Potential falsifications of the theory of evolution

Which specific mutations to produce is not a decision that the cell makes. When E. coli run out of glucose and start to starve they do not sense the presence of lactose and then mutate specific genes to produce a lactase enzyme. What E. coli do is sense starvation through DNA damage and increase the random mutation rate, some of which randomly produce an enzyme that is capable of metabolizing the lactose (as well as randomly duplicating the gene in some clones). That is what we OBSERVE when these natural engineering systems are at work.If you want to call that "sentience" then go for it, but at least understand what you are deeming to be sentient.Edited by Taq, : No reason given.

But he wasn't talking about NGE when he wrote that, he was talking about the whole of evolution. You had asked if evolution was non-random with regards to fitness. He answered no, it is definitely non-random, and in this, as I already explained in Message 765, we all agree. This is because natural selection very non-randomly selects the most fit organisms to pass their genes on to the next generation. However, what those mutational modifications to those genes actually do to improve fitness is definitely non-deterministic.Regarding NGE and determinism, as I said in Message 763, it's like an inexpert archer firing at a target and ending up with this: That the arrows hit or at least come close to the target is the part that is to some extent deterministic. The particular process of aiming an arrow at a target means that it is much more likely you'll hit the target than the car or the cat. But what part of the target you hit is much less deterministic, and what prize you'll get for hitting the target is not deterministic at all and is anyone's guess. If cells are sentient then so is your iPod.As we keep telling you, Shapiro insists on misusing terminology in ways that leave what he says open to broad misinterpretation, as you keep demonstrating.--PercyEdited by Percy, : Spelling.

Mutations are necessary, but their randomness is not. If they were Lamarckian and strictly determined by the genome and the environment, then evolution might work even better than it actually does.* But the evidence is that they aren't. The theory explains how despite the randomness of mutations w.r.t. fitness, adaptive evolution nevertheless takes place. * It is possible that the random deviations from strict "hill climbing" may be useful under certain circumstances; consider for example Lenski's bacteria, where the fixation of an apparently neutral mutation was a stepping stone to subsequent adaptation. On the other hand, why would Lamarckian optimization have to seek out local peaks by stepwise increments of fitness? As it is a purely imaginary mechanism, there is no reason why it should be limited in this way.Edited by Dr Adequate, : No reason given.

Taq writes; I understand what you are saying in re mutations and fitness. I am still going over papers & opinions including Shapiro's before I will be convinced that in fact all mutations are non-random with regard to fitness.

Shapiro wrote; I agree the biochemical systems are the source of the mutations but Shapiro goes on farther to say these biochemical systems may lead us to find what kind of guidance may be incorporated in genome change.

Taq writes; The question is how do we know the mutations that are capable of metabolizing the lactose are in fact random, couldn't they be programmed with the enzyme for that purpose?

I disagree.
I think you continue to twist Dr. Shapiro's ideas to your own ends.
And I've written to Dr. Shapiro to see if we can clear this up.

Great. I am not intentionally trying to twist Dr. shapiro's words.
What are you telling him?

We know this by a couple of routes one is a probabilistic analysis.So for example lets take a simple point mutation as the starting point. If we know the genome size and the point mutation rate, either the base rate or an increased one, then we can estimate the amount of growth/generations required before every single point mutation should have occurred. If we the plate out a specific number of cells then we can compare the number of lactose metabolising colonies that appear to estimates based on the mutation rate under the assumption of randomness. If there is a significant deviation from these estimates this would suggest some non-random phenomenon.The other method now available to us is long term longitudinal genetic studies where we can actually capture a representative snapshot of the genomes of a bacterial population over many generations and trace the origin of novel genetic traits and their evolutionary trends in the population.It is these sort of methodologies that caused early phenomena thought to be examples of directed mutation, such as in Cairns' experiments with E.coli in the 80s, to be appreciated as a result of hyper-mutability.Surely if this really was a programmed response we would expect it to have a much higher occurrence in the right conditions?TTFN,WK

They could, but they aren't. During stress the E. coli upregulate the expression of DinB which codes for an error prone polymerase that fixes gaps in the DNA (also called translesion repair). These gaps occur throughout the genome, not just in the lac gene responsible for lactose metabolism. In fact, this same SOS response also mutates ampD which is responsible for beta-lactam resistance (source). So these mutations happen throughout the genome and are not informed by the presence of lactose or beta-lactams. The enzyme simply finds damaged DNA and fixes it with a few mutations thrown in.

In the case of the SOS response in E. coli, the guidance is towards DNA gap repair by an error prone polymerase that incorporates de novo mutations.

Got an answer. That was quick!My statement is in red. Looks like Shapiro just re-iterated what I said. This, I think, is a working definition of "sentient" as used by Shapiro.I'm going to ask him something else.
Stay tuned.

I have lost all hope that we will get a straight answer from Shapiro. His answers are as dodgy as a politicians. He tries to swing any question back to his genetic engineering systems even if the question is asking about something else.

Invite him to participate in this thread and explain what he really means.--Percy

I told him about the thread and gave him the address.In the meantime, here's his reply re: random. He's bound and determined to use "highly non-random but also highly non-deterministic" instead of "random".I haven't got access to the P factor paper he mentions, but I found this one:A novel mechanism for P element homing in Drosophila, PNAS June 8, 1999 vol. 96 no. 12 6856-6861 SourceThis is literally the first sentence of that paper.