Originally posted by C Hess Natual selection is simply the process whereby organisms with "bad" mutations are weeded out (they can't survive long enough to reproduce), leaving only those mutations that are either neutral or beneficial. The end result will appear designed (for obvious reasons), but it really is not. How is this still a problem for you to understand?
Originally posted by RJHinds How does 'natural selection' REALLY work?
https://www.youtube.com/watch?v=OBDUY2rLt_4
Seriously? This guy claims that bacteria becomes resistent to antibiotics because they lose information. And one example of losing information is when information is added through horisontal gene transfer.
Say what you will about these creationist videos, but they're often good for a laugh. Thank you. 🙂
Originally posted by C Hess Seriously? This guy claims that bacteria becomes resistent to antibiotics because they lose information. And one example of losing information is when information is added through horisontal gene transfer.
Say what you will about these creationist videos, but they're often good for a laugh. Thank you. 🙂
Okay, he did not mention the possibility of horizontal gene transfer as a possible way to gain gene information to become resistant to antibiotics. However, he is correct that resistance to some antibiotics occurred from losing gene information.
Originally posted by RJHinds If a human becomes immune to malaria by getting the mutant sickle cell, did he get it by a gain of information or a loss?
Sickle cell anemia is caused by a substitution mutation in the HBB gene. That means that part of the gene is overwritten with new information. You could say that the gene lost the previous information, but at the same time gained new information. Thus, the answer is: both.
Protection from malaria comes through sickle cell trait though, so that means you carry this mutation from only one of your parents, which in turn means that you don't develop the sickle cell anemia.
Originally posted by C Hess Sickle cell anemia is caused by a substitution mutation in the HBB gene. That means that part of the gene is overwritten with new information. You could say that the gene lost the previous information, but at the same time gained new information. Thus, the answer is: both.
Protection from malaria comes through sickle cell trait though, so that means you ca ...[text shortened]... rom only one of your parents, which in turn means that you don't develop the sickle cell anemia.
Okay, I understand that you can look at it that way. But the new information that was gained is wrong information that replaced the right information that was originally there. Do you agree that it lost the right information originally there which was replaced by wrong information?
So was it the wrong information that replaced the right information that made the person unable to get malaria or was it because of the loss of the right information that made the person unable to get malaria?
Yes, I do understand that they believe that both parents have to have the sickle cell mutation in order to pass on the ability of the child to develop sickle cell disease. But I am referring to malaria in this case. Have the scientists decided which one exactly is the cause of immunity to malaria?
Originally posted by C Hess Let's say that life comprises all of ten organisms. If one of them carries a mutation that prevents it from reproducing, that doesn't mean that all ten of them dies. You do realise that, right?
Yes, that means you now have 10% less going forward. You also realize
that more bad things happen than good when it comes to mutations, and
loosing more than you gain will at some point end it all? You can have 5
good mutations with 20 bad and if one of those bad is bad enough it does
not matter how many good ones you have if they all happen to same
group of organisms.
Originally posted by KellyJay Yes, that means you now have 10% less going forward. You also realize
that more bad things happen than good when it comes to mutations, and
loosing more than you gain will at some point end it all? You can have 5
good mutations with 20 bad and if one of those bad is bad enough it does
not matter how many good ones you have if they all happen to same
group of organisms.
The truth is that mutations are relatively rare. It doesn't happen with every single reproduction, and when it does happen, the most common form of mutation is actually neutral, not bad. Those nine organisms will probably reproduce for generations before the next mutation occur.
Originally posted by RJHinds Okay, I understand that you can look at it that way. But the new information that was gained is wrong information that replaced the right information that was originally there. Do you agree that it lost the right information originally there which was replaced by wrong information?
So was it the wrong information that replaced the right information that ...[text shortened]... n this case. Have the scientists decided which one exactly is the cause of immunity to malaria?
There is no wrong or right information. It's all relative. Because sickle cell anemia is pretty bad, scientists expected this particular mutation to have been weeded out long ago, and in most parts of the world it's rare. The reason it's still fairly common in parts of the world where malaria is common, is because it's actually a beneficial gene in those parts, so it gets naturally selected for. All is relative.
Mind you, this mutated version of the HBB gene can't be completely selected for, because if everyone carried it, everyone would have sickle cell anemia, instead of just the sickle cell trait.
Originally posted by KazetNagorra How are you quantifying "information" in this context?
I was referring to "information" in the context of copying errors when DNA replicates or is transcribed into RNA.
The following reference describes what happens if the code in DNA becomes changed in some way, and the effect that would have on the proteins it codes for:
Copying errors when DNA replicates or is transcribed into RNA can cause changes in the sequence of bases which makes up the genetic code.
Changes to individual bases
Remember that a set of three bases in a gene in DNA codes for a particular amino acid.
A gene will be made up of a string of these codes rather like a string of 3-letter words in a sentence. We'll use that as a simple analogy. Take the sentence:
the big fox bit the dog but not the boy
Suppose one letter got changed in this by accident. Suppose, for example, the "d" in dog got replaced by a "p". The sentence would now read:
the big fox bit the pog but not the boy
Clearly this doesn't make complete sense any more. Would that matter if the same thing happened in a gene? It depends!
If you look back at the table, there are several amino acids which are coded for by more than one base combination. For example, glycine (Gly) is coded for by GGT, GGC, GGA and GGG. It doesn't matter what the last base is - you would get glycine whatever base followed the initial GG.
That means that a mutation at the end of a codon like this wouldn't make any difference to the protein chain which would eventually form. These are known as silent mutations.
Alternatively, of course, you could well get a code for a different amino acid or even a stop codon.
If a stop codon was produced in the middle of the gene, then the protein formed would be too short, and almost certainly wouldn't function properly.
If a different amino acid was produced, how much it mattered would depend on whereabouts it was in the protein chain. If it was near the active site of an enzyme, for example, it might stop the enzyme from working entirely.
On the other hand, if it was on the outside of an enzyme, and didn't affect the way the protein chain folded, it might not matter at all.
Inserting or deleting bases
The situation is more dramatic if extra bases are inserted into the code, or some bases are deleted from the code. Using our example sentence from above, and keeping the three letter word structure:
If you insert a single extra base:
the big fro xbi tth edo gbu tno tth ebo y
An extra "r" is inserted in "fox". If the sentence still has to be read three letters at a time (as in DNA), everything from then on becomes completely meaningless.
If you delete a single base:
the big fxb itt hed ogb utn ott heb oy
This time the "o" in "fox" has been deleted. And again, because we have to read the letters in groups of three, the rest of the sentence becomes completely wrecked.
So does this matter? Well, of course it does! Large chunks of the protein will consist of completely wrong amino acid residues.
We've looked so far at inserting or deleting one base. What if you do it for more than one?
The effect is the same unless you add or delete multiples of three bases - without changing any other codons. If you added an extra three bases between two existing codons, then essentially you are just adding an extra word.
the big fox bit the xjy dog but not the boy
That extra word represents an extra codon in the DNA, and so an extra amino acid residue in the protein chain. Does this matter? It depends where it is in the chain (Is it important to the active site of an enzyme, for example?), and whether it affects the folding of the chain.
What if the three bases were inserted so that they broke up an existing codon? Here is the same extra "word", "xjy", dropped in the word "bit". Everything is then reshuffled into groups of three letters.
the big fox bxj yit the dog but not the boy
You can see that the effect is again fairly limited. It will change one codon completely, and introduce an extra codon. That would give you one different amino acid and one extra amino acid in the chain. Again, how much that would affect the final protein depends on where it happens in the chain.
Deleting a whole codon again leaves most of the protein chain unchanged. Again, whether the function of the protein is affected depends on where the missing amino acid should have been and how critical it was to the way the protein folded.
Sickle cell anaemia (US: anemia)
This is so called because red blood cells change their shape from the normal flexible doughnut shape to a much more rigid sickle shape - rather like a crescent moon.
It results from the change of a single base in a gene responsible for making one of the protein chains which makes up haemoglobin (US: hemoglobin).
The affected part of the gene should read:
...C T G A C T C C T G A G G A G A A G T C T...
....Leu ...Thr ...Pro ...Glu ...Glu ...Lys ...Ser ....
What it actually reads in someone suffering from sickle cell anaemia is:
...C T G A C T C C T G T G G A G A A G T C T...
....Leu ...Thr ...Pro ...Val ...Glu ...Lys ...Ser ....
The effect of this single change is to make the haemoglobin temporarily polymerise to make fibres after it has released the oxygen that it carries around the body. This changes the shape of the red blood cells so that they don't flow so easily - it makes them sticky, especially in small blood vessels. This can cause pain and lead to organ damage.
Originally posted by C Hess The truth is that mutations are relatively rare. It doesn't happen with every single reproduction, and when it does happen, the most common form of mutation is actually neutral, not bad. Those nine organisms will probably reproduce for generations before the next mutation occur.
Yet you still think that one random mutation will build upon an old one to
produce something as complex as a nervous system over time.
Originally posted by C Hess There is no wrong or right information. It's all relative. Because sickle cell anemia is pretty bad, scientists expected this particular mutation to have been weeded out long ago, and in most parts of the world it's rare. The reason it's still fairly common in parts of the world where malaria is common, is because it's actually a beneficial gene in those part ...[text shortened]... ryone carried it, everyone would have sickle cell anemia, instead of just the sickle cell trait.
We look at this from opposite viewpoints. I believe what God made was right and thus a mutation error to that original would be wrong. Try to look at it from my point of view to understand what I am saying and then answer the questions, please.
Originally posted by C Hess Protection from malaria comes through sickle cell trait though, so that means you carry this mutation from only one of your parents, which in turn means that you don't develop the sickle cell anemia.
To be more specific, sickle cell anemia changes the gene that encodes hemoglobin, changing one of the amino acids in such a way that the hemoglobin proteins clump together into rod-like structures. If there are some non-clumping hemoglobins and some clumping hemoglobins then the result is short rod like structures that protect against malaria. If all the hemoglobins are the clumping form, then the result is long rod-like structures that causes sickle shaped cells that cause problems.
I have a mutation called MTFHR c677t which I believe also provides some malaria prevention, but is less harmful than sickle cell anemia in the homozygous form (which I am). It does have some bad side effects and some good side effects. It is a change of exactly one base pair in the DNA from a C to a T.
14 Jan '15 17:34
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