May 23, 2004 - May 29, 2004 Archives
Entropy may seem to be at first a simple concept but when trying to apply these concepts correctly one invariably runs into frustrating issues and areas of confusion. In this posting I intend to explore some of these confusions and I hope to explain how one applies entropy calculations correctly.
The Scientist reports that paternal mitochondria have been found in the muscle cells of a sufferer from myopathy, by a team from the Beth Israel Deaconess Medical Center and Harvard Medical School. This means that paternal mitochondria not only find their way into the oocyte (the female egg cell), as Ankel-Simons and Cummins reported in 1996, but also can continue into the mature organism. What effect does it have on Mitochondrial Eve?
John Wilkins has written a FAQ on the probability of abiogenesis.
What Louis Pasteur and the others who denied spontaneous generation demonstrated is that life does not currently spontaneously arise in complex form from nonlife in nature; he did not demonstrate the impossibility of life arising in simple form from nonlife by way of a long and propitious series of chemical steps/selections. In particular, they did not show that life cannot arise once, and then evolve. Neither Pasteur, nor any other post-Darwin researcher in this field, denied the age of the earth or the fact of evolution.
From the early views of Aristotle, through the research by Louis Pasteur to abiogenesis research, Wilkins shows how these fascinating concepts evolved.
A worthy addition to the Probability of Abiogenesis FAQs
There are quite a few genes that are known to be highly conserved in both sequence and function in animals. Among these are the various Hox genes, which are expressed in an ordered pattern along the length of the organism and which define positional information along the anterior-posterior axis; and another is decapentaplegic (dpp) which is one of several conserved genes that define the dorsal-ventral axis. Together, these sets of genes establish the front-back and top-bottom axes of the animal, which in turn establishes bilaterality—this specifically laid out three-dimensional organization is a hallmark of the lineage Bilateria, to which we and 99% of all the other modern animal species belong.
There are some animals that don't belong to the Bilateria, though: members of the phylum Cnidaria, the jellyfish, hydra, sea anemones, and corals, which are typically radially symmetric. A few cnidarian species exhibit bilateral symmetry, though, and Finnerty et al. (2004) ask a simple question: have those few species secondarily reinvented a mechanism for generating bilateral symmetry (so that this would be an example of convergent evolution), or do they use homologous mechanisms, that is, the combination of Hox genes for A-P patterning and dpp for D-V patterning? The answer is that this is almost certainly an example of homology—the same genes are being used.
Continue reading Bilateral symmetry in a sea anemone (on Pharyngula)
The results of the Second Panda Poll, PP2, show that the readers of this blog overwhelmingly think that the case against evolution should not be taught in the public schools. In response to the question,
The arguments against evolution are unsound and should not be taught as science in the public schools,
nearly 90 % of respondents strongly agreed or agreed. Approximately 10 % disagreed or strongly disagreed.
Introduction to Shannon entropy
Motivated by what I perceive to be a deep misunderstanding of the concept of entropy I have decided to take us onto a journey into the world of entropy. Recent confusions as to how to calculate entropy for mutating genes have will be addressed in some detail.
I will start with referencing Shannon’s seminal paper on entropy and slowly expand the discussion to include the formulas relevant for calculating the entropy in the genome.
But first some warnings
Speaking of bathroom walls...check out this long thread on Creationist genetics. It's an enlightening peek into the mind of a creationist. I had originally commented on the curious tale of Jacob and Laban in the book of Genesis, in which Jacob is able to modify the coat color of sheep and goats by having them mate in front of appropriately colored sticks. I pointed out that this is nonsense—genetics doesn't work that way.
We then got many overwrought comments from a creationist, Susan Williams, defending the Bible. Confronted with a story that contradicts plain, simple, observable biology, she resorts to the Rush Limbaugh defense: it's just a joke, you aren't supposed to take it literally.
That's fine with me. I wonder, though, why creationists insist on defending as literally true other tales from the Bible that contradict the scientific evidence? As long as they are willing to give God a sense of humor and a willingness to illustrate his lessons with allegory and jokes, why not carry that to it's logical conclusion and recognize that the Bible is not a scientific document?
With any tavern, one can expect that certain things that get said are out-of-place. But there is one place where almost any saying or scribble can find a home: the bathroom wall. This is where random thoughts and oddments that don’t follow the other entries at the Panda’s Thumb wind up. As with most bathroom walls, expect to sort through a lot of oyster guts before you locate any pearls of wisdom.
I ran across the following interesting website
Phylogenetic trees of taxa are often created and used for the calculation of ancestral traits of the internal nodes of these trees. However, seldom are these ancestral traits visualized in an intuitive manner.
Ancient Wings allows users to see how the ventral hindwing of 54 butterflies in the genus Bicyclus have changed over time. By clicking on each of the nodes within the evolutionary tree, the user can see how eyespots’ sizes and positions relative to the wing have evolved. The ancestral wing pattern traits were calculated using COMPARE 4.4, a program by Emilia Martins of Indiana University. The phylogenetic tree and its historical calibration are by Antonia Monteiro of SUNY at Buffalo.
The paper, “Ancient Wings: animating the evolution of butterfly wing patterns”, and the program can be found at this website.
Since we have seen some poorly argued claims about entropy and its relevance to evolution, I will explore the concepts of entropy as they apply to genome evolution and will show that the evidence shows how simple processes like variation and selection are sufficient to explain the evolution of complexity or information/entropy in the genome.
While various ID authors (here and elsewhere) have argued that such natural processes are unable to explain the evolution of information in the genome, it should be clear that the actual evidence contradicts any such suggestions.
In the past I have argued with various people on the topic of entropy. Jerry Don Bauer a.k.a. Chronos has shown some interesting confusions as to the concept of entropy and believes that he has shown that using the laws of entropy he has shown that macro-evolution could not have happened.
A new genetic analysis of man’s best friend could help scientists explain why a border collie has knack for herding or why poodles sport a curly coat. In the May 21 issue of Science, researchers at Fred Hutchinson Cancer Research Center report the first extensive genetic comparison of domestic dog breeds.
The study, led by Fred Hutchinson researchers Drs. Elaine Ostrander, Leonid Krugylak and graduate student Heidi Parker, revealed distinct DNA blueprints for each of the 85 varieties of purebreds that were analyzed as well as similarities between certain breeds. The researchers expect that understanding these genetic relationships will help them uncover the genes responsible for the physical features and behaviors unique to each breed as well as the diseases to which they are commonly susceptible, such as cancer, deafness, blindness, heart disease and hip dysplasia.
The findings also have generated excitement among those who study diseases of the human animal. Because at least half of the more than 300 inherited canine disorders-including a number of cancers-resemble specific diseases of man, many scientists believe that the dog genome holds a wealth of information that will benefit human health.
There are a number of things claimed for this study, most of which confirm things that we already knew or suspected.
- The nearest relatives of dogs are wolves.
- Dog breeds are genetically distinct.
- Dog breeds cluster into four large groups. One is more closely related to wolves, and includes the Alaskan Malamute and Siberian Husky. Another includes mastiff-like breeds. The third includes herding dogs. The fourth comprises hunting dogs.
- The analysis is being used to find genetic bases for various canine diseases.
The clustering noted above is shaking up some notions of the history of certain breeds:
Noticeably absent from this ancient cluster were several breeds long regarded as the most ancient by breeders, including the Pharaoh Hound and the Ibizan Hound – depicted on Egyptian tomb walls. The researchers said their analysis indicated that the modern representatives of these breeds were recreated in more recent times from combinations of other breeds. The researchers also found genetic evidence for a recent origin of the Norwegian Elkhound, believed to be of ancient Scandinavian origin.
I think that it is important to note that this study is based on microsatellite analysis, not whole-genome data. The claim of the headline and press release that this study “may benefit human health” appears to be a long way from turning possibility into performance. It seems certain that the canine study will be useful in helping track down genetic diseases in dogs, but to have that carry over to humans we would have to know that many of the same microsatellite markers exist in both species, and that has not yet been established as far as I can tell. (As an organismal biologist skimming bioinformatics, though, I could easily be wrong on this. I would be grateful to anyone who can point to work where this has been accomplished.) Some microsatellite studies show useful cross-species comparisons are possible, and other studies show that they don’t work so well, depending upon the particular species under consideration. By contrast, comparative genomics has already identified the genetic basis of a human disease, Bardet-Biedl Syndrome (BBS).
Since I seem to be on a roll, I thought I’d take a look at a claim that’s made frequently by ID proponents, namely that archaeology uses a design detection procedure akin to that allegedly formalized by Dembski’s Explanatory Filter. (Gary Hurd: Feel free to interject/comment/correct at will.)
Gene duplication is mentioned as one example in which information and complexity in the genome can increase leading to biochemical novelty and even irreducibly complex systems. Despite this ID proponents object to gene duplication as a relevant mechanism. I will explore some of the objections and show how science has and is addressing these objections. I intend to show that the objections raised by ID proponents are mostly without merit.
Behe mentions in this 2003 interview that
My current work is an attempt to model the evolution of new protein functions through gene duplication. Gene duplication is purported to be a major pathway for the Darwinian evolution of biochemical novelty. However, as in other areas, Darwinists have not closely examined whether gene duplication can realistically do all that they ascribe to it. I hope to help them out in this area by asking those questions.
It seems that Behe may not be familiar with the research on gene duplication when he states that
The hitch, as always, is that Darwinists virtually never explain in any detail how natural selection would actually get from protein A to protein B after the gene for protein A duplicated. After all, gene duplication just leaves you with a second copy of the same gene — nothing different. The problem is, as everyone agrees, that the duplicated gene is much more likely to suffer a deleterious mutation than a beneficial one. Nonetheless, Darwinists hope that the occasional beneficial mutation just might come along. However, they never look very deeply into the matter. It turns out that to acquire some new functions, such as the capacity to bind a new molecule, multiple mutations would be expected to be needed, not just a single mutation. The requirement for multiple mutations would quickly render gene duplication an untenable explanation, since a duplicated gene would be riddled with deleterious mutations before acquiring several positive ones.
Fifteen months ago Paul Nelson made available a “discussion paper” on Ontogenetic Depth to serve as background for an ISCID chat. In that paper he claimed that
The ontogenetic depth of a handful of extant animals (from the model systems of developmental biology) is known with precision.
That’s 15 months ago. In the chat itself Nelson cut and pasted the same claim from the background paper, and said further that
But, as I said at the beginning, the start of any scientific answer begins with correctly understanding the problem. Ontogenetic depth helps to do that. This is what any candidate theory of animal origins has to explain. it is not itself an explanation, but a description.
So somehow or other, ontogenetic depth provides a problem for biology to explain, but we’re not told what the problem is - we are not given the metric Nelson uses to describe the problem. That’s of no particular help in “correctly understanding the problem.”