Introducing Geremy (and Behe)

Hey, why don’t we proceed to look at a large collection of genetic data from most living primates instead of just chimps and humans? That could be informative.

For example, there’s this:

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Looking at the reference, I see what it was supposed to mean: there has been no introgression from other ape lineages into the human lineage for several million years. That isn’t surprising. Again, whatever did you think it meant?

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This is supposed to be your introductory thread @Geremy, so welcome to PS. From the little exchange we had and you with others, I deduced you are fond of citing papers you don’t understand or you just misrepresent what the authors say. That’s not a good practice. You are dealing with budding and veteran scientists on PS, you will get called on it if that continues. Welcome once more :+1:

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CrisperCas after reading the other paper with a larger mtDNA sample size(although I hate to see non coding DNA ignored) than Huang used, I have no problem accepting that point as falsified, so thanks for the link.

I don’t think that your assessment of the coding sections of coding Y chromosome comparison between humans and the great apes. Additionally, I have linked a paper that provides evidence that the large human specific non coding region of the Y chromosome interacts with chromosome 1 to regulate testicular protein synthesis, making it very divergent from both chimpanzees and all of the great apes. Here’s the link:
https://genome.cshlp.org/content/17/4/433.full

I am also very aware of both the genetic similarities between humans and chimpanzees and the average of 25% difference in how those genes are transcribed during the first days of after conception as you can read about here:

I would love see evidence that one could either gradually or suddenly create such a difference in gene transcription (independent of the hypothesis of common descent) using known evolutionary mechanisms without the evolutionary pathway result in the dead end such as miscarriage etc.

I would love to see you explain what your alternative proposal would be. Why are you unwilling to submit your ideas to examination?

And gradual changes in transcription rate are fairly easy to accomplish by slight mutations in transcription factor binding sites. Probably in other ways too.

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Indeed. In addition to @John_Harshman’s reply, I would add this off-the-top-of-my-head list of ways to alter overall mRNA levels (which is probably what @Geremy means by “gene transcription”) via very modest changes (often no more than one base):

Changing the stabilities of the mRNAs, by slightly changing motifs recognized by RNA binding proteins that mediate turnover.

Changing the stabilities of the mRNAs, by slightly changing motifs that are targeted by small RNAs (microRNAs).

The origination of new microRNAs (as explained nicely by @NLENTS).

Changing the concentrations of one or more transcription factors (or other regulatory proteins), by changing their rates of synthesis or turnover. (Mechanisms alluded to above apply here as well.)

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I’m not sure why you include that last condition. It amounts to saying you want to see how evolution would accomplish this task if it did not include negative selection. Which is obviously unrealistic.

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As a mouse molecular geneticist in the late 1980s-early 1990s, it was obvious from my own work and talking with others that there is an enormous amount of unnecessary transcription–in fact, it is what we would expect from neutral and Darwinian mechanisms, primarily the former.

For the reasons others have pointed out, I think that global changes in transcription are far more likely than specific ones.

You seem to be speculating with little or no knowledge of the complexity of the regulation (or lack thereof) of transcription.

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Off to a bad start, aren’t we?

Then you should refer to their supplement which includes a tree with essentially identical topology produced from full-length mtDNA. Or the tree I also included, which used full-length mtDNA sequences.

This is just confused. The analysis was for full sequences, with sequence identity higher between humans and chimpanzees than between either and gorilla. If anything, you’ve got the conclusion precisely reversed! The gene loss in chimpanzees means that there are several coding regions shared by humans and gorillas not found in chimpanzees, but this is more consistent with large deletions than anything else.

In the future, you should actually make sure the paper says the thing you claim it says, or you have independently confirmed the claim. Because I ran BLAST on the sequence and got hits on Pan Ychr.

So… yeah.

You realize they had to exclude a bunch of genes because there was differential regulation within species, right? So that’s already evidence enough. You can, and do, see differential regulation. If the cause of the differences is something that can get fixed, and it does, then you’ll have differential regulation between descendant populations.

No clue what you were trying to say with this. Try again.

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We have those mutations, and we are doing just fine.

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The gene loss in chimpanzees means that there are several coding regions shared by humans and gorillas not found in chimpanzees, but this is more consistent with large deletions than anything else.

To me this speculation it is possible that there has been gene loss in chimpanzees it’s possible there hasn’t been. This why I think the way population genetics is used makes molecular evolution unfalsifiable, because one can invoke any number of speculative scenarios required to make even contrary data fit. I know that population genetics was invented to study the characteristics of infer fertile populations, applying it to species with no gene flow sort of makes it a theory of everything in biology, just one that can’t be independently tested.

I have to learn how to use BLAST myself, I had actually looked up an interview with the woman who originally made the discovery, which claimed the sequence was unique to humans, I think they framed her statement in a way that isn’t correct:

You can do that with any explanation. It is not possible to come up with some explanation for a set of observations, which when contradicted by some other observation, you can’t then just invent some new ad-hoc hypothesis to explain away.

All we can over hope to do is compare the relative fit of different explanatory models to the data we currently have. Yes, it is strictly speaking always possible to invoke some obscure combination of phenomena to explain away data that appears not to fit your model, but in that case you complicate your model. Thus science also includes a preference for simpler hypotheses-heuristic, commonly referred to as Occam’s razor.

The goal is to try to explain as much as the data as possible, with as simple a predictive model as you can come up with. The key word there is predictive. The models should lead you to have expectations of the data. It is not enough to just account for the data after the fact with piles of rationalizations.

That’s why evolution, while a somewhat complicated model, is a scientific theory, as it does actually lead to having expectations of the data(consilience of independent phylogenies).

That’s also why “design” isn’t a scientific theory, as it predicts nothing, and only accounts for the data in ad-hoc fashion “Oh so this is what we find? Well that’s just what the designer wanted”. That’s why evolution is in principle falsifiable, as it really can fail to fit the data, and why design is intrinsicically unfalsifiable, as anything you see could have been what some obscure designer wanted to design for it’s own inscrutable reasons of will and whim.

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No I’m pretty sure you wouldn’t love to see genetic experiments on human embryos to try to recreate stages in our evolutionary past.

The evidence we have now is the best we can hope for without time machines and embryonic experimentation. Comparative evidence between individuals, and between species, shows how our evolution occurred.

If you want more specific evidence of how the molecular biology of transcription regulation evolves, there’s articles such as this:

https://www.nature.com/articles/nature23902

In these papers they show how transcription factor proteins evolve and change their regulatory properties over time, mutation by mutation. They further go on to show, in the last paper, how the historical outcome of transcription factor evolution is not a rare miraculous occurrence, but just one among many possible evolutionary trajectories that could just as easily have happened.

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That’s an understatement. They fall into the standard misunderstanding of what “junk DNA” means by equating it with non-protein-coding DNA. But her statement is still problematic. Her intuition told her that functionless DNA couldn’t exist, so she set out to prove it. That’s a bad approach to science. Then she found a couple of small segments in heterchromatin that have functions, which she uses to conclude, apparently, that all of it has function. If you find a needle in a haystack, does that show that the entire haystack consists of needles?

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This is true of every single theory in science. There are always outliers and noise in the data. What matters is the signal. If the signal is much stronger than the noise then the hypothesis is supported.

Population genetics is no different than what is done in other theories and fields of science. Scientists use models to understand how the Sun works, as one example. Population genetics is just an idealized model of how genetics works in a population.

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Aren’t the oldest algae fossils also fossils of unicellular eukaryotes?

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The ones I’ve written weren’t.

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This is just a off-hand rejection of statistics.

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By my understanding, in all practical terms this is not possible. Could you explain how there could be no gene loss in a lineage for 6 million years?.

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Sorry I took so long to answer this question, but yes from an earlier study:

http://darwinsdaemon.com/Pubs/Khona16_AlgalResearch.pdf

Of the several single-celled eukaryotes, the green chlorophyte Chlamydomonas reinhardtii is preferred as a vital system in studying stress-inducible responses for two main reasons. First, it harbours a host of such stress-responsive genes; but, their functional significance in altering the metabolism for adaptation remains unexplored and second being the ease with which the physio- logical changes occurring in the cell vis-à-vis the stress can be studied [19,36]. It has been used to study responses to various abiotic stress agents such as osmolytes, temperature, irradiation, nutrient starvation, heavy metals and oxidative stressors [17,34,39,58,67,68,73,82]. Being versatile, it displays varied responses to different stress conditions…

The same article looked at a related species and mentions:

Palmelloidy was induced in Chlamydomonas eugametos in response to chloroplatinic acid [49]. Multiple layers of cell walls in these palmelloids suggested that probably the cells continue to divide in the mother cell i.e. they are unable to separate after division and remain encased in a common membrane.

It’s also interesting to note what happened when the palmelloid condition was irreversible:

Palmelloids induced after 24 h of NaCl stress took ~4 h for complete dissociation while the palmelloidy induced after 36 or 48 h of stress was found to be irreversible accompanied with cell death (data not shown).

I think what I am saying about this experiment is reasonable in view of the evidence.