To summarize, here is what Hallet and Maxwell did:
Acquired a colony of bacteria with known genotype for the gyrA gene. This bacterium is known to be susceptible to the antibacterial quinolone
Induced random misrepair mutations in the gyrA gene
Applied quinolone to the colony
Discovered that some of the bacteria were not killed by the quinolone
Sequenced the gyrA gene of some of the bacteria that survived the quinolone
Discovered that one resistant bacterium had a gyrA genotype that was different from the original colony’s genotype (where the original genotype’s 317th nucleotide was an A, the resistant genotype’s 317th nucleotide was a G)
Discovered that the gyrase protein produced by the mutant allele was also different from the original protein of the colony
Isolated the gyrase protein that was produced by the mutant gyrA allele
Tested the function of this mutant protein under varying levels of quinolone
Discovered that the mutant protein could tolerate 10 times more quinolone than the original protein, and still function properly
They showed that random mutation created a new allele (i.e., added information that did not previously exist), that the new allele produced a novel protein, and that the novel protein outperformed the original protein. Thus, the mutant bacteria were selected for by the quinolone regime.
There is no other way to explain this data other than with a beneficial, information-adding, random mutation.
Thus, by your definition, Hallet and Maxwell demonstrated the reality of macroevolution (along with the reality of beneficial mutations).
I love when evolutionists point to antibiotic resistance as evidence of evolutionary change.
So do I.
However, bacteria acquire this information through plasmids, from a process called horizontal gene transfer.
Not in this case, they didn’t. The genetic information for quinolone resistance did not exist in this colony prior to this experiment. This was verified by genetic sequencing and by the fact that the founders of the colony were killed by quinolone.
Thus, there was nowhere from which this information could have been horizontally transferred.
Furthermore, the change in information content was exactly one base pair. Evoking HGT to explain a one-base-pair difference is overkill.
Thus, HGT is an absurdly poor explanation for what these researchers observed.
Mutations can potentially account for the origin of antibiotic resistance, but involve mutational processes that are contrary to evolution. These mutations usually eliminate transport genes, and regulatory control systems.
This may be true in some cases, but, in Hallett and Maxwell 1991, the mutation did not affect any transport genes or regulatory genes in any way: the mutation only affected the final protein product.
Here is a link to the abstract of the Hallett and Maxwell 1991 article again: I think you need a subscription (or an institution that has a subscription) to the journal Antimicrobial Agents and Chemotherapy to view the full text, though. If you can get access (e.g. from a local university), I recommend you read it.
Please tell us how to measure the complexity of an organism.
I believe Dennis answered this question, back in Message 196:
The length and diversity of amino acid sequences in nucleotides that provide the instructions for the production of protiens and instructions for the size, shape, and (inter)function of complex systems that are found in complex organisms and unique to specific species. This complexity is explained by the large amount of information found in DNA sequences. If you need further clarification, google it.
And, in Message 133, I believe he settled on the teaspoon as his unit of measure.
So, if we start with the premises that...
Amino acid sequences provide instructions for the production of proteins and complex systems of organisms.
The length and diversity of amino acid sequences is a surrogate measure for the complexity of an organism.
The length and diversity of amino acid sequences can be measured in either nucleotides or teaspoons.
...I don’t think it surprises anybody that Intelligent Design is the conclusion.
Please tell us how to measure the complexity of an organism.
I did, twice now. If you can't use the previous explanations to figure out why you are more complex than a single celled organism (though this is debatable as well in your case), then perhaps this is not the right forum for you. I really don't know how to explain it any better than that (or better than my quoted scientist).
You have a lot to learn about both science and interpersonal communication, son.
Your previous explanations for how you measure information or complexity of DNA were:
"In teaspoons? I didn't know I was allowed to invent a measuring system. I like teaspoons.
This depends on what you are asking. Humans have some 3 billion base pairs, and that are arranged into 24 distinct chomosomes, that arrange molecules ranging from 50 to 250 MBP (that would be million base pairs...I shortened it)." Message 133
(a non-answer, or, at best, an indirect, unclear answer)
"I already told you in my previous message. In base pairs, chromosomes, and teaspoons." Message 140
(a very problematic answer, because I’m pretty sure the organism with the most base-pairs---and thus, consequently, the most information and complexity---is either an amoeba or a flowering plant)
"...mentioned above. Loss mutations are found in the hundreds, that result in a non-functional genetic sequence, protein, or structure." Message 161
"My secret for measuring information is genetic complexity." Message 193
(a new, equally-ambiguous buzzword to use in place of “information”)
“The length and diversity of amino acid sequences in nucleotides that provide the instructions for the production of protiens and instructions for the size, shape, and (inter)function of complex systems that are found in complex organisms and unique to specific species. This complexity is explained by the large amount of information found in DNA sequences. If you need further clarification, google it.” Message 196
(complete nonsense: amino acid sequences don’t have nucleotides in them, and don’t provide instructions for making proteins---rather, they kind of are proteins)
So, there are three possibilites:
You didn’t really answer the question.
You answered the question, but your answer was nonsensical.
You answered the question, but your answer doesn’t support the conclusions you want to make.
This is not very promising for you, I’m afraid.
Edited by Bluejay, : entered the word "how" where it should have been.
Edited by Bluejay, : Formatting and links for quotes
Edited by Bluejay, : "and thus, consequently, the most information and complexity"
I have no idea who you are, but you have offered no scientific opinion whatsoever.
Well, I won’t deny that. Science is based on a foundation of logic. As such, science can’t happen until the logic is taken care of, and the logic here clearly has not yet been taken care of.
So, let me try my best to point out why nobody likes your answers about measuring genetic information:
If you believe that genetic information or genetic complexity is measured in nucleotides, then am I to understand that the organism with the largest genome (i.e. the most nucleotides) is the most complex, or has the most information?
This is the implication of using nucleotides as metric.
The problem I see immediately is that this does not jive well with your comments in Message 219:
So, you are saying that if random letters are changed in a book to any random letters, eventually, you will have a completely new book with a coherant message?
In this comment, you emphasize the importance of “message coherence.” So, I assume from this that you think message coherence is somehow important to understanding mutation, genetic complexity and genetic information. (Feel free to correct me if I’ve made a bad assumption here).
Now, I can’t imagine how one might use nucleotides (or chromosomes or teaspoons) to measure “message coherence.” So, from my point of view, your argument doesn’t seem to be enjoying much internal consistency. I suggest that it is because you haven’t actually formed a coherent idea about what “information” is, nor about how it relates to genetics, mutation or macroevolution.
Furthermore, there’s this statement from the same message:
Dr Adequate writes:
Does the gain of a plasmid constitute a "genetic loss" --- or a genetic gain?
Genetic gain. Continue.
You have affirmed the existence of HGT, and have now affirmed that it is a genetic gain.
Genetic gain is an increase in information, as measured in nucleotides, and thus, by your definition, is an example of macroevolution.
Yet, you say that it is not macroevolution.
This tells me that you haven’t actually formed a coherent idea about what macroevolution is either, nor about how it relates to genetics, information or mutation.
I hope this at least gives you an idea of why everybody has given you so much pressure over this.
Actually, it’s a “Free for All” thread, even though we’ve been treating it like a science thread: that’s why nobody is stepping in to stop us from mocking each other so blatantly. In a real science thread, we’d have had moderators stepping in telling us to cool it down, and maybe suspending a few of us, by now.
But, I’m confused as to why you think my arguments are just opinions about your beliefs. All I have done is present pretty good evidence that your argument is not internally consistent, which is more than enough to topple it on logical or scientific grounds. Your only response so far has been to get annoyed with me and accuse me of being confrontational.
I really don’t like offending or irritating people. So, what, exactly, can I do that you won’t take as a personal insult?
The doc and I are on this because I quoted a scientist earlier on that compared the information found in DNA to be different from that of specific chemical arrangements, much like the words in a book. If you want to jump into our posts, I'm diggity, but read back a bit so you are up to speed on whats going on.
I have kept up with your and Dr A’s discussion up until this point quite well, Dennis. And, my point still stands.
With Dr A, you argue that there is some importance to the arrangement of letters and “coherence” of a message in determining its information content.
Then, you get upset with me and accuse me of not keeping up with the discussion when I say that you argue that there is some importance to the arrangement of letters and “coherence” of a message in determining its information content.
What the hell?
Do you, or do you not, think that the arrangement of nucleotides is part of the definition of “genetic information”? Your argumentation so far suggests that you do think this is the case, but you only ever seem to get upset when I ask you about it, and I'm left trying to put together the indirect clues that you're leaving behind in your responses to me and to others on this thread.
If you do include arrangement of nucleotides in your definition of "information," how do you measure the arrangement, and how do you determine whether or not a particular arrangement contains more information than another particular arrangement? Surely not by nucleotides or teaspoons?
Although I am not convinced the entire spectrum of organic life came from antibiotic resistance (HGT), it is still a valid point. Mooving on.
There have been at least two or three examples of bacteria evolving antibiotic resistance given in this thread. At least two of them cannot be credibly explained by HGT. In fact, I already made this point in Message 167, but you have not yet responded to it. I assume it just got lost in the swarm, which is understandable and not really offensive to me. Even so, I would still like you to account for this before you continue to assert and/or imply that HGT is how it all went down, as you have been doing.
My example (Hallett and Maxwell 1991) was demonstrated to be a random point mutation (an “A” replaced with a “G”), and not an HGT event. It was a random change in nucleotide arrangement that had an advantageous (and no apparent deleterious) effect on the bacteria’s fitness.
So, this is why I’m asking you whether or not the arrangement of nucleotides in the DNA is part of “genetic information.”
If it is, I have just shown you an increase in genetic information, and, consequently, macroevolution by means of random mutation, and have thus just defeated your argument here.
Your message had no evidences to refute mine, just opinions. How do you expect me to respond to an opinion?
By either demonstrating that my opinion is inaccurate or by agreeing with it. That’s what debate is, Dennis.
But, I’m somewhat perturbed by your characterization of my posts. As far as I can tell, I presented a paper in my first post that contained strong evidence for mutation as the source of new genetic information (Hallett and Maxwell 1991*), and no real evidence has been presented by either one of us since then.
* Note: this links to the abstract; you may need a subscription to see the full text
That paper is my evidence that refutes your argument. You can check out my arguments and explanations associated with that paper in Message 139 and Message 167.
think that the arrangement of nucleotides is part of the definition of “genetic information”?
...I'm not a geneticist, so I would not know how it is measured. I do know that only specific nucleotide arrangements and codons produce useful information.
Excellent. I’m not a geneticist either, so let’s see if we can do it without actually having to measure information content or usefulness.
Let’s just work with a strict all-or-nothing dichotomy: let’s assume that information content is either 1 (has useful information) or 0 (has no useful information), with no possible in-between values.
What we need now is a way to tell which specific nucleotide arrangements produce useful information, and which don’t. Once we can do that, we can then proceed to determine whether those information-containing sequences can come about by random mutation.
However, I don’t think there is a way to tell whether or not a given DNA sequence contains any useful information. The only way to tell would be context-specific (i.e. how the given sequence interacts with the other molecules that are involved in realizing its function), which really isn’t all that helpful.
Lane is pretty clear that natural selection was not involved.
He's really not. He's contrasting the rapidness of the symbiotic emergence of eukaryotes with the typical gradualness of other evolutionary events. That he used "natural selection" in his description of one of the two options he was comparing is not indicative of his excluding it from the other option.
Here's the quote again:
quote:The transition to complex life on Earth was a unique event that hinged on a bioenergetic jump afforded by spatially combinatorial relations between two cells and two genomes (endosymbiosis), rather than natural selection acting on mutations accumulated gradually among physically isolated prokaryotic individuals.
The first of the two options he is comparing is endosymbiosis. The second option contains three parts: (1) natural selection; (2) acting on mutations; and (3) accumulated gradually. Your interpretation of it acts like the first part (natural selection) is the only part of the option.
In reality, the options are:
Natural selection acting on symbiotic relationships that happen rapidly.
Natural selection acting on mutations that accumulate gradually.
Do you see how this is a more appropriate interpretation of what Lane and Martin said?
I am not saying that NS was not involved after the jump from prokaryote to eukaroyte, or that NS & mutation were not involved in prokaryote prior to the jump. But the jump per Lane & Martin was a "unique event", that did not rely on NS.
I see what you're getting at.
The trouble is that mutations also create a kind of "jump" that doesn't involve NS; and NS only gets involved after those little mutational "jumps" too.
This goes back to Granny's original explanation: Lane & Martin's comment suggests that, what happened in the "jump" from prokaryote to eukaryote is "symbiosis + natural selection" rather than "mutation + natural selection." This is what makes them call it a "unique event": symbiosis is less common than mutation as a mechanism of evolution.
Because it allows the ecological and/or physiological networking of entire independent genomes into a single, collaborative unit, symbiosis can be thought of as adding several useful, new traits or alleles at the same time. This makes it "bigger" than more typical mutations.
And, the endosymbiotic origin of organelles almost certainly didn't happen in a single, giant "jump": for example, there are many kinds of eukaryotic cells alive today that absorb prokaryotes by phagocytosis, then, for whatever reason, fail to digest them, and simply let the prokaryotes live, grow and reproduce inside them, creating a co-habitation relationship that is midway between separate organisms and fully-symbiotic organisms.
Some papers I have been reading are leaning toward the hypothesis that Macro evolution, or the transition to complex entities, does not rely on NS and mutation, but on genetic information engineering processes and are almost instant in nature compared to the gradualness of micro evolution.
There are so many usages of the term "macro-evolution" that I groan every time I hear someone use the word. "Transition to complex entities" is not a description I've ever heard for it before, though.
There does seem to be a fad of finding new mechanisms for evolution these days. I'm not sure what drives people to think evolution needs new mechanisms, but I figure I'll just let them have their fun and assume that it must be contributing something of value to science (otherwise why would they be doing it?).
At any rate, don't get hung up on "macro-evolution": none of the definitions that people give it are really that meaningful in the long run.
Way to put me on the spot, man!. I don't know anything else: I just have some lecture notes from an undergraduate plant diversity course that don't say anything more than what I already wrote, and memory of a couple slides the professor showed.
Now I understand what happened. I had heard this Rickettsia/mitochondria story before, and I got the details of it confused with the details of a Cyanobacteria/chloroplast example from my plant diversity course. In the Cyanobacteria/chloroplast example, the eukaryote (which did not lack mitochondria) engulfed the bacterium, but took a long time before getting around to digesting it within the vacuole. This gave the bacterium enough time to photosynthesize and reproduce inside the host cell. It became a mutualism, because, while the bacterium is protected from predators, the host cell is able to uptake excess photosynthate from the bacterium.
I still don't have a taxon name for the organism, nor any more details than this, such as, how the bacterium gets minerals (which it can't photosynthesize). I suspect that, since the vacuole is used to eject waste products after the prey is consumed, it may double as a waste reservoir, and may thus have waste products from the host cell from which to extract minerals.