So you don't know what the first life evolved from but you have faith that it did and evolution explains how all life came to exist?
The question mark is my way of asking what your saying instead of trying to put words in your mouth
If that is your method of asking a question, I recommend you re-evaluate your communication methods. There's a difference between asking a question a question like "What do you think about ABC?" compared to "You don't know A but you must believe B?" But I thank you for clarifying afterwards that it is a question, as it was originally interpreted as an assertion.
Regarding the question itself: no. Religion has no middle ground. Everything MUST be "known" or explained for the religion to work out. Science has an alternate: not knowing. The options in science are not "it's definitely true" or "it's faith that it's true." It's either true, or not fully supported. So even though there is a good working idea of how things came to be, the fact still remains that there is not compelling reproducible evidence that really proves it. That does NOT mean I have faith that the working idea is correct, since it has not been proven to be correct. It is what it is: unknown for the time being. And that's ok in science, but not religion.
REGARDLESS, evolution is a separate process, just as learning how to drive is a separate knowledge set from building a car. It doesn't matter how you get a car, whether you buy it, or your parents give it to you, or you steal it: you still know how to drive it. So too does evolution drive the change in life over time, REGARDLESS of where the life came from.
The question, once again, is what did the first life on earth evolve from?
What you are describing is abiogenesis, not evolution.
And you have to explain how whale fossils are found in inland places such as Michigan and the other inland places that is to far from the ocean. You also have to explain sea shells found on mountain tops.
No, that's not necessary.
You seem to continually skip around from topic to topic. Everytime you're proven wrong in one area, you leave it pretending it doesn't exist, to move onto your next poor excuse or copied and pasted outdated garbage. Why don't you pick one and stick to it?
Here are a few topic suggestions:
- The "new information" you said can never come about and I proved you wrong about
- How you don't understand microevolution, let alone how it genetically differs from macroevolution
- What genetics tells us about evolution
- How bacteria gain antibiotic resistance without exogenous genetic information
Wait wait. You pick a topic. You generally lack the integrity to see it through to the end, but try your hardest.
I will admit there was more new information then i thought from mutations, but Dr. Spetner cleared that up for me.
We can go here.
How bacteria gain antibiotic resistance without exogenous genetic information
Antibiotic Resistance as an Example of Evolution
Spetner: Continuing his effort to show the evolutionary efficacy of beneficial mutations, Max presented in his essay the acquisition of antibiotic resistance by microorganisms as an example of evolution. He said one can “demonstrate a beneficial mutation … with laboratory organisms that multiply rapidly, and indeed such experiments have shown that rare beneficial mutations can occur. For instance, from a single bacterium one can grow a population in the presence of an antibiotic, and demonstrate that organisms surviving this culture have mutations in genes that confer antibiotic resistance.” Such an experiment shows that “de novo beneficial mutations” can arise.
My response to this is that I have shown in my book that mutations leading to antibiotic resistance fail the test of representing the mutations necessary for evolution. I summarize that argument here. All antibiotics are derived from microorganisms. Recall the story of the serendipitous discovery of penicillin by Alexander Fleming in 1928, when he noticed that his plate of Staphylococcus bacteria was clear in the vicinity of a bread-mold contaminant. The mold was found to produce something that could lyse and kill the bacteria. That something was a molecule later named penicillin. Afterwards, other antibiotics were found to be produced by other microorganisms, such as soil bacteria. Soil has long been recognized in folk medicine as a cure for infections.
The antibiotics produced by these microorganisms serve them as a defense against attack by other microorganisms. Some microorganisms are endowed with genes that grant resistance to these antibiotics. This resistance can take the form of degrading the antibiotic molecule or of ejecting it from the cell. Unfortunately for human health care, the organisms having these genes can transfer them to other bacteria making them resistant as well. Although the resistance mechanisms are specific to a particular antibiotic, most pathogenic bacteria have, to our misfortune, succeeded in accumulating several sets of genes granting them resistance to a variety of antibiotics.
The acquisition of antibiotic resistance in this manner qualifies as evolution only in the sense that it is an adaptive hereditary change. It is an example only of Evolution B. It is not the type of evolution that can make a baboon out of a bacterium. The genetic change is not the kind that can serve as a prototype for the mutations needed to account for Evolution A. The genetic changes that could illustrate the theory must not only add information to the bacteriumÂ’s genome, they must add new information to the biocosm. The horizontal transfer of genes only spreads around genes that are already in some species.
It turns out, however, that a microorganism can sometimes acquire resistance to an antibiotic through a random substitution of a single nucleotide, and this is the kind of example Max presented. Streptomycin, which was discovered by Selman Waksman and Albert Schatz and first reported in 1944, is an antibiotic against which bacteria can acquire resistance in this way. But although the mutation they undergo in the process is beneficial to the microorganism in the presence of streptomycin, it cannot serve as a prototype for the kind of mutations needed by NDT. The type of mutation that grants resistance to streptomycin is manifest in the ribosome and degrades its molecular match with the antibiotic molecule. This change in the surface of the microorganismÂ’s ribosome prevents the streptomycin molecule from attaching and carrying out its antibiotic function. It turns out that this degradation is a loss of specificity and therefore a loss of information. The main point is that Evolution A cannot be achieved by mutations of this sort, no matter how many of them there are. Evolution cannot be built by accumulating mutations that only degrade specificity.
In the final paragraph of my original critique, I said the following:
The mutations needed for macroevolution have never been observed. No random mutations that could represent the mutations required by NDT that have been examined on the molecular level have added any information. The question I address is: Are the mutations that have been observed the kind the theory needs for support? The answer turns out to be NO! Many have lost information. To support NDT one would have to show many examples of random mutations that add information. Unless the aggregate results of the genetic experiments performed until now is a grossly biased sample, we can safely dismiss Neo-Darwinian theory as an explanation of how life developed from a single simple source.
Max: You cite the fact that some bacteria grown under selective pressure of this antibiotic become resistant through a mutation that “degrades the molecular match with the antibiotic molecule” representing “a loss of specificity and therefore a loss of information.” Some streptomycin resistance mutations do, as you point out, reflect mutations of the ribosomal protein S12 which cause loss of binding of this antibiotic, which you interpret as “loss of information.” However, you ignore other mutations of this protein that do not lead to loss of antibiotic binding (e.g. Timms et al., Mol Gen Genet 232:89, 1992). According to your formulation, these mutations would not represent a loss of information, yet they are represent natural mutations that are adaptive under conditions of exposure to streptomycin. Would you accept that this kind of mutation is a good model for an adaptive evolutionary change consistent with Neo-Darwinian Theory?
Spetner: You misunderstood the paper by Timms et al., which you cited. All of the adaptive mutations reported in that paper show reduced binding of the streptomycin molecule. The 12 adaptive mutations reported in the S12 protein fall into two categories. There was no example of what you claimed I ignored. Five of those mutants are designated as streptomycin resistant (Smr), and seven are designated as streptomycin dependent (Smd). All 12 of them, in the words of the authors “reduce the affinity of the ribosome for streptomycin.” Perhaps you would like to point out to me where in that paper they mention mutations in S12 do not lead to reduced binding, and which you claim I have ignored.
Max: My citation of this paper was based on its description of the streptomycin-dependent mutants, which require streptomycin for growth as a result of mutations in the S12 protein. Clearly such mutants have not lost streptomycin binding completely; however it is possible that they have reduced binding affinity, so that according to your criteria-which I do not accept as valid-they might have “lost information.” However, your whole argument about streptomycin seems to be based on the misconception that streptomycin works by binding to the S12 protein. In fact, as mentioned in the Timms paper, the binding is primarily to the 16S ribosomal RNA, not to S12, and the mutations in the S12 protein function to decrease streptomycin by stabilizing a specific conformation of the 16S rRNA that does not bind streptomycin well (Carter et al., Nature 407: 340, 2000; Moazed & Noller, Nature. 327:389, 1987; Gravel et al., Biochemistry. 26:6227, 1987; Montandon et al, EMBO J. 5:3705, 1986; Pinard et al, FASEB J. 7:173, 1993; Melancon et al., Nucleic Acids Res. 16:9631, 1988).
[LMS: I DON’T KNOW HOW MAX CAN CLAIM THAT MY “WHOLE ARGUMENT” IS “BASED ON A MISCONCEPTION.” HE IS THE ONE THAT INITIALLY WROTE OF STREPTOMYCIN BINDING TO THE S12 PROTEIN. HE SAID “MOST S12 SEQUENCES BIND STREPTOMYCIN.” (SEE BELOW.) IF THERE IS ANY MISCONCEPTION, IT IS HIS. I JUST WENT ALONG WITH HIM IN THAT BECAUSE I DON’T THINK THE ARGUMENT HINGES ON EXACTLY WHERE THE BINDING SITE IS. EXACTLY IN WHICH PROTEIN OF THE RIBOSOME THE BINDING TAKES PLACE IS IRRELEVANT TO THE ARGUMENT.]
A mutation that causes a specific conformational change in another molecule that in turn prevents efficient binding of a third molecule does not necessarily suggest a “loss of information” to me, even if your protein information metric were valid.
[LMS: IT IS NOT CORRECT TO SAY THAT A SPECIFIC CONFORMATIONAL CHANGE PREVENTS EFFICIENT BINDING. ITÂ’S THE OTHER WAY AROUND. A SPECIFIC CONFORMATION IS REQUIRED FOR EFFICIENT BINDING. CHANGE THAT CONFORMATION AND THE EFFICIENCY OF BINDING IS LOST (OR THERE MAY BE NO BINDING AT ALL). THE LOSS OF SPECIFICITY IS A LOSS OF INFORMATION. THE ABOVE STATEMENTS OF MAX SHOW THAT HE DOES NOT UNDERSTAND THE RELATIONSHIP OF SPECIFICITY TO INFORMATION, AND THAT POINT IS PERHAPS THE SOURCE OF MUCH OF HIS DIFFICULTY.]
There are several other ways of considering how mutations affect information. In my view, even if all S12 mutations that caused streptomycin resistance abolished antibiotic binding, a reasonable argument could still be made that such mutations represent a gain of information rather than a loss. In the universe of all the possible S12 amino acid sequences that can function in the ribosome, essentially all S12 proteins found in “wild-type” bacteria (i.e., those grown in the absence of streptomycin) bind to this antibiotic. The S12 sequences that allow bacterial growth in the presence of streptomycin represent a small subset of the universe of functional S12 sequences. Therefore by growing bacteria in streptomycin we select for a specific and small subset of possible S12 sequences; thus it might be argued that we have forced a small increase the information content of the genome by narrowing the choice of S12 sequences.
Spetner: The set of S12 proteins that allow bacterial growth in streptomycin (i.e., that do not bind to the antibiotic) form a disparate subset of the universe of S12 proteins. My intuition tells me that the set that binds (the susceptible set) is smaller, and therefore has a smaller entropy, than the set that does not bind (the resistant set). Mutations that appear in the presence of the antibiotic convert one subset to the other. A mutation that transfers the enzyme from a low-entropy set to a higher-entropy set loses information; it does not gain it.
Max: There are many sequences of S12 proteins in a variety of “wild type” bacteria. Different species of Gram negative bacteria are commonly sensitive to streptomycin despite variations in S12 sequence; organisms with S12 mutations are very rarely found except under streptomycin selection. Therefore, MY intuition tells me that most S12 sequences bind streptomycin and that the set of S12 sequences conferring streptomycin resistance is smaller than the set conferring sensitivity. What supports your “intuition” that the susceptible set is smaller and therefore has smaller entropy?
[LMS: MAXÂ’S INFERENCE THAT LEADS TO HIS INTUITION IS BASED ON A FLAWED ARGUMENT. ONE CANNOT CONCLUDE FROM THE RARITY OF BACTERIA WITH S12 MUTATIONS THAT MOST SEQUENCES LEAD TO BONDING. MOST BACTERIA HAVE THE SAME S12 SEQUENCE. HE IS CONFUSING THE NUMBER OF ORGANISMS WITH THE NUMBER OF POSSIBLE AMINO-ACID SEQUENCDES. MY INTUITION ON THIS POINT IS SO STRONGLY SUPPORTED BY THE NATURE OF MOLECULAR BONDING, THAT I AM AMAZED THAT MAXÂ’S INTUITION TELLS HIM THE OPPOSITE. BEFORE I DESCRIBE THE RELEVANT FEATURES OF THE BONDING OF LARGE MOLECULES, LET ME SAY THAT THE BONDING HAS A SPECIFICITY MUCH LIKE THAT OF A KEY IN A LOCK. THE SET OF KEYS THAT WILL OPEN A PARTICULAR LOCK IS MUCH SMALLER THAN THE SET OF KEYS THAT WILL NOT OPEN IT, AND THEREFORE, THE FORMER SET HAS A LOWER ENTROPY THAN THE LATTER SET. THE KEY-LOCK ANALOGY IS SUPPORTED BY THE FOLLOWING WELL-UNDERSTOOD MECHANISM FOR BONDING BETWEEN LARGE MOLECULES.
NONCOVALENT BONDS, SUCH AS HYDROGEN BONDS, VAN DER WAALS ATTRACTIONS, AND IONIC BONDS ARE MUCH WEAKER THAN COVALENT BONDS, AND IT IS THEY THAT ARE RESPONSIBLE FOR BINDING BETWEEN LARGE MOLECULES SUCH A PROTEINS. IF THE CONFORMATIONAL SHAPES OF TWO MOLECULES DO NOT MATCH WELL, THEN NO MORE THAN A FEW SUCH BONDS CAN FORM BETWEEN THEM. SINCE THESE BONDS ARE WEAK, THE FEW BONDS THAT FORM ARE EASILY BROKEN BY THERMAL MOTION, AND WE SAY THE MOLECULES DO NOT BIND TO EACH OTHER. IF, HOWEVER, THE SHAPES OF TWO MOLECULES CONFORM TO EACH OTHER OVER A LARGE AREA, THEN MANY NONCOVALENT BONDS CAN FORM. THE SUM TOTAL OF THESE MANY BONDS IS STRONG ENOUGH TO RESIST THE DISRUPTING FORCES OF THERMAL MOTION, AND WE SAY THE MOLECULES BIND TO EACH OTHER. SINCE THE SHAPES OF LARGE MOLECULES ARE IRREGULAR, IT IS UNLIKELY THAT THE SHAPES OF TWO MOLECULES CHOSEN AT RANDOM WILL MATCH EACH OTHER OVER A WIDE AREA. THEREFORE, IT IS ELEMENTARY THAT THE NUMBER OF DIFFERENT MOLECULES THAT FORM A GOOD MATCH TO ANY GIVEN MOLECULE IS MUCH SMALLER THAN THE NUMBER THAT FORM A POOR MATCH.]
However, I want to make it clear that I don’t buy your interpretation of certain specific mutations as reflecting a “loss of information.” You state that the “information content of an enzyme is the sum of many parts, among which are: level of catalytic activity, specificity with respect to the substrate, strength [and specificity] of binding to cell structure, [and] specificity of the amino-acid sequence devoted to specifying the enzyme for degradation.” This formulation is vague, non-quantitative, not supported by clear logic, not accepted in the scientific literature (to the best of my knowledge; please educate me if I am wrong), and in my view not useful.
Spetner: Ed, the level of your argument here is quite low. You have seen this entire section (above), and you took from the introduction my list of what characteristics can contribute to the information content of an enzyme and criticized it for being non-quantitative (followed by other pejorative epithets). Is that supposed to be some sort of debating tactic? In any case, the tactic is out of place in this discussion. From the context of what I wrote, it should have been clear to you that this partial list of characteristics that can contribute to the information in an enzyme was an introduction to my quantitative estimate of one of the characteristics of specificity of an enzyme. After I showed how one might calculate the information related to a type of specificity, I showed how a mutation that appeared to enhance activity on a new substrate actually reduced the information by about 50%.
It is elementary that specificity translates into information and vice versa. Have you ever played 20 questions? With the YES/NO answers to 20 judicious questions, one can discover a previously-chosen number between 1 and a million. If the questions are well chosen, those YES/NO answers can be worth one bit of information each, and 20 bits can specify one object out of a million. Twenty bit of information translates to specificity of one part in a million. Ten bits - to one part in a thousand.
The Zip codes in the US also demonstrate that specificity and information are two sides of the same coin and go hand in hand. An address in the United States can be completely specified by the nine-digit zip code. One digit of information will narrow down the address from being anywhere in the United States to being in just a few states. Thus if the first digit is a 6, the address is located somewhere in Illinois, Missouri, Kansas, or Nebraska.
A second digit of information will add specificity by narrowing down the address further. A 3, 4, or 5 in the second digit puts the address in Missouri. A 3 in the second digit puts it in the eastern portion of the state. Two digits of information are more specific than one.
A third digit of information is still more specific, narrowing down the address even more, making it still more specific. If the third digit is a 1, the address is specific to St. Louis and its suburbs. The next two digits of information pin down the address to within a few blocks. The remaining 4 digits of information can locate a specific building. Thus, it is clear that the information contained in the digits of the zip code translate into specificity.
There is no question about it: SPECIFICITY = INFORMATION.
Not only have I made it clear above that my criterion for gain/loss of information is quantitative, and supported by logic and the conventional understanding of these notions in information theory, I included that section in my first critique of your posting. You chose not to relate to it at all, and instead you made up the above criticism out of thin air.
Max: In my previous comments about your calculation of the “information gain or loss in a mutation” I made some criticisms which you called “pejorative epithets” and which you suggested were “some sort of debating tactic” or “made out of thin air"; but you did not address any of the criticisms substantively, so I will repeat them with more detail in hopes that you will address them. 1. I suggested that your formulation is vague and non-quantitative and not supported by clear logic. You have stated:
Spetner: The information content of an enzyme is the sum of many parts, among which are:
Level of catalytic activity
Specificity with respect to the substrate
Strength of binding to cell structure
Specificity of binding to cell structure
Specificity of the amino-acid sequence devoted to specifying the enzyme for degradation