Mexican blind cavefish (Astyanax mexicanus)

I don’t really start threads as a rule and do not want to start another. General question. Do brainless organisms like sponges and jellyfish show mutations in their genomes?

That’s the link I provided above. The counter shows you didn’t open that link. How did you find it since you didn’t get it from me?

Why not just admit you didn’t read the paper?

Yes, clearly.

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New mutations in brainless bacteria have been observed and mapped for decades now. Mutation rates in species like sponges and jellyfish are probably going to be derived from phylogenetic methods instead of in real time, but those papers do exist.

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That seems to be due to disease.

How in the world did you get that from the paper?

Fossils?

What possible reason would the complexities of cellular life (depurination, indels, polymerase errors, chromosomal inversions/deletions/duplications, etc) affect all animals except sponges and jellyfish?

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What specifically is the word “that” in your response referring to? Are you suggesting that all observed genetic variation in sponges and cndiarians is caused by disease? Even if that were true (it isn’t!), they would still be mutations.

That is one method of doing it:

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Unwarranted assumption. He may not have got it from the paper. He may have contracted measles.

Even so, looking at “DNA methylation” and “genes encoded by DNA” and “mutations to those genes” is to deal with the effect and not the cause. Clearly, the causes leading to this blind fish’s phenotype are 1. Its dark environment, and 2. The diminished function in the visual sensory area of its brain.

That is I believe the indisputable reason why the species mutated in the first place – no matter how many generations were involved and no matter how it played out at the genetic molecular level.

Understand I am not arguing for or against your or the paper’s theories. I am simply saying you are looking at the effect and not the cause.

Congratulations. You’ve rediscovered Lamarckism, an idea science examined and rejected over 200 years ago.

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How are those clearly the causes? You need some mechanisms and evidence.

Also, why don’t these fish grow eyes when they are in an environment with light?

I would suggest that you look at a simple experiment involving bacteria and antibiotics done by Joshua and Ester Lederberg back in the 1950’s. They started with a single bacterium, and grew a population of bacteria from that single founding bacteria. They let the bacteria grow in a heavy lawn in a petri dish, and then they used a felt applicator to stamp the bacteria on other plates, just as you would with a rubber stamp and an ink pad. The plates they stamped the bacteria on had antibiotics in them. What they found is that they got a few bacteria that were resistant to antibiotics. More importantly, the resistant colonies of bacteria were found at the same position on each of the stamped plates. This meant the resistant bacteria came from the same spot in the lawn of bacteria.

What this tells us is that the resistant bacteria already acquired the mutation for antibiotic resistance before they were exposed to antibiotics. Exposure to antibiotics didn’t cause the mutations. Mutations are independent of the needs of the organism. It is experiments like this one which led scientists to conclude that mutations are not guided in a teleological fashion like you are describing.

You can read the paper here:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC169282/

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I agree the resistance was there but how do you know it was due to mutation?

Further, help me to understand why this study is remarkable? By the 1950’s it was well-documented that bacteria were developing resistant strains to antibiotics. So I think this next statement could very well be unfounded:

How do you know that? Contrary to what you are claiming, how do you know that ancestors to these bacteria were not exposed to antibiotics many or several generations earlier in another host?

This experiment does not bear that out.

The point of the study was to investigate the order of events that lead to antibiotic resistance, no one’s suggesting it was the first study to identify resistance. The study tested whether exposure to antibiotics caused mutations that led to resistance, or whether randomly-occurring resistance mutations were merely selected for in antibiotic-containing environments. It demonstrated that the latter was true.

Sure, some distant ancestor of the bacteria probably encountered some natural antibiotics, but the point is that the ancestral culture that the bacteria in the experiment descended from was not resistant to antibiotics. The study demonstrated that in these bacteria, resistance arose randomly, independent of the presence or absence of antibiotics in their environment.

Yes it did, because it demonstrated that resistance mutations occurred in the absence of antibiotics. If mutations were influenced by the needs of the organism, we’d expect to see bacteria in the presence of antibiotics experiencing resistance-causing mutations at a higher rate, but we don’t.

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First you said

Then you said

How did you not just contradict yourself?

I’m not sure the system counts clicks from the person who posted the link.

Very easily. The experiment enabled the researchers to pinpoint precisely when the resistance mutations in the experimental bacteria occurred, and it was in the absence of antibiotics (i.e. when the bacteria were being cultured in media without antibiotics). Whether the ancestors encountered antibiotics or not is irrelevant to this fact.

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More evidence that @r_speir didn’t read the paper.

He clearly doesn’t know what replica plating is, or why one might do it.