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Henry J



Posts: 4013
Joined: Mar. 2005

(Permalink) Posted: June 20 2009,17:54   

Quote
whether she has a headache


Is there a variable for the amount of aspirin that's available?

Henry

  
dvunkannon



Posts: 1377
Joined: June 2008

(Permalink) Posted: June 21 2009,22:26   

From the MEDAL (Missouri Estimation of Distribution Algorithms Laboratory blog

Quote
John H. Holland will give a keynote speech at GECCO-2009 on July 12, 2009 (Sunday), 10:40am-11:40am. The talk is entitled Genetic Algorithms: Long Ago [Past] and Far Away [Future] and the abstract of the talk follows:

It was in the mid-50’s of the 20th century when I realized that Fisher’s fundamental theorem could be extended from individual alleles to co-adapted sets of alleles, without linearization. That led to a realization that recombination, rather than mutation, was the main mechanism providing grist for the natural selection mill. There was little theory concerning recombination in those days, but now recombination is a standard explanation for biological innovations, such as swine flu.

Much later, in the early 1990’s, GA’s provided the “adaptive” part of rule-based models of complex adaptive systems (CAS), such as the artificial stock market pioneered at the Santa Fe Institute. Tag-based signal processing occurs in systems as different as biological cells, language acquisition, and ecosystems. CAS models offer a unified way to study the on-going co-evolution of boundary and tag networks in these systems


--------------
I’m referring to evolution, not changes in allele frequencies. - Cornelius Hunter
I’m not an evolutionist, I’m a change in allele frequentist! - Nakashima

  
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: June 23 2009,19:10   

Quote (Steve Schaffner @ June 19 2009,13:33)
Quote (slpage @ June 19 2009,13:09)
I am still wondering why they think that constraining the outcomes to a constant population size is biolgically realistic.

It's a feature of many population genetics models. It has the advantage of being simple. How accurate it is depends a lot on what organism you're looking at.

Of course, there's a big difference between using models to analyze how particular aspects of evolution work and trying to model the entire process well enough to say whether it can occur.

Which is sort of my point.  Their claim is that this is state of the art and realsitic, yet they appear to have employed certain parameters for simplicity rather than realism.

Constant population size is one of my pet peeves with Haldane's model as well.

  
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: June 23 2009,19:13   

Quote (Henry J @ June 19 2009,16:16)
Quote
Of course, there's a big difference between using models to analyze how particular aspects of evolution work and trying to model the entire process well enough to say whether it can occur.

Well, that's just being picky! :p

But yeah, if populate size is allowed to go way up, then the simulation would have to deal with food shortages (i.e., fitness would drop across the board if population gets too large for the food supply).

Henry

I don't mean just allowing it to grow willy nilly - that is not realistic, either.  But if they want to claim 'most realistic' then it seems to me employing non-universal constraints negates that claim.

I also gather that while deleterious mutations are allowed to accumulate and not reduce, that beneficials are allowed to be lost.  Is that correct?

  
Steve Schaffner



Posts: 13
Joined: June 2009

(Permalink) Posted: June 23 2009,19:44   

Quote (slpage @ June 23 2009,19:13)
I don't mean just allowing it to grow willy nilly - that is not realistic, either.  But if they want to claim 'most realistic' then it seems to me employing non-universal constraints negates that claim.

True, but I doubt variation in population size would have much effect on the long-term fate of the population.
Quote

I also gather that while deleterious mutations are allowed to accumulate and not reduce, that beneficials are allowed to be lost.  Is that correct?

I haven't been running the program, but I haven't seen anything obviously wrong with how they handle beneficial and deleterious mutations. In the real world, deleterious mutations of very small effect really do accumulate, and most beneficial mutations really are lost.

  
AnsgarSeraph



Posts: 11
Joined: June 2009

(Permalink) Posted: June 24 2009,21:24   

I've been in touch with Dr. Wes Brewer, who maintains the MENDEL code. He's still working on the Linux flavors and hopes to have a production copy soon. He's not comfortable posting it on a public site, at the moment, but said that I could privately supply the link to people here who want it.

The "big deal" aspect of it is that this is version 1.4.5. It looks like the source code is packaged in "cgi-bin/cmendel" and "cgi-bin/fmendel" (but that's just from the README . . . I don't know code so I didn't open any files).

Anyone who wants this thing can email me @

whitebriar - gmail - com

—Sam

  
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: June 25 2009,03:08   

Quote (AnsgarSeraph @ June 24 2009,21:24)
I've been in touch with Dr. Wes Brewer, who maintains the MENDEL code. He's still working on the Linux flavors and hopes to have a production copy soon.

Mah, a java version would be better IMHO - install apache etc ????

Then it would work on Linux, Windows, MacOS anything that has a JVM in fact.

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
Zachriel



Posts: 2594
Joined: Sep. 2006

(Permalink) Posted: June 25 2009,08:41   

The calculation of "working fitness" is seemingly broke. From Mendel's Accountant:

      do i=1,total_offspring
          work_fitness(i) = work_fitness(i)/(randomnum(1) + 1.d-15)
       end do


We can test this by taking a series of fitnesses k from 1.001 to 2,

 For k = 1 To 1000
      Cells(k, "a") = 1+ k / 1000
      Cells(k, "b") = Cells(k, "a") / Rnd
  Next k


This is a typical result:

9 Average
31 St.Dev.
362% Relative St.Dev.
1.04 Min
533 Max

The original distribution of k has a Relative St.Dev. of 19%. It's worse for fitnesses distributed between 0.5 and 1.5 or 0.5 and 1. (Just like the phylogenetic fitness, the calculation is not normalized. And why ÷Rnd^1? Why not ÷Rnd^½ or ÷Rnd^¾?) This single operation eliminates the vast majority of the signal from genetic or phylogenetic fitness.

A more reasonable calculation is Roulette Wheel selection.

I have a working version of Gregor's Bookkeeper. I'll post on that in the next few rotations.


-
Fixed a problem.

--------------
There is only one Tard. The Tard is One.

   
Zachriel



Posts: 2594
Joined: Sep. 2006

(Permalink) Posted: June 25 2009,10:03   

Ranking is the actual measure, not the nominal working fitness. If we just look at 1000 trials, comparing the actual rank to the expected rank, a perfect fitness signal will have a St.Dev. of zero; 1,2,3,4,5 ...

Ranking of random fitness has a St.Dev of about 410 from the expected rank. Using (1 + k / 1000)÷Rnd the St.Dev between the expected rank and the actual rank is about 320-350. A very weak signal.

This is sorted by Working Fitness. What was ranked 863 is now first on the list.

Phylo      Working       Phylo
Fitness     Fitness       Rank
1.863   15,077.64      863
1.526     5,482.23      526
1.759       591.73       759
1.298       369.09       298
1.413       274.25       413
1.986       207.86       986
1.781       194.58       781
...

Of course, there are many other sources of noise that dilute the fitness signal, but this is the most egregious departure from model realism.


-
A different run than the previous. They're both typical and should be easy to verify.

--------------
There is only one Tard. The Tard is One.

   
dvunkannon



Posts: 1377
Joined: June 2008

(Permalink) Posted: June 25 2009,10:07   

Quote (Zachriel @ June 25 2009,09:41)
The calculation of "working fitness" is seemingly broke. From Mendel's Accountant:

      do i=1,total_offspring
          work_fitness(i) = work_fitness(i)/(randomnum(1) + 1.d-15)
       end do


We can test this by taking a series of fitnesses k from 1.001 to 2,

 For k = 1 To 1000
      Cells(k, "a") = 1+ k / 1000
      Cells(k, "b") = Cells(k, "a") / Rnd
  Next k


This is a typical result:

9 Average
31 St.Dev.
362% Relative St.Dev.
1.04 Min
533 Max

The original distribution of k has a Relative St.Dev. of 19%. It's worse for fitnesses distributed between 0.5 and 1.5 or 0.5 and 1. (Just like the phylogenetic fitness, the calculation is not normalized. And why ÷Rnd^1? Why not ÷Rnd^½ or ÷Rnd^¾?) This single operation eliminates the vast majority of the signal from genetic or phylogenetic fitness.

A more reasonable calculation is Roulette Wheel selection.

I have a working version of Gregor's Bookkeeper. I'll post on that in the next few rotations.


-
Fixed a problem.

I assume you mean the scaling of fitness by total population fitness used in routlette selection, correct?

I'm not following the dissection of MA, is work_fitness being used to drive a selection algorithm? If so, the division by rnd() is equivalent to assuming that all selection takes place after a night of drinking heavily.

Roulette selection assumes that details don't matter - of several equally snappily dressed men at the bar, the one with the clean fingernails will not be selected much more frequently than the rest with dirty fingernails. Is this "realistic"? What does MA assume about sexual selection?

A lot of GAs use tournament selection to maintain a more constant selection pressure. I think you could argue that tournament selection models some part of the sexual selection process.

ETA - or give users a choice of selection algorithm.

--------------
I’m referring to evolution, not changes in allele frequencies. - Cornelius Hunter
I’m not an evolutionist, I’m a change in allele frequentist! - Nakashima

  
Zachriel



Posts: 2594
Joined: Sep. 2006

(Permalink) Posted: June 25 2009,11:00   

Quote (dvunkannon @ June 25 2009,10:07)
I assume you mean the scaling of fitness by total population fitness used in routlette selection, correct?

Yes, the scaling determines probability of successful reproduction.  

Quote (dvunkannon @ June 25 2009,10:07)
I'm not following the dissection of MA, is work_fitness being used to drive a selection algorithm? If so, the division by rnd() is equivalent to assuming that all selection takes place after a night of drinking heavily.

Close, but not quite. Actual reproductive success involves more than mating selection. There is still a strong component of phylogenetic health involved. Reproductively healthier individuals will tend to mate more often and produce more offspring, even when they mate randomly. (Perhaps you should spend more time in bars—for observational purposes, of course.)

Quote (dvunkannon @ June 25 2009,10:07)
Roulette selection assumes that details don't matter - of several equally snappily dressed men at the bar, the one with the clean fingernails will not be selected much more frequently than the rest with dirty fingernails. Is this "realistic"?

Yes. Minor differences tend to have minor effects. There is no amplification for discernment. Like the bar at 10 PM rather than 1 AM (i.e. after only moderate alcohol consumption).

Quote (dvunkannon @ June 25 2009,10:07)
What does MA assume about sexual selection?

It doesn't (as far as I know).

--------------
There is only one Tard. The Tard is One.

   
Zachriel



Posts: 2594
Joined: Sep. 2006

(Permalink) Posted: June 25 2009,20:47   

Gregor's Bookkeeper is now workable enough to report some results. But first the implementation.

Gregor's Bookkeeper doesn't keep track of all mutations, just their cumulative effect. The only concern at this point is average fitness and genomic decay. But it does allow us to inspect the population to see what is happening. Bells and whistles don't matter much in the face of the claim that Mendel's Accountant has overthrown 150 years of biological science. We eagerly anticipate replicating this exciting discovery.

Each member of the population is comprised of a collection of genes. Mutations can occur randomly in any member and any gene. Most mutations are very nearly neutral.  



Beneficial mutations are often dominant because they can cover for the activity of a weaker partner. But sometimes alleles can combine effects, or deleterious mutations can sometimes even be dominant. This aspect of the model is still unsatisfying, so we're leaving Dominant = 50%, Recessive = 50%.



Phylogenetic Fitness is normalized. That means Environmental Noise scales properly with fitness.  



PhyloIndex holds the sort of the Phylogenetic Fitness. We take those with the highest Phylogenetic Fitness to enter the mating round (after eliminating those with very low fitness).



Those with higher Phylogenetic Fitness are more likely to mate and produce a large number of offspring. The first step is to create an accumulation of normalized fitnesses. Then we use this table to determine winners and losers. Finally, we select a random allele from each Parent.



Other aspects include allowing normal variations in population, average offspring and mutation rates over time.

--------------
There is only one Tard. The Tard is One.

   
midwifetoad



Posts: 3551
Joined: Mar. 2008

(Permalink) Posted: June 25 2009,21:28   

I think you left out the smoke and mirror generators and the obfuscationizer.

--------------
”let’s not make a joke of ourselves.”

Pat Robertson

  
Zachriel



Posts: 2594
Joined: Sep. 2006

(Permalink) Posted: June 26 2009,07:31   

Quote (midwifetoad @ June 25 2009,21:28)
I think you left out the smoke and mirror generators and the obfuscationizer.

Mirrors are easy, but modeling smoke. That's hard.

--------------
There is only one Tard. The Tard is One.

   
Henry J



Posts: 4013
Joined: Mar. 2005

(Permalink) Posted: June 29 2009,13:34   

Quote (Zachriel @ June 26 2009,06:31)
Mirrors are easy, but modeling smoke. That's hard.

And hazardous to the health.

  
Zachriel



Posts: 2594
Joined: Sep. 2006

(Permalink) Posted: July 02 2009,09:25   

Quote (Zachriel @ June 25 2009,11:00)
 
Quote (dvunkannon @ June 25 2009,10:07)
{snipped} ... equivalent to assuming that all selection takes place after a night of drinking heavily.

(Perhaps you should spend more time in bars—for observational purposes, of course.)

I trust, dvunkannon, that your field work is progressing well.

Quote (dvunkannon @ June 25 2009,10:07)
A lot of GAs use tournament selection to maintain a more constant selection pressure. I think you could argue that tournament selection models some part of the sexual selection process.

I've been thinking about your analogy and suggestions. Roulette seems to emulate relative fecundity. Those with higher fecundity will tend to mate with those of higher fecundity simply because they mate and produce offspring more often. (Wimps pass out in the corner, rarely mating.) But Tournament does tend to pair those with like-fecundity, so I suppose it does seem like sexual selection. I may try that next. I thought about some more explicit method, but that might be beyond what we are trying to accomplish with this model.

--------------
There is only one Tard. The Tard is One.

   
Zachriel



Posts: 2594
Joined: Sep. 2006

(Permalink) Posted: July 02 2009,09:25   

There was some question about the mutation algorithm. It's based on a mirror of this RndGamma distribution. {The lip at 1.000000 is due to cutting off the maximum effect at an arbitrary level.}



The probability distribution of mutational effect tends to be very small, with larger effects increasingly rare.



The routine usually returns a multiplier of just a little more than one (favorable), or a multiplier of just a little less than one (deleterious).

Deleterious and favorable mutational effects have an identical distribution, except that favorable mutations are generally much rarer. I'm using the Excel Application GammaDist function. It's not a perfect distribution, but should be more than sufficient for our purposes.

--------------
There is only one Tard. The Tard is One.

   
Zachriel



Posts: 2594
Joined: Sep. 2006

(Permalink) Posted: July 02 2009,09:27   

The qualitative results of Gregor's Bookkeeper are fairly straightforward. If the rate of reproduction is low compared to the mutation rate, that is, if many offspring are mutants rather than clones, then deleterious mutations will tend to accumulate in genomes. (They will actually eventually accumulate with any finite population.)

But every once in a while, a significant and favorable mutation will sweep through the population. For a given ratio of favorable to beneficial mutations, the larger the population, the less the fitness will drop before a beneficial mutation has a chance to sweep through the population. So for a given setting, just dial-up the population (or reproductive rate) to avoid genomic meltdown.

Now consider a large population that has been divided into small isolated groups. Many will meltdown. But some, by chance, will experience favorable mutations that will sweep the population. Then if the population is allowed to grow, this subpopulation can avoid genomic meltdown and experience further gains in fitness. Lots of branches, most of which fail, but a few that then prosper. Adaptive radiation.

And we have yet to account for sexual selection, or hybridization.

--------------
There is only one Tard. The Tard is One.

   
midwifetoad



Posts: 3551
Joined: Mar. 2008

(Permalink) Posted: July 02 2009,10:11   

Forgive me for having trouble with the meltdown concept. Is there an observed instance in the real world of a reproducing population going extinct due to the accumulation of deleterious mutations?

What would that look like?

--------------
”let’s not make a joke of ourselves.”

Pat Robertson

  
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: July 02 2009,10:19   

Quote (midwifetoad @ July 02 2009,10:11)
Forgive me for having trouble with the meltdown concept. Is there an observed instance in the real world of a reproducing population going extinct due to the accumulation of deleterious mutations?

What would that look like?

http://www.uncommondescent.com/

ba-dum-tish!

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
Zachriel



Posts: 2594
Joined: Sep. 2006

(Permalink) Posted: July 02 2009,10:46   

Quote (midwifetoad @ July 02 2009,10:11)
Forgive me for having trouble with the meltdown concept. Is there an observed instance in the real world of a reproducing population going extinct due to the accumulation of deleterious mutations?

What would that look like?

In asexual populations, it's rather easy to understand. If most offspring are mutants, they are nearly always of lower fitness. Organisms such as bacteria have low individual mutation rates, and most offspring are exact clones. Even then, they often recombine genetic material.

It's a bit different in sexually reproducing species such as vertebrates. Bottleneck populations, species that have had their habitat severely reduced, or varieties near range edges, are believed to suffer mutational meltdown. Reproductive rates and numbers of viable offspring tend to decline due to inbreeding, and that can make the species vulnerable to extinction. It's a problem with many species being pushed to the brink by humans.

Hybridization can sometimes reinvigorate a species.

--------------
There is only one Tard. The Tard is One.

   
midwifetoad



Posts: 3551
Joined: Mar. 2008

(Permalink) Posted: July 02 2009,11:22   

I'm still a bit confused. It is commonly argued, and has been for many decades, that low population numbers lead to extinction, even if the remaining members are protected.

But I fail to get the relevance for TOE. Extinction seems to be a rather common event at geological time scales, so what's the problem for the theory?

I'm thinking the definition of deleterious is rather arbitrary unless it is exposed to selection. What prevents us from defining all niche specializations as deleterious at geological time scales, since specialization puts a population at risk for extinction.

--------------
”let’s not make a joke of ourselves.”

Pat Robertson

  
Zachriel



Posts: 2594
Joined: Sep. 2006

(Permalink) Posted: July 02 2009,11:52   

Quote (midwifetoad @ July 02 2009,11:22)
I'm still a bit confused. It is commonly argued, and has been for many decades, that low population numbers lead to extinction, even if the remaining members are protected.

But I fail to get the relevance for TOE. Extinction seems to be a rather common event at geological time scales, so what's the problem for the theory?

The claim is that genetic meltdown affects even normal-size populations. Of course, Mendel's Accountant ignores many factors that mitigate against the claim.

 
Quote (midwifetoad @ July 02 2009,11:22)
I'm thinking the definition of deleterious is rather arbitrary unless it is exposed to selection. What prevents us from defining all niche specializations as deleterious at geological time scales, since specialization puts a population at risk for extinction.

You're right in general.

Presumably, Mendel's Accountant is considering absolute fitness, meaning populations can precipitously degrade if the fecundity drops below a certain level. If they were serious, they would investigate under which circumstances they would not see meltdown, and explore this boundary in more detail. But their purpose is apologetics dressed up as science. I certainly wouldn't consider any such simulation to be anything more than qualitatative unless carefully matched to a biological situation. It doesn't even account for sexual selection; and without empirical verification, it is subject to simple mistakes such as the calculation of "working fitness" noted above. They see what they want to see.

--------------
There is only one Tard. The Tard is One.

   
midwifetoad



Posts: 3551
Joined: Mar. 2008

(Permalink) Posted: July 02 2009,12:29   

I'd think if you were trying to model a natural phenomenon, you would have an example in mind. Something from the real world to model. But maybe that's just me.

I haven't heard of any decline in the fecundity of asexual organisms. All the species I know of that are listed as in danger of extinction seem to be in danger due to reduction of or rapid change in habitat,  or due to introduction of diseases or predators. Neither of these causes involves genetic entropy.

I just wonder what observation led to the genetic entropy hypothesis.

--------------
”let’s not make a joke of ourselves.”

Pat Robertson

  
Bob O'H



Posts: 1956
Joined: Oct. 2005

(Permalink) Posted: July 02 2009,13:52   

Quote (midwifetoad @ July 02 2009,12:29)
I'd think if you were trying to model a natural phenomenon, you would have an example in mind. Something from the real world to model. But maybe that's just me.

Mendel's Accountant is meant to be used to make a general point about evolution, so they don't want  to burden the model with the specifics of one system.

Quote
I haven't heard of any decline in the fecundity of asexual organisms. All the species I know of that are listed as in danger of extinction seem to be in danger due to reduction of or rapid change in habitat,  or due to introduction of diseases or predators. Neither of these causes involves genetic entropy.

Well, yes.  I'm a bit cynical about a lot of conservation genetics: far too many people doing it use species of great conservation concern, like fruit flies.

In think there has been some work showing it happens in nature, but there are so many other threats as well.

Quote
I just wonder what observation led to the genetic entropy hypothesis.

The Fall.

Sanford is a YEC, so his argument is that things have been getting worse since The Fall, and all we can do is pray.

--------------
ID theorists don’t postulate a designer for their arguments. - Crandaddy
There is no connection between a peppered moth, natural selection, and religion that I can see. - FtK

   
Henry J



Posts: 4013
Joined: Mar. 2005

(Permalink) Posted: July 02 2009,14:12   

Quote (midwifetoad @ July 02 2009,11:29)
I just wonder what observation led to the genetic entropy hypothesis.

Observation? Observation? We don't need no steeenkin pathetic-level-of-detail observation!!111!!eleven1!!

  
dvunkannon



Posts: 1377
Joined: June 2008

(Permalink) Posted: July 02 2009,23:51   

Quote (Zachriel @ July 02 2009,10:25)
Quote (Zachriel @ June 25 2009,11:00)
   
Quote (dvunkannon @ June 25 2009,10:07)
{snipped} ... equivalent to assuming that all selection takes place after a night of drinking heavily.

(Perhaps you should spend more time in bars—for observational purposes, of course.)

I trust, dvunkannon, that your field work is progressing well.

Quote (dvunkannon @ June 25 2009,10:07)
A lot of GAs use tournament selection to maintain a more constant selection pressure. I think you could argue that tournament selection models some part of the sexual selection process.

I've been thinking about your analogy and suggestions. Roulette seems to emulate relative fecundity. Those with higher fecundity will tend to mate with those of higher fecundity simply because they mate and produce offspring more often. (Wimps pass out in the corner, rarely mating.) But Tournament does tend to pair those with like-fecundity, so I suppose it does seem like sexual selection. I may try that next. I thought about some more explicit method, but that might be beyond what we are trying to accomplish with this model.

I'm glad you found the analogy helpful!

in re: field work and observation - piss poor at the moment. The result of living in New Jersey while dating a Czech supermodel that lives in Prague.

--------------
I’m referring to evolution, not changes in allele frequencies. - Cornelius Hunter
I’m not an evolutionist, I’m a change in allele frequentist! - Nakashima

  
Zachriel



Posts: 2594
Joined: Sep. 2006

(Permalink) Posted: July 03 2009,17:01   

Quote (slpage @ June 23 2009,19:10)
Constant population size is one of my pet peeves with Haldane's model as well.

Experimenting with Gregor's Bookkeeper.

VARIABLE POPULATION and FECUNDITY: Setting the number of Parents and the number of Children such that they vary (e.g. 20% relative standard deviation), they tend to achieve a higher fitness. This is apparently because when the population bottlenecks, it weeds out the weaklings. This is somewhat analogous to variations in climate, such as plenitude followed by drought.

TIME: The typical pattern is to watch the fitness slowly ebb away, but then suddenly spring back. If you quit too soon, you would never see this. As long as the population is large enough to be reasonably stable to avoid extinction for long enough, you will see a sawtooth pattern; a slow slide down in fitness, then a sudden increase as a significant favorable mutation sweeps through the population.

DOMINANCE: Still not happy with this feature. As might be expected, setting the fitter allele to be more dominant leads to greater fitness. This might be considered a cheat though. Setting an arbitrary allele to be dominant, it still often leads to greater fitness. An interesting test was to set dominance on a sliding scale, 1/G for G = 1 to numG (G for gene). This means that for some genes, the dominant gene is deleterious, for others favorable. Interestingly, this also leads to greater fitness.

SHAKING the BOX: It almost seems that anything that adds a bit of complex motion allows those with the highest fitness to rise to the top. Need more data.



DIFFERENCES between Gregor's Bookkeeper and Mendel's Accountant:

  * Multiplicative fitness.
  * Roulette Wheel mating, rather than the odd "divide by random" method.
  * Can handle very large populations and generations—if you're willing to wait.
  * Raised limit on the effect of favorable mutations. Adjusted some other settings.

--------------
There is only one Tard. The Tard is One.

   
dvunkannon



Posts: 1377
Joined: June 2008

(Permalink) Posted: July 06 2009,12:19   

Thinking about the problem of evolving a code, I just wanted to bounce some ideas off of anyone that wants to answer...

Here is a genome design:
6*26 bits of data to build a phenotype, followed by
64*8 bits of coding table

The coding table works like this. Each entry contains an 8 bit string. Each 8 bit string mapt to a list of affinities to a subset of 32 characters:

127 -> 20% A, 40% F, 40% J

This table of affinities would be salted with entries that guarantee A-Z have some entry with high affinity.

The GA works like any binary coded GA. To create a phenotype, run the data section of the genome through the code table 6 bits at a time. The 6 bits are like the three codons in DNA, mRNA, and tRNA. Taken as an index, they give an 8 bit value. The 8 bit value gives a set of affinities, and you spin the roulette wheel to see which letter you get. That letter is the phenotypic expression of the 6 bits you started with. Continue to loop until you've finished the data section of the genome.

To score a phenotype, compare with the string A .. Z and take the sum of the squared error at each position (ex target D, actual A, error is 3).

I think that if it works, you'll eventually get a population with the code table filled with at least one copy of each high affinity 8 bit string.

Comments? Is choosing 32 useful entries out of 256 too easy or too hard?

--------------
I’m referring to evolution, not changes in allele frequencies. - Cornelius Hunter
I’m not an evolutionist, I’m a change in allele frequentist! - Nakashima

  
midwifetoad



Posts: 3551
Joined: Mar. 2008

(Permalink) Posted: July 06 2009,13:00   

My little program seeks to build words through cumulative selection. The scoring algorithm is based on the frequency of letter pairs and triplets occurring in actual words. I've built frequency tables for a number of languages.

Selecting just on the relative frequency of pairs and triplets, it builds 7, 8, 9 and ten letter words in very few generations, involving just a few thousands mutations.

More interesting to me is the fact that it builds long word-like strings that look like words and are perfectly pronounceable, but aren't in the dictionary. Also interesting (to me) is the fact that it often ignores dictionary words in selecting the most fit. But despite being word blind, it builds words.

I don't want to read too much biology into this, but I think it blows away Behe's claim that long strings can't be the result of a selection algorithm that is unaware of a goal or target.

My program doesn't have a target or halting condition and continues to produce unique strings for hundreds of generations. I prevent getting stuck on a high scoring mother by periodically killing off the most fit child. Literally, every fourth generation, the most fit bites it.

I don't know if this simulates anything in nature, but to me it indicates that a rather mindless algorithm can do things beyond the ken of rocket scientists.

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”let’s not make a joke of ourselves.”

Pat Robertson

  
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