complexity, from what I've heard, while the amount of genes do not, which suggests ot a lot of people that it has some other important functuions that haven't been worked out yet, that do not involve proteins.

[elfinchilde]

As a side note, figuring out what, if anything, "junk DNA" does is something being researched at the moment, since it otherwise seems strange that so much of DNA would not be being used. the amount of junk DNA also tends to increase with organism complexity, from what I've heard, while the amount of genes do not, which suggests ot a lot of people that it has some other important functuions that haven't been worked out yet, that do not involve proteins.

one theory has to do with evolution: that people/all creatures are essentially made of different insensate cells which got together, because it was beneficial for them. In time, as the whole organism evolved, some of these unnecessary cells lost their function (like the human appendix), but their genome still remains within, becoming 'junk DNA' (otherwise known as non-sense DNA).

The other thing that is interesting is this: diseases which kill, tend to start from the ends of the cells. Also, all cells die natural programmed deaths: there is a time frame for life. The process is known as apoptosis: programmed cellular death. Enzymes known as telomerases are responsible for 'eating' up DNA sequences.

It is because of this that we have death. Since on a micro-level, what is death but the loss of genes.

Man seeks for immortality. But the only cells that are immortal are cancer cells. Their telomerases have stopped functioning. So cancer cells are the only ones that grow and grow, and live forever. (perhaps poetry has it right, intuitively: that death is the only immortal thing. Ironically, immortality is to be found in what brings death.)

Which brings us back to junk DNA. Quite a large proportion of them are found at the end of the cells. So when the telomerases start eating up DNA, these go first. In essence, they become infantry soldiers who fall first in the line of fire, such that the important leaders (ie, the sense DNA) are still protected for a while.

That's one postulated function.

[nightning]

As a side note, figuring out what, if anything, "junk DNA" does is something being researched at the moment, since it otherwise seems strange that so much of DNA would not be being used. the amount of junk DNA also tends to increase with organism complexity, from what I've heard, while the amount of genes do not, which suggests ot a lot of people that it has some other important functuions that haven't been worked out yet, that do not involve proteins.

True... but there are also DNA elements within called transposons (http://en.wikipedia.org/wiki/Transposon), or the jumping genes (not really genes at all :dry:). They cut and paste themselves within the genome (can probably duplicate themselves as well). Scientists are not exactly sure whether transposons in the cell does anything useful. The common hypothesis is that these are parasitics DNA sequences that rides on the organism's genome. The cell evolved mechanisms to "tolerate" these parasites. When transposons manages to insert themselves into coding regions... the cell has enzymes that removes the offensives junk from the mRNA so that only proper proteins are expressed... Sometimes the transposons are "bad" and the cell fails to remove the junk... in that case you get diseases.

That's the theory I prescribed to anyhow... It's interesting to note that the more complex the organism, the more of these transposons exists in the genome. Also that much of the non-coding regions consists of short sequences repeated over and over again. They might be spacers necessary for DNA histone folding (how DNA is packaged up into chromosomes)... but some of those can also be mutated transposons.

[ygolo]

True... but there are also DNA elements within called transposons (http://en.wikipedia.org/wiki/Transposon), or the jumping genes (not really genes at all :dry:). They cut and paste themselves within the genome (can probably duplicate themselves as well). Scientists are not exactly sure whether transposons in the cell does anything useful. The common hypothesis is that these are parasitics DNA sequences that rides on the organism's genome. The cell evolved mechanisms to "tolerate" these parasites. When transposons manages to insert themselves into coding regions... the cell has enzymes that removes the offensives junk from the mRNA so that only proper proteins are expressed... Sometimes the transposons are "bad" and the cell fails to remove the junk... in that case you get diseases.

That's the theory I prescribed to anyhow... It's interesting to note that the more complex the organism, the more of these transposons exists in the genome. Also that much of the non-coding regions consists of short sequences repeated over and over again. They might be spacers necessary for DNA histone folding (how DNA is packaged up into chromosomes)... but some of those can also be mutated transposons.

Ar these pathological versions of Homeobox (http://en.wikipedia.org/wiki/Homeobox) genes?

From a computer geek's perspective... Self-modifying code can pack a lot more useful information than in the same amount of static code.

Also, continuing with the analogy with the genetic algorithms, it was found that putting genes in the algorithm that modify other genes in our virtual chromosomes makes punctuated equilibrium in the population of solutions more likely (my theory is that the fitness landscape changes with these genes to have multiple plateaus).

[nightning]

Ar these pathological versions of Homeobox (http://en.wikipedia.org/wiki/Homeobox) genes?

From a computer geek's perspective... Self-modifying code can pack a lot more useful information than in the same amount of static code.

Also, continuing with the analogy with the genetic algorithms, it was found that putting genes in the algorithm that modify other genes in our virtual chromosomes makes punctuated equilibrium in the population of solutions more likely (my theory is that the fitness landscape changes with these genes to have multiple plateaus).

Hmmmm could be convergent evolution by these two sets of genes. I'm not sure. My guess is they share similarities but have arisen differently. Homeobox genes evolved to serve the cell, transposon evolved to serve itself.

Self-modifying code... Hmmmm the question is how do you get it to modify the way you want it so that it will do what you want it to when placed under a changing environment in which you have no control over?

[ygolo]

Hmmmm could be convergent evolution by these two sets of genes. I'm not sure. My guess is they share similarities but have arisen differently. Homeobox genes evolved to serve the cell, transposon evolved to serve itself.


So what is your take on Richard Dawkins' notion of "selfish genes." Couldn't it be said that even the genes that don't harm the host organism are acting out of self-preservation. No?


Self-modifying code... Hmmmm the question is how do you get it to modify the way you want it so that it will do what you want it to when placed under a changing environment in which you have no control over?


That, in practice, turns out to not be too different from having static code do what is desired under environments where we have no control. Well-designed self-modifying code tends to be as robust as well-designed static code. However, the space savings can be immense. The usual place where I use it is in embedded systems for creating polymorphic (http://en.wikipedia.org/wiki/Polymorphism_in_object-oriented_programming) interrupt behavior. Many hackers also use polymorphism (http://en.wikipedia.org/wiki/Polymorphic_code) of this sort to bypass security features and hide viruses. This unfortunately gives the technique a bad rep.

(If you couldn't tell by now, I am fascinated with the links between biology and computing)

[nightning]

So what is your take on Richard Dawkins' notion of "selfish genes." Couldn't it be said that even the genes that don't harm the host organism are acting out of self-preservation. No?
I'm afraid I've been "brain washed" early in my scientific career on the selfish gene theory. (I can only blame my 1st year biology prof on it... crazy Rosie... a brilliant geneticist... but still crazy.) I prescribe fully to that line of thinking. The purpose in life for everything... even down to sequences of DNA is to survive... Obviously nothing last forever... it decays, decomposes, breaks down, whatever. So to keep on living forever, you make copies of yourself... from the "baby genes" to "mini mes". Inertia more or less applies to everything... even genes are "lazy". Why do more work than you have to? Forget about extra enzymes... The shorter your sequence... the faster you can replicate yourself... Being able to make 3 copies of yourself in the time your opponent can make 2 is so much better. Afterall resources are limited.

Some genes (like the transposons and viruses) op for the parasite route... piggy back themselves on the suckers. Other genes rather prefer to cooperate to ensure their own survival. (Sure, your rate of replication will be slower, but at least you guarentee you survive to leave some copies.

It's not much different than survival strategies of many animal species... a sort of gull for example. Some hunt their own fish, other steals it from the hunters. It's game theory played out in the biological world. I have more than a passing interest on this topic. :yes:



That, in practice, turns out to not be too different from having static code do what is desired under environments where we have no control. Well-designed self-modifying code tends to be as robust as well-designed static code. However, the space savings can be immense. The usual place where I use it is in embedded systems for creating polymorphic (http://en.wikipedia.org/wiki/Polymorphism_in_object-oriented_programming) interrupt behavior. Many hackers also use polymorphism (http://en.wikipedia.org/wiki/Polymorphic_code) of this sort to bypass security features and hide viruses. This unfortunately gives the technique a bad rep.

(If you couldn't tell by now, I am fascinated with the links between biology and computing)
Ah! Object oriented programming... I've always been meaning to learn more about it. But never gotten the time and energy to do so. Yes... I see what you mean now.

Biological systems and computing, if I know more about computing perhaps I would be too. I like dynamic system interactions. ^^