Thank you, Opus. So, if I understand you right, there are mutations that restore fitness that also do not belong to the class of "reversion" mutations that Anderson talks about. I am guessing that is what you mean by "Promoter-Up" mutations. The key claim here, I think, is that you have supposedly random mutations that not only increase fitness (a necessarily contingent quality and not absolutely dependent on increased complexity), but more importantly increase informational complexity beyond the originally observed state of complexity, something that could support Darwinian theory, even though it contradicts the predictions of the generalized second law of thermodynamics. I think we already established in this discussion that terms like "gain of function" are not probative, because, as Anderson showed, gains in function can arise from loss of information, where events like loss of repressor genes are concerned, which result in increased performance of a certain function already encoded in the genetic design. But I take it you are speaking of gain of information, not just gain of function.
When you get a chance, could you take a look at this article about Darwinism and the deterioration of the genome?
He makes some interesting claims, such as the fact that mutations are not entirely random, and that the structure of the genome does not fit with the hypothesis that the whole genome is the product of random change. Also, he insists on the extreme rarity of beneficial mutations, with several citations to support his claim. Perhaps you and Mina disagree with the author's conclusion, however, in which case we should certainly discuss this further:
All of the beneficial mutations located in my search of the literature involving almost 20 million references were loss mutations and mutations such as sickle cell anemia that have a beneficial effect only in very special circumstances. In most situations they have a decidedly negative effect on the organism’s health. Not a single clear example of an information-gaining mutation was located. It was concluded that molecular biology research shows that information-gaining mutations have not yet been documented. While such negative findings do not in and of themselves prove creation, they support the conclusion that an Intelligent Designer formed the original genomes of each created kind.
One alternative way of looking at this problem is the following: if we start by assuming beneficial, information-gaining mutations are sufficiently frequent, why did e.g. Dobzhansky's fruitfly experiments completely fail to reveal any? After deliberately increasing the mutation rate by application of radiation, and after many generations, the only mutations that occurred were deleterious, e.g. loss of wings. And even if you argue that such mutations could be beneficial in certain environments, e.g. a windy island where a winged fly could be easily blown out to sea, they are clearly information-losing mutations, not information-gaining. I see problems with Darwinian predictions whichever aspect of biology you look at.
And notwithstanding whatever scientific evidence for Darwinism there may be, the dogmatic problems remain. A God who created death is simply not the God of the Christians. A universe that arose out of cycles of destruction and spontaneous creation would seem on the contrary to support pagan theories of the Deity, like the three aspects of the Hindu god Shiva.
I started on the article that you suggested that I read. I wasn't particularly efficient, because I consider this a conversation rather than a debate. That will be evident once you see how far I have gotten. But first I want to relieve your mind about promoter up mutations, the gain of information achieved is not novel, strong promoters already have this information (typically in bacteriophage that wants to overexpress their gene products as fast a possible). Promoter up mutations are pervasive because they often only require a single base pair change. If you want to know why most promoters are purposefully weak, we can go into that later. And my advise to Dobzhansky is to lower the radiation dose, wait longer, and be more patient, but then again I have only started working with fruit flies a few months ago and I am already tired of having them fly into my mouth when harvesting embryos for protein purification.
I am sure I have read it already, but can you recap the evidence that absolutely all life had to live forever. It appear to be the crux of the problem here rather than scientific evidence. It is not a situation that would allow a sustained environment in our current biosphere, but that doesn't mean it didn't happen. And I confess that I have read this entire 66 page and growing thread, but remember almost none of it.
This is where I am with the article you have chosen for so far (comments on the abstract and the beginning of the article) with quoted text in red
:An evaluation of DNA/RNA mutations indicates that they cannot provide significant new levels of information.
This is wrong unless his definition of information doesn’t include a beneficial effect. Instead, mutations will produce degradation of the information in the genome. This is the opposite of the predictions of the neoDarwinian origins model.
Degradation of information is a weird term here. I don’t know what he is talking about because I do not know what the neoDarinian origin models (there must be more than one, right?) are and I do not really care what they are.Such genome degradation is counteracted by natural selection that helps maintain the status quo.
I he means defects, absolutely, he hit the nail on the head with this statement. Degradation results for many reasons, two of which are reviewed here. 1) there is a tendency for mutations to produce a highly disproportionate number of certain nucleotide bases such as thymine and 2) many mutations occur in only a relatively few places within the gene called “hot spots,” and rarely occur in others, known as “cold spots.”
I do not know why he picks out thymine. There are hot spots, they tend to be repetitive sequence elements. The other spots used to be called cold spots, but they represent the normal rate of mutations. There is no impact of hot versus cold on the role of mutations in evolution. In other words, the normal mutation rate for a given gene is 1 per 10 million (+/- a factor of 10) in a population of bacteria, and hot spots are around 1 in 10,000 (+/- a factor of 10). There is plenty of time for 1 per 10 million. An intensive review of the literature fails to reveal a single clear example of a beneficial information-gaining mutation. Conversely, thousands of deleterious mutations exist, supporting the hypothesis that very few mutations are beneficial. These findings support the creation origins model.
Again, I am not sure what he means by information and what he thinks is not information. There are many examples of beneficial mutations. The author also seems to ignore the fact that evolved organisms are near perfection for their environmental niche. If you change their environment (temperature, salinity, nutrient compositions, etc.) beneficial mutations are evident that might be silent or detrimental in the prior environment. This is already documented. Why are there thousands upon thousands of research papers on detrimental mutations and let us say only a few hundred or less of the papers that show that beneficial mutations occur? It is because detrimental mutations have financial and health consequences. The research will be funded by NIH and the Department of Agriculture and published in the limited and costly space of Journals. If you want to do a new experiment on the acquirement of beneficial mutations based on environmental change with a new organism or a new environmental situation/requirement, it is doubtful you would be funded because the proof of concept has already been established, the probability of discovering something novel (very important for basic research) is low and only a small fraction of research proposals with high probability for novel and significant contributions are funded. I suspect there are a lot more studies of this sort in industry-related journals rather the research journals and he probably should do his literature search there (it is not going to be indexed in PubMed, unfortunately).An evaluation of the literature and an analysis of the original data reveals many serious problems with Dawkins’ mutation/selection model. A major problem is the computer program contains human designed foresight that evolution does not possess. Intermediate word sets are chosen only because the program is designed to select for changes that match its predetermined goal.
I might have the same objection, but I have done the same thing with totally random DNA sequence with a selective pressure and having no idea what the result would be. Here is an example (done by someone I know): when whole genome sequences became available for organisms from the third domain of life, Archaea (they are prokaryotic extremophiles that contain related proteins that are only found in eukaryotes and not bacteria and vice versa), a researcher found a gene encoding a protein that was related to a class of bacterial transcriptional regulators that bind to specific DNA sequences (transcription is RNA synthesis). The regulation of gene expression is primarily mediated (ultimately) by regulating transcription and little or nothing was known about the regulation of gene expression in Archaea. They are difficult grow in a laboratory and no genetic system was available. The researcher cloned the gene, expressed the protein in E. coli and purified it to see if it would bind nonspecifically to DNA (with weak affinity; that is, most of the interaction affinity is due only to the spacing and negative charges of the phosphate (PO4-) separating individual deoxyribose moities of DNA). It did bind nonspecifically, but he had no way of finding out if it bound tightly to a specific sequence in the archaeal genome due to the near impossibility of doing genetics (optimal growth conditions of 100 C (the temperature water boils) and anaerobic, which means no agar petri dishes, no air allowed, and the melting and degradation of any DNA that you might would want to get into the cell). To get around this problem he used an in vitro evolution technique called SELEX. It is kind of the modern way to get proteins or RNA with new activities that didn’t exist previously in nature by starting with totally random DNA (we are just too dumb to figure out how to do this type of genetic engineering ourselves currently). In this case a totally random ~20 (might be 16, I forget) base pair DNA molecule was synthesized on a machine with predetermined flanking DNA sequences on each side (more about this later). This corresponds to 420 different sequences and he made enough DNA to have four copies of each possibility. He then allowed a relatively small amount his protein to bind to this DNA under nonspecific conditions (high micro-molar concentrations of DNA). Because nonspecific protein-DNA interactions are transient (that is, the on and off rates of binding/releasing to/from DNA is rapid), if his protein binds DNA specifically (not all proteins of this type do), it will exchange, with time, onto DNA having greater and greater similarity to its preferred binding sequence and it will remain bound to these more preferred DNA sequences for longer periods of time. I won’t go into the details but there are lots of ways of isolating DNA bound to protein from free DNA, which was done. This isolated DNA was amplified by 25 rounds of DNA replication using the predetermined flanking sequences to design DNA primers to replicate the random region. The technique is called PCR, which I am guessing you are familiar with and won’t go into it further except to note that the heat resistant DNA polymerase comes from the same archaeal species (Pyrococcus furiosus). Twenty five rounds is the number of doublings E. coli achieves after 8-12 hours. He then used this DNA for binding to his protein at more stringent conditions (a lot less protein and a lot less DNA, but still with a large excess of DNA over protein. The DNA that bound to his protein was again isolated and amplified by PCR. This procedure was repeated about 6 to 8 times (I can’t remember), each time making the conditions more stringent (ultimately down to the low nanomolar concentration range). He sequenced this DNA and found that he selected an interrupted palindromic sequence from random DNA. I don’t remember the sequence, but is was of this sort: 5'-GGCTTACaggGTAAGCC-3' (the complementary DNA strand has the same capitalized letter sequence going right to left [in the 5' to 3' direction]; agg is the interruption). He found this sequence upstream of just a couple of genes in the Pyrococcus genome and he cloned the genes into an E coli plasmid for in vitro transcription using the (human/eukaryotic-like) Pyrococcus RNA polymerase and (human/eukaryotic-like) basal transcription factors TBP and TFIIB and found that his (bacterial-like) protein and the palindromic sequence were essential for the transcription of these genes but not other Pyrococcus genes.One major problem is that this model does not include lethal mutations. Every single product of the program can survive and “reproduce” until the goal is reached. As a result, there is no limit to the “beneficial changes” available for selection, and every single change to each goal letter increases “fitness” and is thus selected for the next generation (Spetner, 1997, pp. 163-170). This model is totally unrealistic because most expressed mutations are deleterious and, as a result, the favorable mutations almost always “become swallowed in the flood of bad mutations” (Hoyle, 1999, p. 20). Hence, “only mutations of small effect are likely to be beneficial” (Bell, 1997, p. 56).
First off, I do not buy into abiogenesis occurring on earth. I do not find it reasonable (it is beyond what I can comprehend) and I stopped reading abiogenesis-related papers about five years ago (although this research topic is worthwhile for many other reasons). I also do not buy into the above statement. Let’s start with a microorganism and how and/or why it got here is a matter of one’s faith. For me, I would prefer God to start with some bacterial species (I know more about them than archaea) along with some bacteriophage (viruses that infect bacteria), the latter so that I do not have to write about the evolutionary lag phase when they were not in existence. Oh, and some of these chosen bacteria have a sex pilus and a DNA plasmid episome that can integrate in and out of the bacterial chromosome carrying along duplicated bacterial genes to other bacteria during intercourse. They are not needed and I do not use them for this story, but sex sells. These bacteria created an environment on earth that made it possible for them to devolve into less adaptive and less fit organisms like eukaryotes (from yeasts to humans). I say this because bacteria can survive quite well without us eukaryotes, but we eukaryotes cannot survive without bacteria. Now a eukaryote might say we have an evolved archeaeon for our nucleus, an evolved cyanobacteria for our chloroplast, an evolved eubacteria for our mitochondria and an evolved bacteriophage T7-related RNA polymerase for our mitochondrial RNA polymerase (I didn’t want to leave our bacteriophage friends out), but we eukaryotes can’t do squat, metabolically, compared to prokaryotes. I added this opinion of mine because I think we need to have more humility and focus ourselves why God created this environment for us to exist (for me it is spelled out primarily in the Gospel of St Matthew and I will forever be struggling to live up to those expectations without thinking about it first). Back to the issue on hand with a warning, I am not an evolutionary biologist, I have never taken a class on it nor have I read a book or article about evolution (per se), I am not interested in it (I consider it a done deal based on comparative protein structure and enzymatic mechanisms and of course phylogenetic relationships of DNA and proteins), there are others here that are more knowledgeable than I am in this particular area (Minasoliman (I hope I spelled that correctly) and Heorhij, for example). The refuting scenario that follows came to mind because of the recent metagenomic sequencing project, The Sorcerer II Global Ocean Sampling Expedition, in which DNA extracted from ocean waters is being sequenced by the Craig Venter machines and programs used to shotgun sequence the human genome. A lot of the DNA found turned out to be from cyanophage, a bacteriophage which infects cyanobacteria (life-giving blue green algae in Opus118-speak, or “pond scum” in Aposphetic). These cyanophage, en masse, contain a lot of genes, including photosystems I and II (for photosynthesis) and other metabolic (anabolic and catabolic) enzymes, from cyanbacteria, other metabolic enzymes without bacterial counterparts, and a bunch of other proteins that we have no idea what they do because all we have is DNA sequence and no known homologs. Some viruses kill the cell no matter what (lytic), some rest a spell like rats until it looks like the boat is going to sink (lysogenic). Viruses are good incubators for evolution because they are not alive, incorporate (duplicate) preexisting genes from bacteria by chromosomal integration or inadvertent recombination (both happen), have 100-1000 progeny per infected cell in less than 15 minutes, compared to 1 bacterial genome in 20 minutes max, no constraints on the evolving gene being toxic at some point because they are going to kill the cell in a few minutes any way or whenever they feel like it if they are lysogenic, less dependent on precise DNA replication (leading to more errors/mutations) because of the number their progeny with each infection cycle, and they are probably the first to sense and adapt to changes in the environment (meaning a selective pressure on the duplicated genes they already harbor) because they need to grab as much of the cell’s resources and the cellular environmental resources as fast as they can while they are killing off the cell (once they go lytic on you, if they were lysogenic). This is one way to refute the lethality problem proposed above, there are others I could propose if viruses didn’t exist and do not exist now which is perhaps overdoing it.
That's it so far. I am still contemplating on some text that I wrote about evolution in higher eukaryotes, I decided to use RNA splicing as a mechanism to that avoids lethality but I do not have the facts on the tip of my tongue and describing the topic is a bit complex.