"Why must we cling to an outmoded view of life that spun from minds eager to rid science of intelligent causes? We need a biology for the Information Age, where intelligent causes are well known. Intelligence, and only intelligence, explains codes, messages, software, error-correction routines, networks, and hierarchical systems of all the above. Step aside, Charlie. You had your day. You did your damage. We have a lot of repair work to do." (from an article linked below)
Citrate-eating bacteria? As Michael Behe mentioned:
"Now, wild E. coli already has a number of enzymes that normally use citrate and can digest it (it's not some exotic chemical the bacterium has never seen before). However, the wild bacterium lacks an enzyme called a "citrate permease" which can transport citrate from outside the cell through the cell's membrane into its interior. So all the bacterium needed to do to use citrate was to find a way to get it into the cell. The rest of the machinery for its metabolism was already there. As Lenski put it, "The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions."
Bacteria evolving in the lab?
Nope. After over 30,000 generations, Citrate eating bacteria are apparently the result of a system failure or the recovery of a system previously displayed by the organism. No matter how Darwinists try to spin it, they cannot show that E. Coli actually added an information container with new information to the genome.
1 Two species, Flavobacterium sp. K172 and Pseudomonas sp. NK87, were identified that degrade nylon compounds.
Much research has flowed from this discovery to elucidate the mechanism for the apparently novel ability of these bacteria.2 Three enzymes are involved in Flavobacterium K172: F-EI, F-EII and F-EIII, and two in Pseudomonas NK87: P-EI and P-EII. None of these have been found to have any catalytic activity towards naturally occurring amide compounds, suggesting that the enzymes are completely new, not just modified existing enzymes. Indeed no homology has been found with known enzymes. The genes for these enzymes are located on plasmids:3 plasmid pOAD2 in Flavobacterium and on two plasmids, pNAD2 and pNAD6, in Pseudomonas.
Apologists for materialism latched onto these findings as an example of evolution of new information by random mutations and natural selection, for example, Thwaites in 1985.4 Thwaites’ claims have been repeated by many, without updating or critical evaluation, since.
Is the evidence consistent with random mutations generating the new genes?Thwaites claimed that the new enzyme arose through a frame shift mutation. He based this on a research paper published the previous year where this was suggested.5 If this were the case, the production of an enzyme would indeed be a fortuitous result, attributable to ‘pure chance’. However, there are good reasons to doubt the claim that this is an example of random mutations and natural selection generating new enzymes, quite aside from the extreme improbability of such coming about by chance.6
Evidence against the evolutionary explanation includes:
- There are five transposable elements on the pOAD2 plasmid. When activated, transposase enzymes coded therein cause genetic recombination. Externally imposed stress such as high temperature, exposure to a poison, or starvation can activate transposases. The presence of the transposases in such numbers on the plasmid suggests that the plasmid is designed to adapt when the bacterium is under stress.
- All five transposable elements are identical, with 764 base pairs (bp) each. This comprises over eight percent of the plasmid. How could random mutations produce three new catalytic/degradative genes (coding for EI, EII and EIII) without at least some changes being made to the transposable elements? Negoro speculated that the transposable elements must have been a ‘late addition’ to the plasmids to not have changed. But there is no evidence for this, other than the circular reasoning that supposedly random mutations generated the three enzymes and so they would have changed the transposase genes if they had been in the plasmid all along. Furthermore, the adaptation to nylon digestion does not take very long (see point 5 below), so the addition of the transposable elements afterwards cannot be seriously entertained.
- All three types of nylon degrading genes appear on plasmids and only on plasmids. None appear on the main bacterial chromosomes of either Flavobacterium or Pseudomonas. This does not look like some random origin of these genes—the chance of this happening is low. If the genome of Flavobacterium is about two million bp,7 and the pOAD2 plasmid comprises 45,519 bp, and if there were say 5 pOAD2 plasmids per cell (~10% of the total chromosomal DNA), then the chance of getting all three of the genes on the pOAD2 plasmid would be about 0.0015. If we add the probability of the nylon degrading genes of Pseudomonas also only being on plasmids, the probability falls to 2.3 x 10-6. If the enzymes developed in the independent laboratory-controlled adaptation experiments (see point 5, below) also resulted in enzyme activity on plasmids (almost certainly, but not yet determined), then attributing the development of the adaptive enzymes purely to chance mutations becomes even more implausible.
- The antisense DNA strand of the four nylon genes investigated in Flavobacterium and Pseudomonas lacks any stop codons.8 This is most remarkable in a total of 1,535 bases. The probability of this happening by chance in all four antisense sequences is about 1 in 1012. Furthermore, the EII gene in Pseudomonas is clearly not phylogenetically related to the EII genes of Flavobacterium, so the lack of stop codons in the antisense strands of all genes cannot be due to any commonality in the genes themselves (or in their ancestry). Also, the wild-type pOAD2 plasmid is not necessary for the normal growth of Flavobacterium, so functionality in the wild-type parent DNA sequences would appear not to be a factor in keeping the reading frames open in the genes themselves, let alone the antisense strands.
Some statements by Yomo et al., express their consternation:
‘These results imply that there may be some unknown mechanism behind the evolution of these genes for nylon oligomer-degrading enzymes.
‘The presence of a long NSF (non-stop frame) in the antisense strand seems to be a rare case, but it may be due to the unusual characteristics of the genes or plasmids for nylon oligomer degradation.
‘Accordingly, the actual existence of these NSFs leads us to speculate that some special mechanism exists in the regions of these genes.’It looks like recombination of codons (base pair triplets), not single base pairs, has occurred between the start and stop codons for each sequence. This would be about the simplest way that the antisense strand could be protected from stop codon generation. The mechanism for such a recombination is unknown, but it is highly likely that the transposase genes are involved.
Interestingly, Yomo et al. also show that it is highly unlikely that any of these genes arose through a frame shift mutation, because such mutations (forward or reverse) would have generated lots of stop codons. This nullifies the claim of Thwaites that a functional gene arose from a purely random process (an accident).
- The Japanese researchers demonstrated that nylon degrading ability can be obtained de novo in laboratory cultures of Pseudomonas aeruginosa [strain] POA, which initially had no enzymes capable of degrading nylon oligomers.9 This was achieved in a mere nine days! The rapidity of this adaptation suggests a special mechanism for such adaptation, not something as haphazard as random mutations and selection.
- The researchers have not been able to ascertain any putative ancestral gene to the nylon-degrading genes. They represent a new gene family. This seems to rule out gene duplications as a source of the raw material for the new genes.8
The chromosome of P. aeruginosa has 6.3 million base pairs, which makes it one of the largest bacterial genomes sequenced. Being a large genome means that only a relatively low mutation rate can be tolerated within the actual chromosome, otherwise error catastrophe would result. There is no way that normal mutations in the chromosome could generate a new enzyme in nine days and hypermutation of the chromosome itself would result in non-viable bacteria. Plasmids seem to be adaptive elements designed to make bacteria capable of adaptation to new situations while maintaining the integrity of the main chromosome.
Stasis in bacteriaP. aeruginosa was first named by Schroeter in 1872.10 It still has the same features that identify it as such. So, in spite of being so ubiquitous, so prolific and so rapidly adaptable, this bacterium has not evolved into a different type of bacterium. Note that the number of bacterial generations possible in over 130 years is huge—equivalent to tens of millions of years of human generations, encompassing the origin of the putative common ancestor of ape and man, according to the evolutionary story, indeed perhaps even all primates. And yet the bacterium shows no evidence of directional change—stasis rules, not progressive evolution. This alone should cast doubt on the evolutionary paradigm. Flavobacterium was first named in 1889 and it likewise still has the same characteristics as originally described.
It seems clear that plasmids are designed features of bacteria that enable adaptation to new food sources or the degradation of toxins. The details of just how they do this remains to be elucidated. The results so far clearly suggest that these adaptations did not come about by chance mutations, but by some designed mechanism. This mechanism might be analogous to the way that vertebrates rapidly generate novel effective antibodies with hypermutation in B-cell maturation, which does not lend credibility to the grand scheme of neo-Darwinian evolution.11 Further research will, I expect, show that there is a sophisticated, irreducibly complex, molecular system involved in plasmid-based adaptation—the evidence strongly suggests that such a system exists. This system will once again, as the black box becomes illuminated, speak of intelligent creation, not chance. Understanding this adaptation system could well lead to a breakthrough in disease control, because specific inhibitors of the adaptation machinery could protect antibiotics from the development of plasmid-based resistance in the target pathogenic microbes.
- Kinoshita, S., Kageyama, S., Iba, K., Yamada, Y. and Okada, H., Utilization of a cyclic dimer and linear oligomers of ε-aminocapronoic acid by Achromobacter guttatus K172, Agric. Biol. Chem. 39(6):1219–1223, 1975. Note: A. guttatus K172 syn. Flavobacterium sp. K172. Return to text.
- Negoro, S., Biodegradation of nylon oligomers [review], Applied Microbiology and Biotechnology 54:461–466, 2000. Return to text.
- A plasmid is an extra-chromosomal loop of DNA in a bacterium. Such loops of DNA, unlike the chromosomal DNA, can be swapped between different species of bacteria. An individual bacterium can have several types of plasmid, and multiple copies of each. Return to text.
- Thwaites, W.M., New proteins without God’s help, Creation/Evolution 5(2):1–3 (issue XVI), 1985. Return to text.
- Ohno, S., Birth of a unique enzyme from an alternative reading frame of the preexisted, internally repetitious coding sequence, Proceedings of the National Academy of Sciences USA 81:2421–2425, 1984. Return to text.
- Truman, R., Protein mutational context dependence: a challenge to neo-Darwinism theory: part 1, Journal of Creation 17(1):117–127; Truman, R. and Heisig, M., Protein families: chance or design? Journal of Creation 15(3):115–127. Return to text.
- As of the date of writing, no Flavobacterium sp. genome has been sequenced. Return to text.
- Yomo, T., Urabe, I. and Okada, H., No stop codons in the antisense strands of the genes for nylon oligomer degradation, Proceedings of the National Academy of Sciences USA 89:3780–3784, 1992. Return to text.
- Prijambada, I.D., Negoro, S., Yomo, T. and Urabe, I., Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolution, Applied and Environmental Microbiology 61(5):2020–2022, 1995. Return to text.
- Bacterial Nomenclature Up-to-date, Deutsche Sammlung von Mikroorganismen und Zellkulturen GmbH, Braunschweig, Germany.
, 18 September 2003. Return to text.
- Truman, R., The unsuitability of B-cell maturation as an analogy for neo-Darwinian Theory, March 2002;
, 22 August 2003. Return to text.
May I refer you to this post to consider the operations of the "simple cell" to some extent?
More DNA Repair Wonders Found 10/07/2010
Oct 7, 2010 — One of the most phenomenal discoveries since the structure of DNA was revealed must surely be the discovery of multitudes of protein machines that repair DNA (01/04/2002). The repair machines are themselves coded by DNA, but DNA would quickly decay into nonsense without them. Another “fundamentally new” repair mechanism was discovered by researchers at Vanderbilt University recently, and other scientists reporting in Nature uncovered more secrets of a “key player” in DNA double-stranded break repair.
Science Daily began its echo of the university press release saying, “Tucked within its double-helix structure, DNA contains the chemical blueprint that guides all the processes that take place within the cell and are essential for life. Therefore, repairing damage and maintaining the integrity of its DNA is one of the cell’s highest priorities.” The wording brings to mind a well-managed business. How can a cell have priorities, integrity, and maintenance?
Explaining that DNA is highly reactive, the article goes on to describe how DNA damage repair is a constant process. “On a good day about one million bases in the DNA in a human cell are damaged.” That’s on a good day. Toxins, reactive oxygen, radiation, and just normal chemical activity in the cell can lead to all kinds of problems. Untreated, these damages can lead to cell death or cancer. The newly discovered mechanism acts on DNA bases that become akylated. This results in “lesions” on the double helix that can impair translation or replication. “To make matters worse, there are dozens of different types of alkylated DNA bases, each of which has a different effect on replication.”
Several known mechanisms can treat the lesions by scanning the DNA chain, something like crewmen on a railroad car, looking for damaged cross-beams, latching onto them and then flipping each one outward and holding it in a special pocket so that other repairmen can attach to the site, fix it, and put it back. The new mechanism found by the Vanderbilt team operates in bacteria. It finds the lesion and, unlike most known glycosylases, flips out both the damaged base and the base it is paired with. Why? “This appears to work because the enzyme only operates on deformed bases that have picked up an excess positive charge, making these bases very unstable,” the article explained. If left alone, the deformed base will detach spontaneously.” This specialized enzyme may attract other repair enzymes to the site, and “speeds up the process by about 100 times.” The enzyme “uses several rod-like helical structures ... to grab hold of DNA.”
What’s more, this enzyme is “considerably different from that of other known DNA-binding proteins or enzymes,” though it bears some resemblance to a family of “very large molecules that possess a small active site that plays a role in regulating the cells’ response to DNA damage.” The article said nothing about evolution.
On another DNA-repair front, today’s Nature described a “protein giant” named BRCA2 that is critically involved in DNA repair, specifically targeting the dangerous double-stranded breaks that can lead to serious health consequences (double-stranded breaks, as the name implies, involve both rungs of the DNA ladder separating). The BRCA2 enzyme, more than 400 kilodaltons in size (containing roughly 400,000 atomic mass units), is a “key player” in the repair, said Lee Zou [Harvard] in Nature,1 commenting on a paper by Jensen et al in the same issue that elucidated the structure of this giant fix-it molecule and explained how it works.2 Since it repairs damage that can lead to breast and ovarian cancers and Fanconi anemia, BRCA2 is of great interest to medical researchers and their patients. Zou described and illustrated four specific functions of this enzyme in the multi-player teamwork process that fixes double-stranded breaks. In addition, the “histone code” (07/26/2006) appears to play a role in regulating the whole repair team. Both articles mentioned evolution only in passing, suggesting possible ancestral relationships, but only in a most cursory and ancillary manner.
1. Lee Zou, “DNA repair: A protein giant in its entirety,” Nature 467, pp. 667–668, 07 October 2010, doi:10.1038/467667a.
2. Jensen, Carreira and Kowalczykowski, “Purified human BRCA2 stimulates RAD51-mediated recombination,” Nature 467, pp. 678–683, 07 October 2010, doi:10.1038/nature09399.
How Darwinism can survive in today’s environment is a tale of the capacity for humans to cling to dogma far beyond whatever usefulness it may have had. Darwinism may have made 19th-century Victorian racists in the British empire feel like they had latched onto something. It may have allowed certain racist totalitarian tyrants to justify their atrocities with a veneer of scientific credibility. That was all before 1951, when the basis of heredity was found to involve a coded language. Shortly after, Crick discovered that one code gets translated by a family of interpreters into another code. Now, in the 21st century, we have whole systems of molecular machines dedicated to preserving the code, and codes upon codes regulating the codes.
Darwin didn’t write code. Software was only beginning to be invented by Babbage in those days. Darwin knew nothing about networks and codes and double-stranded breaks with BRCA2 machinery at the ready, and other complex mechanisms operating even in bacteria, the simplest little blobs of protoplasm he envisioned, that turned out to be more complex than any machinery in Britain. Why must we cling to an outmoded view of life that spun from minds eager to rid science of intelligent causes? We need a biology for the Information Age, where intelligent causes are well known. Intelligence, and only intelligence, explains codes, messages, software, error-correction routines, networks, and hierarchical systems of all the above. Step aside, Charlie. You had your day. You did your damage. We have a lot of repair work to do.
Next headline on: Cell Biology • Genetics • Health • Intelligent Design • Amazing Facts
Really, Darwinists should be ashamed of themselves for driving a horse-and-buggy hypothesis in a digital-highway world. From what we know about information theory, we know that information only comes from intellect (and a rock doesn't have a lot of intellect) and we have found information in spades in the cell. In fact we find that the cell is a constant surprise and we are learning from the cell. Contingencies and redundancies built into the cell in many ways. When is the world going to use their brains and realize that there is no possibility at all that even the simplest of organisms could have been a happy accident?
This is why I am so critical of censorship organizations like the NCSE, phony sites like talk origins and big mouthed idiots like Richard Dawkins. There are indications that we could discover an actual "cure for cancer" by focusing on the cell and various design aspects of interesting possibilities like BRCA2 rather than scanning the skies for little green men broadcasting a radio show and digging around in the dirt looking for some kind of ape that looks something like a human. While guys like Dawkins and Hitchens make millions writing their snide atheistic Darwinist tripe, while Universities watch like watchdogs for any academics that might question the religion of Darwinism, too many people are dying of diseases that might be defeated by actual operational science based on the concept that the cell was designed and that devolution is happening.
Commenters challenge me to quantify information but they are asking with forked tongues, because they know information is not a natural feature and is not material in form or substance, which is actually a problem for them rather than me. If information cannot be material then organisms could not have "arisen" by natural means, as there is no way to explain information. Similarly, there is no way to explain life coming from non-life. But we can quantify information containers. For instance, let's say that the human genome consists of about 3 billion base pairs and 20-25,000 genes. Let us say that we can identify locations on the genome that produce the information to cause the hands to begin to form. We can look within the genome to ascertain to a great extent where the information is for this and we can also study organisms to see if they begin growing "new" containers with new information. We can and we have, and what we find is that actually mutations have a tendency to destroy or distort the information instead of adding something new. Despite the built-in design aspects of organisms that help preserve the information, the human genome is beginning to become devolved. We have lost information and copying errors have managed to get past the quality controls of the cell so that humanity is going to have to wise up and learn more about our genetic code and figure out ways to preserve the information that has not been corrupted.
We are going to keep finding out that the planets and the Sun are entirely too young to fit the idea of long ages. (hint, we already have found this out). We are going to keep finding fossils that have actual mummified flesh and occasionally we will find DNA that has been preserved, all impossible if millions of years are involved. We will find more evidence that man and dinosaur co-existed. We will find that Big Bang and String theory will keep running into insolvable corners and baffling conundrums. We will find more and more "living fossils" as we explore the depths of the oceans and go deep into unfamiliar jungles.
You want to believe in Darwinism? Take a test. Throw a few pieces of junk up into the air a few times ever day and call me when the junk turns itself into a laptop. Maybe you could take a couple of live wires and try to shock a mud puddle to see if a salamander appears. Better yet, enter the state lottery, compared to Darwinism you are an absolute dead-solid lock to win the bazillion dollar prize!
It is time to admit that Darwinism is just not science, it is religion. It is a preposterous proposition in the light of what we now know about organisms. It is nothing more than the last refuge of the anything-but-God crowd and it is time to expose them for what they are. Kooks. Lump them in with the Heaven's Gate crowd and with Scientology. L. Ron Hubbard himself supposedly said that, "The way to make a million dollars is to start a religion." Well, the way to get grant money is to endorse a religion, Darwinism. The way to screw up your scientific career is to actually have a scientific attitude and consider supernatural causes for supernatural things such as life and information. Duh. It is time for the world to wake up and put away the buggywhip!
BTW here is a general clearinghouse site for questions about the fossil record,