Uncommon Descent Serving The Intelligent Design Community

Front loading passes peer review in Cell Cycle

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
Email

1: Cell Cycle. 2007 Jun;6(15):1873-7. Epub 2007 Jun 6. Links

Universal genome in the origin of metazoa: thoughts about evolution.

Sherman M.

Department of Biochemistry; Boston University Medical School, 715 Albany St., Boston, Massachusetts 02118, USA.

sherma1@bu.edu

Recent advances in paleontology, genome analysis, genetics and embryology raise a number of questions about the origin of Animal Kingdom. These questions include:(1) seemingly simultaneous appearance of diverse Metazoan phyla in Cambrian period, (2) similarities of genomes among Metazoan phyla of diverse complexity, (3) seemingly excessive complexity of genomes of lower taxons and (4) similar genetic switches of functionally similar but non-homologous developmental programs. Here I propose an experimentally testable hypothesis of Universal Genome that addresses these questions. According to this model, (a) the Universal Genome that encodes all major developmental programs essential for various phyla of Metazoa emerged in a unicellular or a primitive multicellular organism shortly before the Cambrian period; (b) The Metazoan phyla, all having similar genomes, are nonetheless so distinct because they utilize specific combinations of developmental programs. This model has two major predictions, first that a significant fraction of genetic information in lower taxons must be functionally useless but becomes useful in higher taxons, and second that one should be able to turn on in lower taxons some of the complex latent developmental programs, e.g., a program of eye development or antibody synthesis in sea urchin. An example of natural turning on of a complex latent program in a lower taxon is discussed.

PMID: 17660714 [PubMed – in process]

HT to Gilbert T. for alerting me to this paper.

Comments
[...] Front loading passes peer review in Cell Cycle [...]Universal Genome in the Origin of Metazoa | Uncommon Descent
August 21, 2008
August
08
Aug
21
21
2008
08:40 AM
8
08
40
AM
PDT
I think that Bob is right about genetic entropy in a sense that it seems to lower the total fitness of the species in question. However it lowers the total fitness in multiple fitness landscapes and might improve fitness in a few. For example the antibiotic resistance in bacteria acts just like that increasing fitness against acting antibiotic but the bacteria loses fitness in every other fitness landscape that don't have that antibiotic.Innerbling
September 13, 2007
September
09
Sep
13
13
2007
11:58 AM
11
11
58
AM
PDT
Bob, If you noticed in the article, I definitely referenced Sanford in regards to how information acts in regards to the "fitness" adaptation of a bacteria. So yes! I did answer your question in vivid detail as to how Sanford views Genetic Entropy. As stated before his book is very easy to read and will clear up the misconceptions you seem to have about the limits you seem to think he has on the principle of Genetic Entropy. In fact he does several pages on mutations to what he terms "poly-constrained" information! He definitely does not hold to your view that Genetic Entropy is limited to (a loss of fitness) but also, emphatically, supports its origination in the information of the genome! Please read the book Bob.bornagain77
September 13, 2007
September
09
Sep
13
13
2007
11:23 AM
11
11
23
AM
PDT
Thank you bornagain. I asked you to provide evidence that your definition of genetic entropy accords with Sanford's. You wrote over a thousand words, and didn't answer my request. I guess this means you're not going to, so I think we're done here. BobBob O'H
September 13, 2007
September
09
Sep
13
13
2007
09:24 AM
9
09
24
AM
PDT
I wonder if “form” may be tentatively found (roughly defined) by comparing the differences between Genome sequence similarities with specific gene sequence similarities across phyla. No one has found it yet. But they have figured out what I have already posted- that DNA may lend itself to those forms but the DNA does not determine it.Joseph
September 13, 2007
September
09
Sep
13
13
2007
06:28 AM
6
06
28
AM
PDT
Bob, Since evidence has primary authority in science, let's look at the evidence. If I read you right, You want Genetic Entropy to "only" mean a loss of fitness. Whereas, I hold that Genetic Entropy is a broader overriding principle of biology and includes not only loss of fitness but also loss of functional information, although fitness can "temporarily" be gained for a species. Many times naturalists will offer “conclusive” proof for evolution by showing bacteria that have become resistant to a certain antibiotic such as penicillin. When penicillin was first discovered, all the gram positive cocci were susceptible to it. Now 40% of the bacteria Strep pneumo are resistant. Yet, the mutation to DNA that makes Strep pneumo resistant to penicillin results in the loss of a protein function for the bacteria (called, in the usual utilitarian manner, penicillin-binding-protein). A mutation occurred in the DNA leading to a bacterial protein that no longer interacts with the antibiotic and the bacteria survive. Although they survive well in this environment, it has come at a cost. The altered protein is less efficient in performing its normal function. In an environment without antibiotics, the non-mutant bacteria are more likely to survive because the mutant bacteria cannot compete as well. So as you can see, the bacteria did adapt, but it came at a loss of function in a protein of the bacteria, loss of genetic information in the DNA of the bacteria, and it also lessened the bacteria's overall fitness for survival. Scientifically, it is better to say that the bacteria devolved in accordance with the principle of genetic entropy, instead of evolved against this primary principle of how “poly-constrained information” will act in organisms (Sanford; Genetic Entropy 2005). As well, all other observed adaptations of bacteria to “new” environments have been proven to be the result of such degrading of preexisting molecular abilities. Sometimes a complex adaptation in bacteria is exhibited by naturalists (Hall, gene knockout experiments) that defy tremendous mathematical odds. Yet far from confirming evolution as they wish it would, the demonstration of a complex adaptation of a preexisting protein actually indicates another higher level of complexity in the genetic code of the bacteria that somehow found (calculated) how to adapt a preexisting protein with the very same ability as the protein that was knocked out to the new situation (Behe, Evidence For Design pg. 138). To make matters worse for the naturalists, the complex adaptation of the protein still obeys the principle of genetic entropy for the bacteria, since the adapted bacteria has less overall functionality than the original bacteria did. Thus, even naturalists supposed strongest proof for evolution in bacteria is found to be wanting for proof of evolution since it still has not violated the principle of genetic entropy. Even the most famous cases of adaptations in humans, such as lactase persistence, the sickle cell/malaria adaptation (Behe, The Edge of Evolution 2007), and even long term immune system responses of humans, genetic entropy is still being obeyed when looked at on the level of overall functional genetic information. For naturalists to “conclusively prove” evolution they would have to clearly demonstrate a gain in genetic information that does not in fact decrease functionality of the species. Naturalists have not done so, nor will they ever. The overall interrelated complexity of the information for the integrated whole of a life-form simply will not allow the generation of meaningful information to happen in its DNA by chance alone. “But in all the reading I’ve done in the life-sciences literature, I’ve never found a mutation that added information… All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it.” Lee Spetner (Ph.D. Physics – MIT) “There is no known law of nature, no known process and no known sequence of events which can cause information to originate by itself in matter.” Werner Gitt, “In the Beginning was Information”, 1997, p. 106. (Dr. Gitt was the Director at the German Federal Institute of Physics and Technology) His challenge to scientifically falsify this statement has remained unanswered since first published. Naturalists also claim stunning proof for evolution because bacteria can quickly adapt to detoxify new man-made materials, such as nylon and polystyrene. Yet once again, when carefully looked at on the molecular level, the bacteria still have not demonstrated a gain in genetic information, i.e. though they adapt they still degrade preexisting molecular abilities of the bacteria in order to adapt (genetic entropy). Indeed, it is not nearly as novel as they think it is, for the bacteria are still, only, complacently detoxifying the earth of toxins as they have always been doing for billions of years. Even though naturalists claim this is something brand new, that should be considered stunning proof for evolution, I’m not nearly as impressed, with their stunning proof, as they think I should be (Answers in Genesis; Nylon Eating Bacteria; 2007)! This overriding truth of never being able to violate the entropy of poly-constrained information by natural means applies to the “non-living realm” of viruses, such as bird flu, as well (Ryan Lucas Kitner, Ph.D. 2006). I would also like to point out that scientists have never "naturally" changed any one type of bacteria into any another type of bacteria, despite years of exhaustive experimentation trying to change any bacteria type into any other bacteria type. In fact, it is commonly known that the further scientists deviate any particular bacteria type from its original state, the more unfit for survival the manipulated population will quickly become. As esteemed French scientist Pierre P. Grasse has stated: “What is the use of their unceasing mutations, if they do not change? In sum, the mutations of bacteria and viruses are merely hereditary fluctuations around a median position; a swing to the right, a swing to the left, but no final evolutionary effect.” Needless to say, this demonstrated limit to the variability of bacteria is extremely bad news for the naturalists. Bob I could go on and on, and site evidence after evidence..Yet the very point is that evolutionists have no evidence for evolution that withstands scrutiny; to "conclusively" prove evolution, evolutionists will have to produce solid evidence for for an increase in fitness as well as an increase in obvious functional information for the species. Evolutionists should have countless examples they could produce , since evolution is "a fact of life" yet I can find none anywhere I look! Do you have any examples that can withstand scrutiny Bob"?bornagain77
September 13, 2007
September
09
Sep
13
13
2007
05:22 AM
5
05
22
AM
PDT
I’ve only ever seen you claim that - everything I’ve read by Sanford suggests that he means something else (a loss of fitness).
Loss of function and loss of information are basically the same thing. Function generally requires information. When the informatin is lost the function is lost as well. Sometimes a loss of information creates improved fitness and maybe even function in the same way burning a bridge can have the function of slowing down an invading army.Jehu
September 13, 2007
September
09
Sep
13
13
2007
01:42 AM
1
01
42
AM
PDT
Genetic Entropy is the measurable loss of information ...
I've only ever seen you claim that - everything I've read by Sanford suggests that he means something else (a loss of fitness). If I ordered his book now, it would take over a week to arrive, by which time this thread would have died. So, I'll ask again for you to point me to a definition of genetic entropy that accords with what you're claiming. BobBob O'H
September 12, 2007
September
09
Sep
12
12
2007
10:25 PM
10
10
25
PM
PDT
Joseph, I wonder if "form" may be tentatively found (roughly defined) by comparing the differences between Genome sequence similarities with specific gene sequence similarities across phyla.bornagain77
September 12, 2007
September
09
Sep
12
12
2007
04:18 PM
4
04
18
PM
PDT
Is not the evidence that is currently coming in suggesting similar genotypes across phyla while phenotype appears to be vastly different? That doesn't account for the differences. If anything it tells us that genotype does not determine phenotype. Would not this fact severely hamper the radical front loading scenario? It all depends on where "form" resides. Suggested reading: "Why is a Fly Not a Horse?" by geneticist Giuseppe Sermonti. Chapter VI:
The scientist enjoys a privilege denied the theologian. To any question, even one central to his theories, he may reply “I’m sorry but I do not know.” This is the only honest answer to the question posed by the title of this chapter. We are fully aware of what makes a flower red rather than white, what it is that prevents a dwarf from growing taller, or what goes wrong in a paraplegic or a thalassemic. But the mystery of species eludes us, and we have made no progress beyond what we already have long known, namely, that a kitty is born because its mother was a she-cat that mated with a tom, and that a fly emerges as a fly larva from a fly egg.
Joseph
September 12, 2007
September
09
Sep
12
12
2007
03:16 PM
3
03
16
PM
PDT
Yes indeed I find it funny that the breeding example used by evo-devo proponents seems to offer exact opposite conclusions when data is researched. My current hypothesis: Front-loaded original species -> Time+RM(genetic entropy)+NS+some not so well known mechanism for example epigenetic modifications -> Multiple sub-species that don't have the front-loaded potential anymore, but retain some of it.Innerbling
September 12, 2007
September
09
Sep
12
12
2007
02:30 PM
2
02
30
PM
PDT
Bob, Yes, He does! Are you asking how Genetic Entropy is related to the loss of Genetic Diversity? Bob, The answer is clear. Genetic Entropy is the measurable loss of information and or function in a genome! If diversity is lost to a sub-species that was present in the parent species it came from, this is clearly the loss of functional information in the genome of the sub-species from the parent species, thus the "sub-speciation" stays within the overriding principle of Genetic Entropy! This rule applies to all known cases of sub-speciation I have looked at! I really don't think I can make this any clearer Bob. I really do recommend Dr. Sanford's book "Genetic Entropy" to you. He truly has a gift for taking a complex subject and breaking it down into easy to learn lessons that are easy to understand. He is much like Dr. Behe in this manner. I believe he can do a much better job of teaching you the principle of Genetic Entropy than I can.bornagain77
September 12, 2007
September
09
Sep
12
12
2007
01:54 PM
1
01
54
PM
PDT
bornagain77 - Sanford may "talk about" neutral mutations, but does he include them in his genetic entropy? Oh, and please answer this question (directly!):
How is this related to the loss of genetic diversity?
I'm asking about your claims. BobBob O'H
September 12, 2007
September
09
Sep
12
12
2007
11:28 AM
11
11
28
AM
PDT
The problem with DNA is that it's hard to know which mutation is beneficial, which neutral and which is negative because we don't know the "islands" of functionality. However to my knowledge there is virtually zero data that supports the claim that the functionality we can get through different encodings of DNA is even nearly as plastic as most Darwinists seem to believe. As we can learn from programming languages the syntax that has to be used is precise and random binary coding offers diminishing returns.Innerbling
September 12, 2007
September
09
Sep
12
12
2007
10:48 AM
10
10
48
AM
PDT
If biology was my specialty I would research which is the mechanism that selects the front-loaded potential. According to New Scientist article mentioned here there could be another mechanism besides natural selection called "epigenetic" modifications. It seems to do subtle chemical changes to DNA according to the nutrition and living habits of the subject. I believe that this could be the thing that changes the way we see change in organisms completely when researched further. Too bad I am not a biologist. Article: New Scientist Men inherit hidden cost of dad's vices 06 January 2006 Rowan Hooper Magazine issue 2533Innerbling
September 12, 2007
September
09
Sep
12
12
2007
10:05 AM
10
10
05
AM
PDT
Bob, Dr. Sanford does talk about neutral mutations (or really the lack thereof). I highly recommend his book to you! It will clear up a lot of the misconceptions we have between each other.bornagain77
September 12, 2007
September
09
Sep
12
12
2007
09:27 AM
9
09
27
AM
PDT
Joseph, Is not the evidence that is currently coming in suggesting similar genotypes across phyla while phenotype appears to be vastly different? Would not this fact severely hamper the radical front loading scenario?bornagain77
September 12, 2007
September
09
Sep
12
12
2007
09:19 AM
9
09
19
AM
PDT
Hopefully we’ll get back to frontloading soon. IMHO-Front loading, like universal common descent, is only good if and only if genotype translates into phenotype. However from what we do know, even though genes and genomes may influence development, they do not determine it. Having an influence over something is not the same as determining it. Workers on an assembly-line influence the product's quality. However they do not determine what the product is.Joseph
September 12, 2007
September
09
Sep
12
12
2007
08:02 AM
8
08
02
AM
PDT
A negative mutational load in the genome, by definition, is the buildup of useless information in the genome that reduces the ability of the species to survive.
How is this related to the loss of genetic diversity? Actually, can you point me to this definition? I couldn't find one on the web, and from what I could find, Sanford didn't seem to be discussing information theory. Also, what about neutral mutations? They are also "useless information". Does Sanford include those in genetic entropy?
Yet the very usefulness of the information in the genome itself can only be measured from the macroscopic level when taking into consideration its positive or negative effects on a species!
Err, no. Precisely the opposite. My understanding of Sanford's genetic entropy is that it was the accumulation of deleterious alleles, which had the effect of reducing mean population fitness - it's the fitness reduction that's key. Hopefully we'll get back to frontloading soon. BobBob O'H
September 12, 2007
September
09
Sep
12
12
2007
07:31 AM
7
07
31
AM
PDT
Bob O'H If you haven't read it, I suggest you read Dr. J.C.Sanford's book "Genetic Entropy"; 2005. Though, in my own personal opinion, he tries to stretch the evidence a bit to far in limiting the span of human existence to fit his YEC for humans of 6000 years. I believe the foundation he lays for the principle of Genetic Entropy is solid in its basic premise and irrefutable as a overriding principle of biology! No, I am not saying that Genetic Entropy has nothing to with the buildup of a negative mutational load. In fact, I am saying quite the opposite in that it is all connected! It is just that Genetic Entropy can be measured in a variety of ways. You seem to be looking at Genetic Entropy from strictly the molecular level. Yet the very usefulness of the information in the genome itself can only be measured from the macroscopic level when taking into consideration its positive or negative effects on a species! A negative mutational load in the genome, by definition, is the buildup of useless information in the genome that reduces the ability of the species to survive. The fact that a negative mutational load is building up in humans can be clearly demonstrated by this following fact. "When first cousins marry, their children have a reduction of life expectancy of nearly 10 years. Why is this? It is because inbreeding exposes the genetic mistakes within the genome (slightly detrimental recessive mutations) that have not yet had time to "come to the surface". Inbreeding is like a sneak preview, or foreshadowing, of where we are going to be genetically as a whole as a species in the future. The reduced life expectancy of inbred children reflects the overall aging of the genome that has accumulated thus far, and reveals the hidden reservoir of genetic damage (slightly detrimental recessive mutations) that have been accumulating in our genomes. (Sanford; Genetic Entropy; page 147) So as you can see Bob the negative mutational load has everything to do with Genetic Entropy yet our ability to measure it effectively is for the large part limited to its effects on the macroscopic level of the species.bornagain77
September 12, 2007
September
09
Sep
12
12
2007
05:27 AM
5
05
27
AM
PDT
Genetic Entropy IS THE LOSS OF INFORMATION!!!!!
OH REALLY????!!!1??? So, does genetic entropy have nothing to do with the buildup of a negative mutation load? "Negative" implies a loss. And a "buildup of a negative mutation load" would definitely be "a degradation of the genome". "Noise" wouldn't necessarily be a "negative".Joseph
September 12, 2007
September
09
Sep
12
12
2007
04:46 AM
4
04
46
AM
PDT
bornagain77 - can you give me a direct answer. Are you saying that genetic entropy has nothing to do with the buildup of a negative mutation load? BobBob O'H
September 11, 2007
September
09
Sep
11
11
2007
10:43 PM
10
10
43
PM
PDT
Bob O'H Ditto to Jehu's comment!bornagain77
September 11, 2007
September
09
Sep
11
11
2007
01:58 PM
1
01
58
PM
PDT
Bob O'H
So, does genetic entropy have nothing to do with the buildup of a negative mutation load? That’s what I glean from reading comments on the web about it.
You have to understand the difference between information and noise.Jehu
September 11, 2007
September
09
Sep
11
11
2007
01:23 PM
1
01
23
PM
PDT
If Michael Sherman is interested in doing research on this paper's implications. Does anyone have any specific ideas for experiments they would like to see performed?idnet.com.au
September 11, 2007
September
09
Sep
11
11
2007
01:10 PM
1
01
10
PM
PDT
Genetic Entropy IS THE LOSS OF INFORMATION!!!!!
OH REALLY????!!!1??? So, does genetic entropy have nothing to do with the buildup of a negative mutation load? That's what I glean from reading comments on the web about it. BobBob O'H
September 11, 2007
September
09
Sep
11
11
2007
11:53 AM
11
11
53
AM
PDT
Atom, You have very keen observation-s of the current state of observed data! I would like to comment, since I support the "strong" ID position of later implementation of information, that the front loaded position, while somewhat tenable, is by no means set in stone for the ID theory. From the evidence we now have, We can say with assurance that we KNOW information was implanted in the genomes! With just as much assurance, from the current evidence, we can state that we are not exactly sure when the precise implementation of information in the genome was inserted! I believe myself, and I know I'm probably in the minority in this view on this site, that since the demonstrated harmful rate of mutations to DNA is known to approach +99.9999%, including the highly touted HOX gene mutations, I believe the information for the genome was implanted as late as parent species! and was not implanted much earlier than that. Many people point to genetic similarities between phyla and say "look proof of relationship!",,yet this is the same type of shabby reasoning that evolutionists use to try to prove monkeys and humans are related. This Similarity , although suggestive, quickly fails under critical analysis! My own take on this is that we have barely touched the surface of understanding functionality in genomes and to infer relationship between phyla is very premature. Especially when the genomes could have required similarity due to required shape space configuration or any number of other functionally similar uses that have no bearing on relationship! Or I could be wrong and it could be relationship,,BUT The very point being that it is very early to be jumping to any solid conclusions! My own take on the preliminary evidence we have so far is that it seems front loading will be very limited in its scope,,,with beneficial adaptations to sub-species occurring, yet, and I believe the evidence for this position is strong, the "front loaded" beneficial adaptation will ultimately come at a loss of the original information that was inserted in the Genome,,Thus I believe staying within the principle of Genetic Entropy and, this is presuming on my part, staying within what is possible for the generation of meaningful information in a genome. Of course all I have, so far, to back this up this claim is the negative mutation rates to DNA,,,Yet until someone demonstrates some radical exception to the current mutation evidence my position holds up with the observed data better than a radical front loading scenario does,,, this includes high populations of bacteria,,,since, as of now, bacteria have never been "naturally" changed into any other type of bacteria (Venter's work is interesting to this point). As well Behe's work in EOE points to a very limited scope for the generation of meaningful information for high populations. I know many objections can be made against my position,,yet I still hold that my position holds up with observed data better that any other current scenario being offered.bornagain77
September 11, 2007
September
09
Sep
11
11
2007
11:49 AM
11
11
49
AM
PDT
I can't stay long but just wanted to jump in with a thought, re the exchange by BornAgain77, Bob OH and Patrick: We observe that: 1) "Lower" lifeforms (such as bacteria) out-reproduce higher lifeforms by leaps and bounds. 2) Life is thought to have originated from lower lifeforms in both NDE and Frontloaded versions of origins. 3) Genetic entropy applies inversely to reproductive rate: the higher the rate, the less affected by genetic entropy. 4) Frontloaded lifeforms would need to stick around with non-degraded information for long time spans (according to FLE scenarios), so they can't become too affected by genetic entropy, in order to complete their "mission" Tying these ideas together, and we solve a puzzle neatly. We have wondered out loud on here why higher lifeforms reproduce so slowly and sparingly compared to lower lifeforms. It is clear to see that such an observed trend cannot be the result of natural selection, because there is no reason decreasing reproductive success would keep being selected for. But maybe we have it backwards: the question isn't why do higher organisms reproduce so sparingly but rather, why do lower lifeforms reproduce so quickly? If Frontloading is true, then we would need our original replicators to be robust against genetic entropy, since they are the root of many branches. The closer to the bottom of the tree, the longer their line will be around, and so the more robust they need to be. Hence they need to reproduce faster in greater numbers. As they diversify and branch out, they get closer to their "terminal" branches, and thus are closer in time to their destination. So as we move up the tree, the less roubst the replicators need to be. The terminal branches can be fully subject to genetic entropy, since they have already reached their destination. This accords well with observation, as much as I am aware. Davescot, others: thoughts?Atom
September 11, 2007
September
09
Sep
11
11
2007
09:40 AM
9
09
40
AM
PDT
Bob, Genetic Entropy IS THE LOSS OF INFORMATION!!!!! Thus a demonstrated lack of diversity, variability, reveals a loss of information thus a degradation of the genome!!!!! Can you see it now?bornagain77
September 11, 2007
September
09
Sep
11
11
2007
09:37 AM
9
09
37
AM
PDT
bornagain - 1. What I wrote doesn't say anything about the truth of the Milner quote. And I wasn't writing about selection - I was writing about a bottleneck. It's this which is the primary cause of the low diversity in crop plants - selection doesn't help of course. I also made no comment about CSI - it's hard enough explaining simple population genetics around here, without having new concepts dragged in. I was well aware of the greater genetic diversity in Africa, but I've no idea about how it relates to genetic entropy, which is the (supposed) degradation of the genome due to fixation of deleterious mutations. I think you need to show how the accumulation of deleterious mutations relates to the information content of genomes. In a desperate attempt to get this thread back on-topic, I'll repeat - do you disagree with DaveScot about frontloading? BobBob O'H
September 11, 2007
September
09
Sep
11
11
2007
09:02 AM
9
09
02
AM
PDT
1 2

Leave a Reply