Dealing a bridge hand is a statistical miracle, yet it happens all of the time. You are committing the Sharpshooter fallacy. The DSB repair system is just one system out of a nearly infinite number of systems that could have evolved. Given the inevitability of evolutionary processes, something will evolve, and that something will be extremely unlikely. In the same way, the very act of dealing cards inevitably results in a pattern of cards that is extremely unlikely.
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This argument is problematic as life has very specific requirements and the claim is not at all scientific as âit could have happened differentlyâ is not a scientific claim. It is just a speculation with very little substance.
Once you start to evolve a complex structure all the elements are dependent on each other. The any sequence will do canard does not apply.
You would first need to show that the specific DSB repair system is required for life to exist. From what I have seen, this isnât the case.
This is the Muller Two Step:
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I donât understand why you are making arguments like this. You are missing Salâs argument here. The issue is not life existing it is complex eukaryotic life existing.
Do you believe that life could exist without a âmemoryâ repair mechanism?
FWIW, Art thinks most biologists donât think there is universal common ancestry of all proteins from a single ancestral sequence.
What do you think? Do you think all proteins/genes descended from a single ancestor? If not, your rebuttal is moot an irrelevent and effectively wrong.
There are an infinite number of ways of making a lock with a matching key, it doesnât make the emergence of a working lock/key system probable by mindless events. Itâs not a sharpshooter fallacy, itâs basic mechanics of the constraints of connecting interlocking/interacting parts.
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I think he is right. I donât think so either.
The more interesting case is that of human evolution. It really looks like like common ancestry there. Why?
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So evolutionary theory/universal common descent (UCD) at the very least needs unexpected events to make it work.
The fair thing to do is to give facts and a variety of estimates of how unlikely an event is. If they decide it meets or doesnât meet their threshhold of a miracle, thatâs up to them. Behe accepts common descent, but he doesnât think random mutation and selection are EXPECTED to achieve changes of that magnitude (though he doesnât cite chromatin evolution explicitly).
I think I can speak for the sentiments of some in the creationist community who were once evolutionists like me. At some point it became apparent that to accept abiogenesis followed by universal common descent meant acceptance of miraculous events to make common descent possible â thus itâs not exactly accurate for evolutionary biologists to represent it as a naturalistic theory even though they believe in their heart it is.
Weâre very very similar to chimps, much more so than we are to trees and starfish.
Hmmm. Are the equivalent events more or less unexpected under design theory than under evolution? If you canât tell, this is not a reason to prefer one over the other.
Then do that. Produce some facts and estimates of the (un)likelinesss of the design of any of the biological systems you have mentioned.
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I am willing to agree with Art that the representation you made about the evolution of proteins was incorrect.
In addition, I acknowledge that your apparent agreement with Art makes my point moot.
As a matter of logic based on the set of facts and representations that you presented, I happen to think I was right. Being moot is not the same thing as being wrong.
Best,
Chris
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This is by a former evolutionist and former non-Christian who is now a professor of cellular biology. She is an Ivy League PhD, and Harvard post-doc. Before providing an estimate that your request, Iâll introduce Change Tanâs background according to her own words (which she gave permission to use), and then provide her estimates in a subsequent comment:
As an exemplary student born in the New China, who grew up under the five -starred red flag , studied dialectical materialism from elementary school, and whose most cherished virtues were to respect, learn from, and follow the examples of my teachers and elders, I (Change Tan) accepted without question the Darwinian evolutionary view that life came from non-life and complicated life from simpler life.
What else could it possibly be? All of my textbooks and all of my teachers taught that principle.
I came to the United States with a Masterâs degree in physical organic chemistry from China. Thinking to apply my knowledge in chemistry to the study of life, I chose biochemistry as my field of study while pursuing my Ph.D. at the University of Pennsylvania, studying signal transduction during frog embryogenesis (how genes interact with each other to control the development of embryos). Tired of reading the reviewersâ criticisms of my manuscripts that âthe results were just based on ectopic overexpressionâ , I was determined to add genetics to my research toolbox, and thus, ended up pursuing postdoctoral training in fly genetics at Harvard Medical School.
Meanwhile, I exposed myself to primary literature and many seminars on current first-hand research by various scientists on diverse topics in biology. Never did I hear any objections to the Darwinian theory of the origin of life or the origin of biodiversity. Darwinian evolution was taken as a given. It was embedded in our reasoning, interpretation of data, and writings.
As I began to teach molecular biology at the University of Missouri in 2006, I discovered that the vital molecular machineries described in the molecular biology textbooks , specifically, the machineries of DNA replication, transcription, and translation, are fundamentally different for bacteria and eukaryotes. The machineries that bacteria use are so fundamentally different from those of eukaryotes that no simple or step-wise adjustments could possibly change one into the other, yet no organisms could survive or propagate without functional DNA replication, transcription, and translation machineries. A natural and logical conclusion from this is that eukaryotes could not have evolved from bacteria. The molecules involved in bacterial and eukaryotic DNA replication, transcription, and translation make this conclusion crystal clear.
Yet how could this be? Everyone around me seemed to be altogether confident that eukaryotes evolved from bacteria.
At first I was thrilled and imagined this to be a great discovery, but soon I began to tell myself: âWait a minute. You must be wrong, Change. Your major is chemistry. You never really studied biology. You only picked up pieces of information from biological science related to your research area on your way as your research required. So many people have spent their entire lives studying evolution. They must have seen what you saw and figured out that the DNA replication, transcription, and translation machineries of bacteria and eukaryotes are not interchangeable and still have been able to determine how eukaryotes evolved from bacteria.â
So, I started to search for the answers evolution biologists might have on the origin of eukaryotes, as well as on the origin of life.
A satisfactory answer has yet to be found.
As stated by Eugene Koonin, a senior investigator at the National Center for Biotechnology Information (National Library of Medicine, National Institutes of Health): âNo direct counterparts to the signature eukaryotic organelles, genomic features, and functional systems exist in archaea or bacteria. Hence, the very nature of the evolutionary relationships between prokaryotes and eukaryotes becomes a cause of bewilderment.â âOf the three domains of life, eukaryotes possess by far the most complex, strikingly elaborate cellular organization that for some might even summon the specter of âirreducible complexityâ (Kurland, et al.,2006) because for most of the signature functional systems of the eukaryotic cells, we can detect no evolutionary intermediatesâ ).
The more I read, the more I think, and the more I learn about the molecular details of bacteria and eukaryotes, the more I am convinced that eukaryotes could not have evolved from bacteria (or archaea, another kind of prokaryotes) and that life could not have evolved from non-life .
Even if itâs all true, it doesnât explain away the evidence for common descent of humans.
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Providence covers it.
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Wrong.You should know better.
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I know who she is. She also writes for AiG, and Iâve read a couple of her articles.
Iâm not holding my breath.
When someone wins the lottery, is that a result of âphysically expected changesâ? That is to say, can we scientifically predict which person will win the lottery each time it is drawn?
If not, whenever a lottery is won, that is a âmiracleâ by your criteria.
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What was the point of that?..
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Ok, as I promised, here is some of the basis of Dr. Tanâs estiamtes. CLASS IS IN SESSION NOW! [reprinted with her permission]
Chemically and naturally, there are many other possible configurations that are energetically indistinguishable from the DNA structure of living cells. Figure 2 shows the configuration of a natural adenine-cytosine deoxyribose dinucleotide (Figure 2 A) and three of its many possible isomers (Figure 2 B-D).
FIGURE 2
FIGURE 2
, let us consider assembling a genomic DNA of only two base pairs (adenine and cytosine on one strand paired with thymine and guanine on the opposite strand), using the components of natural DNAs: nitrogenous bases, deoxyribose, and phosphate acids. Assuming, the top strand (also known as the sense strand or the Watson strand) of our imaginary genome is a dinucleotide with the sequence of 5â-AC-3â, a dinucleotide made of dAMP (deoxyadenosine-5â-monophsphate) and dCMP (deoxycytidine-5â-monophsphate). Since the bottom strand (also known as the anti-sense strand or the Crick strand) is the reverse and complementary of the top strand, its sequence has to be 5â-GT-3â, a dinucleotide made of dGMP (deoxyguanosine-5â-monophsphate) and dTMP (deoxythymidine-5â-monophsphate).
A deoxyribose nucleotide is composed of a deoxyribose sugar ring, a nitrogenous base, and a phosphate group (Figure 3). The nitrogenous base is attached to the deoxyribose sugar ring via a carbon-nitrogen (C-N) bond (Figure 3, boxed with dotted red lines), which is formed from a hydroxyl group (OH) in the sugar ring and an amine group (NH) in the nitrogenous base (Figure 3, bottom). The phosphate group is attached to the sugar ring via a phosphoester (P-O) bond (Figure 3, boxed with dashed red lines), which is formed from a hydroxyl group (OH) in the sugar ring and a hydroxyl group (OH) in the phosphate group (Figure 3, top).
[NOTE : i.e., 5â-pdGMP-pdTMP-3â, or simply 5â-pdG-pdT-3â. The full name of 5â-GT-3â is 5â phosphor-9 (1â-Ă-deoxy-D-ribofuranosyl) guanine 3â oxy-5â phosphor-1 (1â-Ă-deoxy-D-ribofuranosyl) thymine.]
FIGURE 3
FIGURE 3
The numbers of possible isomers of our two-base-pair genome can be calculated in three steps: calculating the isomers of the first strand of the genomic DNA (5â-AC-3â), calculating the isomers of the second strand of DNA (5â-GT-3â), and calculating the total isomers of both strands, as detailed below.
Calculating the number of isomers of the first strand of the genomic DNA
To calculate the number of possible isomers for the first strand of DNA of our imaginary genome, 5â-AC-3â, we need to determine the number of isomers of dAMP, the number of isomers of dCMP, and possible ways of linking them together.
The number of isomers of one dAMP molecule can be calculated by multiplying the number of OH groups in a deoxyribose by the number of amine (NH) groups in an adenine that can be used to form C-N bonds and by the number of linking the molecules to a phosphate group.
Note that deoxyribose exists in five forms in water solutions, each of the forms has three OH groups (red in Figure 4) that can be used to link with an adenine via a C-N bond. The six-membered ring forms are the most stable, while the linear form is the least stable. The two five-membered ring forms are energetically identical, thus, each five-membered ring form will make up 12.5% of the mixture. The two six-membered ring forms are also energetically equal to each other, thus, each making up 37.5% of the mixture. It is interesting that the isomer used in DNA is not the most stable isomer of deoxyribose.
FIGURE 4
FIGURE 4
Adenine exists in two forms in water solutions, thus there are three NH groups in an adenine molecule (N7H, N9H and NH of the NH2 of C6) that can be used to link with the sugar ring via a C-N bond (Figure 5 A). The number of NH groups that can be used to link to the sugar ring via a C-N bond in a cytosine is also three (N1H, N3H and NH of the NH2 of C4) (Figure 5 B). That number is five for guanine (N1H, N3H, N7H, N9H, and NH of the NH2 of C2), and two for thymine or uracil (N1H and N3H) (Figure 5 C-E). The two NH groups of the NH2 of C6 of adenine are indistinguishable and are counted as one, same is true for the NH groups of the NH2 of C4 of cytosine and the NH groups of the NH2 of C2 of guanine.
FIGURE 5
FIGURE 5
Therefore, there are 3 (OH groups for each deoxyribose form) x 3 (NH groups in an adenine) x 5 (forms of deoxyribose) = 45 ways of linking an adenine with a deoxyribose via a C-N bond. The same is true for a cytosine. For a guanine molecule, there are 75 ways to link it with a deoxyribose via a C-N bond. Thymine has 30 such ways. Uracil also has 30 such ways, but it is not a component of DNA, but of RNA.
Now that for each particular deoxyribose form, when one of its three OH groups has been used to link adenine (or any other bases), there will be two OH groups left to be used to link to a phosphate group. Therefore, there are a total of 2 x 45 = 90 ways of linking an adenine, a deoxyribose, and a phosphate group together (Figure 6). That number is 90, 150, and 60 for cytosine, guanine, and thymine, respectively. These are the numbers of isomers of dNMP in which N is an adenine (A), a cytosine (C), a guanine (G), or a thymine (T), excluding all the isomers of deoxyribose that are not a deoxyribose, all the isomers of A/C/G/T that are not A/C/G/T and all the isomers of linking the phospho-group through non-phosphoester bond.
The last step of calculating the isomers of 5â-AC-3â is to determine the possible ways of linking the isomers of dAMP and the isomers of dCMP together. Note that in each of the isomers of dAMP or dCMP, one of the three OH groups of its deoxyribose is occupied by a nitrogenous base, another by a phosphate group. Therefore, there is only one OH left in each isomer of dAMP that can be used to link to the phosphate group of an isomer of dCMP, and vice-versa. Consequently, there are two possible ways to link an isomer of dAMP and an isomer of dCMP. For example, a dAMP and a dCMP can be linked via a phosphodiester bond to form 5â-AC-3â, or 5â-CA-3â.
Taken together, there are 90 x 90 x 2 = 16,200 ways of linking an adenine, a cytosine, two deoxyribose, and two phosphate groups together via C-N bonds and phosphoester bonds (Figure 7), only one of these is our desired DNA sequence 5â-AC-3â.
My interpretation is that a DNA genome is a violation of the law of large numbers, ergo, a statistical miracle. Whether it is a miracle in the theological sense, is a separate question, but this shows one the mechanistic reasons, at least, why life does spontaneously emerge. Observation agrees with chemical theory. And this is the tip of the iceberg.
A lottery, btw, is intelligently designed to guarantee a winner.