Uniformitarianism

[IRQ Conflict]

This statement is misleading, your second source cleary shows this is not the case. Loss of information here is from the perspective of the antibiotic, but why take this perspective?

I didn't read it as being from the perspective of the antibiotic. Where do we see that?

But even without the second source why call it a defect to a trasport mechanism? Does the mechanism exist to transport a substance which is lethal to the bacteria? How can this be so?

I'm not a biologist or a doctor, but I would surmise the transport mechanism is there as a function of the bacteria in general and drugs that are created by man try to exploit this in order to kill the bacteria. Sort of like throwing a grenade on a conveyor belt to take it to the next room where you know the enemy is.

However were we not specifically talking about MRSA bacteria?

Yes, the site I linked to was discussing bacteria in general. Not excluding staff.

In this case resistance is due to a change in the protein which the antibiotic binds to. This isn't a loss of information. It's like changing the locks on your front door.

If you read further down the page it states:

Exposure to antibiotics doesn't cause bacteria to become drug resistant. The above changes in the bacterium that enable it to resist the antibiotic occur naturally as a result of mutation (def) or as a result of genetic recombination (def). Exposure to the antibiotic selects for strains of the organism that have become resistant through these natural processes.

To further this, I looked into the mutation (loss of information) of the MRSA bacteria:

A nucleotide substitution at position 202 (M3) in mecI was detected in three strains (SH15, SH19651, and SH212) which had exhibited mecI RFLP pattern 2. Other base substitutions, M1 in strain SH20 and M2 in strain SH22, generated an amino acid change and a new termination codon, respectively. [he deletion of 28 bases (M5) near the 5' end of the mecI gene was found in MRSA strain SH13, which had shown mecI RFLP pattern 3. This base deletion, shown in Fig. 2A, caused a premature termination at position 33 on the mecI gene.

link


I think I allah akbared this thread, sorry

[BGoodForGoodSake]

This statement is misleading, your second source cleary shows this is not the case. Loss of information here is from the perspective of the antibiotic, but why take this perspective?

I didn't read it as being from the perspective of the antibiotic. Where do we see that?

Well without this perspective how can we call all mutations(not just deletions) loss of information? As the only function lost in most cases is the succeptibility of the bacteria to the drug.

But even without the second source why call it a defect to a trasport mechanism? Does the mechanism exist to transport a substance which is lethal to the bacteria? How can this be so?

I'm not a biologist or a doctor, but I would surmise the transport mechanism is there as a function of the bacteria in general and drugs that are created by man try to exploit this in order to kill the bacteria. Sort of like throwing a grenade on a conveyor belt to take it to the next room where you know the enemy is.

The drugs work because they bind to receptors located in the bacteria's membrane. Change the receptors and the drugs no longer work. It's not a simple conveyer belt. Viruses invade human cells by a similar mechanism. Antibodies also work in a similar manor.

However were we not specifically talking about MRSA bacteria?

Yes, the site I linked to was discussing bacteria in general. Not excluding staff.

In this case resistance is due to a change in the protein which the antibiotic binds to. This isn't a loss of information. It's like changing the locks on your front door.

If you read further down the page it states:

Exposure to antibiotics doesn't cause bacteria to become drug resistant. The above changes in the bacterium that enable it to resist the antibiotic occur naturally as a result of mutation (def) or as a result of genetic recombination (def). Exposure to the antibiotic selects for strains of the organism that have become resistant through these natural processes.

To further this, I looked into the mutation (loss of information) of the MRSA bacteria:

A nucleotide substitution at position 202 (M3) in mecI was detected in three strains (SH15, SH19651, and SH212) which had exhibited mecI RFLP pattern 2. Other base substitutions, M1 in strain SH20 and M2 in strain SH22, generated an amino acid change and a new termination codon, respectively. [he deletion of 28 bases (M5) near the 5' end of the mecI gene was found in MRSA strain SH13, which had shown mecI RFLP pattern 3. This base deletion, shown in Fig. 2A, caused a premature termination at position 33 on the mecI gene.

link

So you ignore the gene substitutions on most of the cases and focus on the one strain which owes its resistance to deletion?

What about SH15?
What about SH19651?
What about SH212?
What about SH20?
What about SH22?

[IRQ Conflict]

This statement is misleading, your second source cleary shows this is not the case. Loss of information here is from the perspective of the antibiotic, but why take this perspective?

I didn't read it as being from the perspective of the antibiotic. Where do we see that?

Well without this perspective how can we call all mutations(not just deletions) loss of information? As the only function lost in most cases is the succeptibility of the bacteria to the drug.

Seems to me your trying to muddy the water and confuse the issue here.

The drugs work because they bind to receptors located in the bacteria's membrane. Change the receptors and the drugs no longer work. It's not a simple conveyer belt. Viruses invade human cells by a similar mechanism. Antibodies also work in a similar manor.

The analogy still works. As would a myriad of others.

So you ignore the gene substitutions on most of the cases and focus on the one strain which owes its resistance to deletion?

The reason I focused on SH13 (strain) M5 (Mutation) was the obvious fact that it's mutation caused the deletion (loss of information) of 28 bases that ultimatley resulted in " a premature termination at position 33 on the mecI gene." This is what is known as a "
Nonsense mutation" which is the cause of cystic fibrosis.

What about SH15?
What about SH19651?
What about SH212?
What about SH20?
What about SH22?

These strains showed no loss of information that I could see, so why would I include them in my example? My goal is simply to show that genetic mutation can and does lead to information loss, to what degree I am unaware but I will continue to study this more.