Since @colewd seems determined to derail the thread “Evidence for common ancestry,” I’ll do him a favor and start this new thread, “Evidence against common ancestry.” Let’s begin by discussing the sequence and waiting time ‘problems’ which @colewd just brought up in the other thread.
Because they’re completely made up by ID advocates, they don’t exist in the real world.
The ‘sequence problem’
The so-called ‘sequence problem’ is from a single study by Axe (2004) in which he estimated the proportion of functional β-lactamases out of all protein sequence space as 1 in 10^77. How did he do this? By taking an already crippled temperature-sensitive β-lactamase domain and mutating it until it no longer worked as a β-lactamase. Needless to say, this is a bad way to test for function in sequence space. Yet he somehow extrapolated from this that any given specified function will only exist at about 1 in 10^77 polypeptides.
It should be obvious how bad this study was for determining the proportion of functional proteins in sequence space. But it’s even worse if you consider how many other experiments have directly refuted Axe. For example, Yamauchi et al. (2002) began with a library of only 10 random polypeptides 140 amino acids in length, and were able to evolve esterase function within just six ‘generations.’ This shows that esterases exist at a rather high proportion within random sequence space.
Nakashima et al. (2007) began with a library of ~10^6 random polypeptides 140 amino acids in length, and were able to evolve DNA-binding function within just five ‘generations.’ This shows that DNA-binding proteins exist at a rather high proportion within random sequence space, thus demonstrating how transcription factors can evolve de novo.
Shahsavarian et al. (2017) began with a library of 2.7 * 10^9 random polypeptides, and found 5 different β-lactamases, showing that β-lactamases exist at a proportion of approx. 1 in 5.4 * 10^8 within random sequence space. This is especially significant because β-lactamase is precisely the enzyme that Axe (2004) looked at, showing that his conclusions are off by about 68 orders of magnitude. This is not a small error.
This research is even being used for important real-life applications. Wang et al. (2016) used the same technique, beginning with a library of 10^9 polypeptides 7 amino acids in length, and they found 7 peptides that bind selectively to ovarian cancer cells, with possible application for cancer treatment. Matsumura et al. (2010) found 19 peptides out of a library of 10^12 random sequences 16 amino acids in length with the ability to inhibit the Bcl-XL enzyme, showing that 1 in ~10^11 polypeptides of this length have this ability, with possible application for therapeutic drugs.
There are many, many more studies like this that I could have cited (for more, see @Rumraket’s post on this topic from The Skeptical Zone). But just one of these studies is enough to show that Axe is completely, utterly, horribly wrong. Many, many, many more than 1 in 10^77 random protein sequences have a specific function. Even as many as 1 in 10^8 random protein sequences have β-lactamase function, which is the specific function that Axe himself was testing for!
So it’s absolutely ridiculous to tout Axe’s paper, or any so-called ‘sequence problem,’ as evidence against common ancestry. Of course, I know that ID creationists aren’t going to let this go anytime soon (if ever), since once they get a paper published in a real peer-reviewed journal, they can’t admit that they could possibly have been wrong.
What about the so-called ‘waiting time problem’?
As it turns out, the ‘sequence problem’ and ‘waiting time problem’ are just two sides of the same coin. Every paper published on the ‘waiting time problem’ thus far has looked at the time until two (or more) pre-specified, coordinated mutations become fixed in a population. But there are many ways to achieve a desired result in real biology, as all of the studies cited above show. So the waiting time ‘problem’ is a non-problem.
However, it gets even worse. One of the recent ID papers published on this topic, by Hossjer et al. (2021), looks specifically at the waiting time in regulatory sequences. As such studies tend to do, they again assumed two pre-specified mutations were needed to achieve the desired function.
But another recent study, by Yona et al. (2018), discovered that no less than 10% of random, 100-nucleotide DNA sequences have the ability to serve as active promoters (regulatory sequences) in E. coli. Ten percent! It’s impossible to understate these findings – ten percent of all sequences 100 nucleotides in length is 10^59 sequences.
Now, I’m not saying that any one of these 10^59 sequences would suffice for whatever desired result evolution is trying to achieve (speaking figuratively – evolution isn’t a purposeful process). But when you’re dealing with this many sequences, is it really reasonable to think that only a single pair of pre-specified mutations will achieve the desired result? No, that’s utterly ridiculous. So no one should be taking these ‘waiting time problem’ publications seriously, especially not if they’re trying to make some overarching conclusion about the real biological world.
Furthermore, the ‘waiting time problem’ assumes that all of the mutations required for a change have to occur simultaneously, presumably because individually they would be deleterious. But I don’t think this is a valid assumption, since many changes in evolution occur without deleterious intermediates.
One very interesting study that examines this idea is Neme et al. (2017). They inserted completely random genes, coding for polypeptides of 65 random amino acids in length, into E. coli bacteria, and observed what happened to the bacteria as a result. What they found is that 52% of the polypeptides decreased the fitness of the host bacterium (slowing its growth), whereas 23% were neutral in effect, and 25% actually increased the fitness of the host bacterium (speeding up its growth).
The same thing was shown by Tretyachenko et al. (2017). They generated ten thousand random 100-amino-acid protein sequences and inserted them into E. coli bacteria. What they found is that the polypeptides were well-tolerated by the E. coli, and that a high proportion (~25%) in fact had defined secondary structures (α-helixes and β-sheets)! Furthermore, the random polypeptides were fairly well-ordered.
What does all this have to do with the ‘waiting time problem’? Mainly, I think it’s applicable because it shows that completely random gene sequences can exist without having any deleterious effect on the host (and indeed do so about 50% of the time). Sometimes they even have a beneficial effect. So it’s totally false to think that any mutation leading up to a functional protein will necessarily be deleterious. This invalidates the ‘waiting time problem’ entirely.
Finally, the ‘waiting time problem’ has also been shown to be false, observationally. The adaptation which originally allowed the HIV-1 group N virus to transmit to humans involved four amino acid changes, each one of which individually is deleterious, and so they all would have had to occur at once (Sauter et al. 2012).
According to Behe’s ID book The Edge of Evolution, which rests entirely on the ‘waiting time problem,’ an adaptation involving four simultaneous mutations should be at or beyond the “edge of evolution,” since (according to Behe) such a change could never have occurred in the entire 4.5 billion year history of the earth. But this change, involving four simultaneous mutations, was observed to happen in just a few decades. Thus, this piece of observational evidence shows that all ‘waiting time’ calculations must be off by many orders of magnitude, most likely for the reasons laid out above.
Conclusion
The ‘sequence problem’ and ‘waiting time problem’ are non-problems. They have been shown observationally to be wrong on many levels, and (in YEC lingo) this is an example of ‘observational science’ not ‘historical science,’ so creationists should (if they were consistent) not disagree with this.
In addition, @colewd, I’m not sure what any of this has to do with common ancestry in the first place. The original thread was about whether all organisms are related through ancestry, not whether evolution is guided or not. Those are two very different questions. Please enlighten us as to how, even if the ‘sequence problem’ and ‘waiting time problem’ are correct, this would demonstrate that all organisms do not share common ancestry.
@colewd, I am absolutely sure that you will take none of this to heart. You have shown yourself to be unwilling to consider evidence against your position time and time again, and I very much doubt that this will be the thing to change your mind. But I hope that someone somewhere will find all of this information useful and interesting.
